Haemaccel

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Emanuel Sikuler - One of the best experts on this subject based on the ideXlab platform.

  • Portal hypertension and blood viscosity
    Journal of Clinical Gastroenterology, 2007
    Co-Authors: Emanuel Sikuler
    Abstract:

    Previous studies, exploring the effect of blood viscosity on portal pressure in portal hypertensive humans and animal models, have shown conflicting results. In a series of studies, in portal vein constricted rats, we investigated effects of reduced blood viscosity on the hyperdynamic circulation, portal pressure, and vascular geometry. Blood was withdrawn at a rate of 0.3 mL/min for 15 minutes followed by 15 minutes of stabilization. The shed blood or Haemaccel was infused at the same rate and volume as used for withdrawal. Hemodynamic measurements were performed using radioactive microspheres. Blood viscosity was measured with an Ostwald viscometer. Vascular hindrance (reflecting vessel geometry) was calculated as resistance/viscosity ratio. In normal and portal hypertensive rats, acute volume replacement with Haemaccel, induced increase in systemic and splanchnic blood flows reflecting mainly changes in viscosity and not in blood vessel geometry. However, 24 hours later, in Haemaccel treated animals, an increased splanchnic arteriolar and porto-collateral vascular hindrance were observed. This indicated vasoconstriction in the porto-collateral vascular bed. The increase in portal venous inflow after acute volume restitution with Haemaccel was prevented by pretreatment with propranolol. Although, caution should be taken in extrapolating these results to humans, we would like to speculate that during a portal hypertensive-related bleeding episode: (1) volume replacement with low viscosity plasma expanders may aggravate the hyperdynamic circulation of portal hypertension. (2) Slow rate volume replacement enables hemodynamic adaptation to occur. (3) Volume replacement maybe more safe in a subject pretreated with propranolol.

  • Late hemodynamic changes following controlled hemorrhage and volume restitution with blood or Haemaccel in anesthetized portal hypertensive rats
    Journal of gastroenterology and hepatology, 2002
    Co-Authors: Nir Hilzenrat, A Yaari, Emanuel Sikuler
    Abstract:

    Background and Aim : In portal hypertensive rats, hemorrhage and acute volume restitution with Haemaccel induced increased cardiac output and portal venous inflow. In the present study, the late hemodynamic effects of this procedure were explored. Methods : Portal hypertension was induced by portal vein constriction. Blood was withdrawn 11.2 ± 3.2 days later, at a rate of 0.3 mL/min, for 15 min, followed by 15 min of stabilization. Haemaccel or blood were infused at the same rate and volume used for withdrawal. Hemodynamic measurements were performed after 24 h, using radioactive microspheres. Viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as resistance/viscosity ratio. Results : Blood viscosity of the Haemaccel group (n = 11), was lower than in the blood group (n = 11): 2.7 ± 0.2 versus 4.0 ± 0.4 (P < 0.01). Arterial pressure, cardiac output, peripheral resistance, portal pressure, portal venous inflow and splanchnic arteriolar resistance were not significantly different. Splanchnic arteriolar and portocollateral hindrance were higher in the Haemaccel group (11.7 ± 5.3 and 1.5 ± 0.6 vs 7.7 ± 3.0 and 0.9 ± 0.4 mmHg × min × 100 gram body weight/mL, respectively, P < 0.05). Conclusion : In portal hypertensive rats, vital organs perfusion, 24 h after hemorrhage and isovolemic volume restitution with Haemaccel and blood, was similar. However, in Haemaccel-transfused animals, a reduction in vascular hindrance, indicating vasoconstriction, was observed in the splanchnic organs, which drain into the portal circulation. Vasoconstriction of the portocollateral vascular bed was observed as well. We suggest that slow-rate volume replacement during a portal-hypertensive-related bleeding episode enables hemodynamic adaptation to occur. Thus, undesirable hyperdynamic changes, which may aggravate secondary bleeding, are attenuated. © 2002 Blackwell Publishing Asia Pty Ltd

  • Blood viscosity, hemodynamics and vascular hindrance in a rat model of acute controlled bleeding and volume restitution with blood or Haemaccel.
    Acta anaesthesiologica Scandinavica, 2001
    Co-Authors: Nir Hilzenrat, Arie Arish, A Yaari, Y Almog, Emanuel Sikuler
    Abstract:

    BACKGROUND: Hemorrhage and volume restitution with commercially available solutions is followed by reduced blood viscosity. Consequent hemodynamic changes may arise not only from the reduced viscosity itself but also from changes in vascular geometry induced by autoregulation processes. Vascular hindrance reflects the contribution of vascular geometry to flow. Our aim was to explore the possible effects of blood volume restitution with Haemaccel or blood, on regional blood flow and vascular geometry. METHODS: Under ketamine anesthesia, blood was withdrawn at a rate of 0.3 ml/min for 15 min followed by 15 min of stabilization. The shed blood or Haemaccel was infused at the same rate and volume as used for withdrawal. Hemodynamic measurements were performed using radioactive microspheres. Blood viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as the resistance/viscosity ratio. RESULTS: Volume replacement with Haemaccel (n=10), compared to blood (n=10), was followed by increased cardiac output and portal venous inflow (37.1 +/- 9.0 and 3.1 +/- 0.5 vs 25.9 +/- 6.8 and 2.2 +/- 0.9 ml x min(-1) x 100 g bw(-1), respectively; P

  • blood viscosity hemodynamics and vascular hindrance in a rat model of acute controlled bleeding and volume restitution with blood or Haemaccel
    Acta Anaesthesiologica Scandinavica, 2001
    Co-Authors: Nir Hilzenrat, Arie Arish, A Yaari, Y Almog, Emanuel Sikuler
    Abstract:

    BACKGROUND: Hemorrhage and volume restitution with commercially available solutions is followed by reduced blood viscosity. Consequent hemodynamic changes may arise not only from the reduced viscosity itself but also from changes in vascular geometry induced by autoregulation processes. Vascular hindrance reflects the contribution of vascular geometry to flow. Our aim was to explore the possible effects of blood volume restitution with Haemaccel or blood, on regional blood flow and vascular geometry. METHODS: Under ketamine anesthesia, blood was withdrawn at a rate of 0.3 ml/min for 15 min followed by 15 min of stabilization. The shed blood or Haemaccel was infused at the same rate and volume as used for withdrawal. Hemodynamic measurements were performed using radioactive microspheres. Blood viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as the resistance/viscosity ratio. RESULTS: Volume replacement with Haemaccel (n=10), compared to blood (n=10), was followed by increased cardiac output and portal venous inflow (37.1 +/- 9.0 and 3.1 +/- 0.5 vs 25.9 +/- 6.8 and 2.2 +/- 0.9 ml x min(-1) x 100 g bw(-1), respectively; P<0.05), decreased viscosity (2.8 +/- 1.3 vs 3.7 +/- 1.3, respectively; P<0.01) and decreased peripheral and splanchnic arteriolar resistance (3.8 +/- 1.1 and 40.9 +/- 7.6 vs 5.2 +/- 1.7 and 61.1 +/- 29.5 mmHg x ml(-1) x min x 100 g bw, respectively; P<0.05). No significant differences between the groups were observed in vascular hindrance and cardiac output distribution. CONCLUSION: Volume replacement with Haemaccel, compared to blood, induced increase in systemic and splanchnic blood flows, reflecting mainly changes in viscosity and not in blood vessel geometry. These results suggest no significant difference in overall activation of autoregulation process between volume restitution with blood or Haemaccel.

  • Systemic and splanchnic hemodynamics following hemorrhage and volume restitution with Haemaccel in portal hypertensive rats: the effect of propranolol.
    Journal of gastroenterology and hepatology, 2001
    Co-Authors: Nir Hilzenrat, Arie Arish, A Yaari, Emanuel Sikuler
    Abstract:

    Background and Aims: Recently, we found in a portal hypertensive rat model that hemorrhage and volume restitution with Haemaccel, a low viscosity plasma expander, induced an increase in cardiac output and portal venous inflow. The present study was conducted to evaluate whether pretreatment with propranolol will attenuate these hyperdynamic changes. Methods: Portal hypertension was induced by portal vein constriction. Treatment was initiated 14–21 days later. Propranolol (30 mg/kg per day) or water were administered for 7 days via a gastric gavage. Under ketamine anesthesia, 18 h after the last given dose, blood was withdrawn at a constant rate of 0.3 mL/min for 15 min followed by a 15-min stabilization. Haemaccel was infused at the same rate and volume used for withdrawal. Hemodynamic measurements were performed after volume restitution in both groups by using radioactive microspheres. Results: Eight rats were studied in each group. In the propranolol-treated animals, portal venous inflow was decreased (2.4 ± 0.8 vs 3.8 ± 0.7 mL/min per 100 g bodyweight; P < 0.01), while splanchnic arteriolar and porto-collateral resistance were increased (52.8 ± 21.0 vs 32.8 ± 13.0 and 6.0 ± 1.4 vs 4.1 ± 0.7 mmHg × min × 100 g bodyweight/mL; P < 0.05, respectively). Cardiac output, mean arterial pressure, heart rate, total peripheral resistance and portal pressure were not significantly different between the two groups. Conclusion: In this model, pretreatment with propranolol prevented the increase in portal venous inflow, which occurs following hemorrhage and volume restitution with Haemaccel. Although caution should be taken in extrapolating data from animal models to humans, our results suggest that volume replacement during a portal hypertensive-related bleeding episode may be safer in a patient treated with non-selective β-adrenoreceptor antagonists.

Nir Hilzenrat - One of the best experts on this subject based on the ideXlab platform.

  • Late hemodynamic changes following controlled hemorrhage and volume restitution with blood or Haemaccel in anesthetized portal hypertensive rats
    Journal of gastroenterology and hepatology, 2002
    Co-Authors: Nir Hilzenrat, A Yaari, Emanuel Sikuler
    Abstract:

    Background and Aim : In portal hypertensive rats, hemorrhage and acute volume restitution with Haemaccel induced increased cardiac output and portal venous inflow. In the present study, the late hemodynamic effects of this procedure were explored. Methods : Portal hypertension was induced by portal vein constriction. Blood was withdrawn 11.2 ± 3.2 days later, at a rate of 0.3 mL/min, for 15 min, followed by 15 min of stabilization. Haemaccel or blood were infused at the same rate and volume used for withdrawal. Hemodynamic measurements were performed after 24 h, using radioactive microspheres. Viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as resistance/viscosity ratio. Results : Blood viscosity of the Haemaccel group (n = 11), was lower than in the blood group (n = 11): 2.7 ± 0.2 versus 4.0 ± 0.4 (P < 0.01). Arterial pressure, cardiac output, peripheral resistance, portal pressure, portal venous inflow and splanchnic arteriolar resistance were not significantly different. Splanchnic arteriolar and portocollateral hindrance were higher in the Haemaccel group (11.7 ± 5.3 and 1.5 ± 0.6 vs 7.7 ± 3.0 and 0.9 ± 0.4 mmHg × min × 100 gram body weight/mL, respectively, P < 0.05). Conclusion : In portal hypertensive rats, vital organs perfusion, 24 h after hemorrhage and isovolemic volume restitution with Haemaccel and blood, was similar. However, in Haemaccel-transfused animals, a reduction in vascular hindrance, indicating vasoconstriction, was observed in the splanchnic organs, which drain into the portal circulation. Vasoconstriction of the portocollateral vascular bed was observed as well. We suggest that slow-rate volume replacement during a portal-hypertensive-related bleeding episode enables hemodynamic adaptation to occur. Thus, undesirable hyperdynamic changes, which may aggravate secondary bleeding, are attenuated. © 2002 Blackwell Publishing Asia Pty Ltd

  • Blood viscosity, hemodynamics and vascular hindrance in a rat model of acute controlled bleeding and volume restitution with blood or Haemaccel.
    Acta anaesthesiologica Scandinavica, 2001
    Co-Authors: Nir Hilzenrat, Arie Arish, A Yaari, Y Almog, Emanuel Sikuler
    Abstract:

    BACKGROUND: Hemorrhage and volume restitution with commercially available solutions is followed by reduced blood viscosity. Consequent hemodynamic changes may arise not only from the reduced viscosity itself but also from changes in vascular geometry induced by autoregulation processes. Vascular hindrance reflects the contribution of vascular geometry to flow. Our aim was to explore the possible effects of blood volume restitution with Haemaccel or blood, on regional blood flow and vascular geometry. METHODS: Under ketamine anesthesia, blood was withdrawn at a rate of 0.3 ml/min for 15 min followed by 15 min of stabilization. The shed blood or Haemaccel was infused at the same rate and volume as used for withdrawal. Hemodynamic measurements were performed using radioactive microspheres. Blood viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as the resistance/viscosity ratio. RESULTS: Volume replacement with Haemaccel (n=10), compared to blood (n=10), was followed by increased cardiac output and portal venous inflow (37.1 +/- 9.0 and 3.1 +/- 0.5 vs 25.9 +/- 6.8 and 2.2 +/- 0.9 ml x min(-1) x 100 g bw(-1), respectively; P

  • blood viscosity hemodynamics and vascular hindrance in a rat model of acute controlled bleeding and volume restitution with blood or Haemaccel
    Acta Anaesthesiologica Scandinavica, 2001
    Co-Authors: Nir Hilzenrat, Arie Arish, A Yaari, Y Almog, Emanuel Sikuler
    Abstract:

    BACKGROUND: Hemorrhage and volume restitution with commercially available solutions is followed by reduced blood viscosity. Consequent hemodynamic changes may arise not only from the reduced viscosity itself but also from changes in vascular geometry induced by autoregulation processes. Vascular hindrance reflects the contribution of vascular geometry to flow. Our aim was to explore the possible effects of blood volume restitution with Haemaccel or blood, on regional blood flow and vascular geometry. METHODS: Under ketamine anesthesia, blood was withdrawn at a rate of 0.3 ml/min for 15 min followed by 15 min of stabilization. The shed blood or Haemaccel was infused at the same rate and volume as used for withdrawal. Hemodynamic measurements were performed using radioactive microspheres. Blood viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as the resistance/viscosity ratio. RESULTS: Volume replacement with Haemaccel (n=10), compared to blood (n=10), was followed by increased cardiac output and portal venous inflow (37.1 +/- 9.0 and 3.1 +/- 0.5 vs 25.9 +/- 6.8 and 2.2 +/- 0.9 ml x min(-1) x 100 g bw(-1), respectively; P<0.05), decreased viscosity (2.8 +/- 1.3 vs 3.7 +/- 1.3, respectively; P<0.01) and decreased peripheral and splanchnic arteriolar resistance (3.8 +/- 1.1 and 40.9 +/- 7.6 vs 5.2 +/- 1.7 and 61.1 +/- 29.5 mmHg x ml(-1) x min x 100 g bw, respectively; P<0.05). No significant differences between the groups were observed in vascular hindrance and cardiac output distribution. CONCLUSION: Volume replacement with Haemaccel, compared to blood, induced increase in systemic and splanchnic blood flows, reflecting mainly changes in viscosity and not in blood vessel geometry. These results suggest no significant difference in overall activation of autoregulation process between volume restitution with blood or Haemaccel.

  • Systemic and splanchnic hemodynamics following hemorrhage and volume restitution with Haemaccel in portal hypertensive rats: the effect of propranolol.
    Journal of gastroenterology and hepatology, 2001
    Co-Authors: Nir Hilzenrat, Arie Arish, A Yaari, Emanuel Sikuler
    Abstract:

    Background and Aims: Recently, we found in a portal hypertensive rat model that hemorrhage and volume restitution with Haemaccel, a low viscosity plasma expander, induced an increase in cardiac output and portal venous inflow. The present study was conducted to evaluate whether pretreatment with propranolol will attenuate these hyperdynamic changes. Methods: Portal hypertension was induced by portal vein constriction. Treatment was initiated 14–21 days later. Propranolol (30 mg/kg per day) or water were administered for 7 days via a gastric gavage. Under ketamine anesthesia, 18 h after the last given dose, blood was withdrawn at a constant rate of 0.3 mL/min for 15 min followed by a 15-min stabilization. Haemaccel was infused at the same rate and volume used for withdrawal. Hemodynamic measurements were performed after volume restitution in both groups by using radioactive microspheres. Results: Eight rats were studied in each group. In the propranolol-treated animals, portal venous inflow was decreased (2.4 ± 0.8 vs 3.8 ± 0.7 mL/min per 100 g bodyweight; P < 0.01), while splanchnic arteriolar and porto-collateral resistance were increased (52.8 ± 21.0 vs 32.8 ± 13.0 and 6.0 ± 1.4 vs 4.1 ± 0.7 mmHg × min × 100 g bodyweight/mL; P < 0.05, respectively). Cardiac output, mean arterial pressure, heart rate, total peripheral resistance and portal pressure were not significantly different between the two groups. Conclusion: In this model, pretreatment with propranolol prevented the increase in portal venous inflow, which occurs following hemorrhage and volume restitution with Haemaccel. Although caution should be taken in extrapolating data from animal models to humans, our results suggest that volume replacement during a portal hypertensive-related bleeding episode may be safer in a patient treated with non-selective β-adrenoreceptor antagonists.

  • acute hemodynamic changes following hemorrhage and volume restitution using a low viscosity plasma expander in anesthetized portal hypertensive rats
    Journal of Hepatology, 1999
    Co-Authors: Nir Hilzenrat, Arie Arish, A Yaari, Emanuel Sikuler
    Abstract:

    Abstract Background/Aim: The aim of this study was to examine, in a portal hypertensive rat model, the hemodynamic changes following hemorrhage and volume restitution with blood and Haemaccel (a low viscosity, volume expander). Methods: Portal hypertension was induced by portal vein constriction. Under ketamine anesthesia, blood was withdrawn at a constant rate of 0.3 ml/min, for 15 min followed by 15 min of stabilization. The shed blood or Haemaccel was infused at the same rate and volume used for withdrawal. Hemodynamic measurements were performed using radioactive microspheres. Blood viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as the resistance/viscosity ratio. Results: Twelve rats were studied in each group. During blood withdrawal, significant reductions in arterial pressure and portal pressure were observed. Volume replacement with blood was accompanied by increased mean arterial pressure and portal pressure to baseline. Arterial pressure following volume replacement with Haemaccel was lower and portal pressure was higher than baseline (128±16 and 17.1±3.9 vs 146±13 and 15.9±3.0 mmHg, respectively; p vs 28.9±3 and 2.9±0.8 ml · min −1 · 100 g bw −1 , respectively; p vs 35.7±3.4% and 4.0±1.3, respectively; p vs 5.0±1.4 and 43.9±12.7 mmHg · ml −1 · min · 100 g bw, respectively; p Conclusion: In this model, volume replacement with Haemaccel induced an increase in cardiac output and portal venous inflow, thus preventing the reduction in portal pressure which might be expected when viscosity is reduced.

A Yaari - One of the best experts on this subject based on the ideXlab platform.

  • Late hemodynamic changes following controlled hemorrhage and volume restitution with blood or Haemaccel in anesthetized portal hypertensive rats
    Journal of gastroenterology and hepatology, 2002
    Co-Authors: Nir Hilzenrat, A Yaari, Emanuel Sikuler
    Abstract:

    Background and Aim : In portal hypertensive rats, hemorrhage and acute volume restitution with Haemaccel induced increased cardiac output and portal venous inflow. In the present study, the late hemodynamic effects of this procedure were explored. Methods : Portal hypertension was induced by portal vein constriction. Blood was withdrawn 11.2 ± 3.2 days later, at a rate of 0.3 mL/min, for 15 min, followed by 15 min of stabilization. Haemaccel or blood were infused at the same rate and volume used for withdrawal. Hemodynamic measurements were performed after 24 h, using radioactive microspheres. Viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as resistance/viscosity ratio. Results : Blood viscosity of the Haemaccel group (n = 11), was lower than in the blood group (n = 11): 2.7 ± 0.2 versus 4.0 ± 0.4 (P < 0.01). Arterial pressure, cardiac output, peripheral resistance, portal pressure, portal venous inflow and splanchnic arteriolar resistance were not significantly different. Splanchnic arteriolar and portocollateral hindrance were higher in the Haemaccel group (11.7 ± 5.3 and 1.5 ± 0.6 vs 7.7 ± 3.0 and 0.9 ± 0.4 mmHg × min × 100 gram body weight/mL, respectively, P < 0.05). Conclusion : In portal hypertensive rats, vital organs perfusion, 24 h after hemorrhage and isovolemic volume restitution with Haemaccel and blood, was similar. However, in Haemaccel-transfused animals, a reduction in vascular hindrance, indicating vasoconstriction, was observed in the splanchnic organs, which drain into the portal circulation. Vasoconstriction of the portocollateral vascular bed was observed as well. We suggest that slow-rate volume replacement during a portal-hypertensive-related bleeding episode enables hemodynamic adaptation to occur. Thus, undesirable hyperdynamic changes, which may aggravate secondary bleeding, are attenuated. © 2002 Blackwell Publishing Asia Pty Ltd

  • Blood viscosity, hemodynamics and vascular hindrance in a rat model of acute controlled bleeding and volume restitution with blood or Haemaccel.
    Acta anaesthesiologica Scandinavica, 2001
    Co-Authors: Nir Hilzenrat, Arie Arish, A Yaari, Y Almog, Emanuel Sikuler
    Abstract:

    BACKGROUND: Hemorrhage and volume restitution with commercially available solutions is followed by reduced blood viscosity. Consequent hemodynamic changes may arise not only from the reduced viscosity itself but also from changes in vascular geometry induced by autoregulation processes. Vascular hindrance reflects the contribution of vascular geometry to flow. Our aim was to explore the possible effects of blood volume restitution with Haemaccel or blood, on regional blood flow and vascular geometry. METHODS: Under ketamine anesthesia, blood was withdrawn at a rate of 0.3 ml/min for 15 min followed by 15 min of stabilization. The shed blood or Haemaccel was infused at the same rate and volume as used for withdrawal. Hemodynamic measurements were performed using radioactive microspheres. Blood viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as the resistance/viscosity ratio. RESULTS: Volume replacement with Haemaccel (n=10), compared to blood (n=10), was followed by increased cardiac output and portal venous inflow (37.1 +/- 9.0 and 3.1 +/- 0.5 vs 25.9 +/- 6.8 and 2.2 +/- 0.9 ml x min(-1) x 100 g bw(-1), respectively; P

  • blood viscosity hemodynamics and vascular hindrance in a rat model of acute controlled bleeding and volume restitution with blood or Haemaccel
    Acta Anaesthesiologica Scandinavica, 2001
    Co-Authors: Nir Hilzenrat, Arie Arish, A Yaari, Y Almog, Emanuel Sikuler
    Abstract:

    BACKGROUND: Hemorrhage and volume restitution with commercially available solutions is followed by reduced blood viscosity. Consequent hemodynamic changes may arise not only from the reduced viscosity itself but also from changes in vascular geometry induced by autoregulation processes. Vascular hindrance reflects the contribution of vascular geometry to flow. Our aim was to explore the possible effects of blood volume restitution with Haemaccel or blood, on regional blood flow and vascular geometry. METHODS: Under ketamine anesthesia, blood was withdrawn at a rate of 0.3 ml/min for 15 min followed by 15 min of stabilization. The shed blood or Haemaccel was infused at the same rate and volume as used for withdrawal. Hemodynamic measurements were performed using radioactive microspheres. Blood viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as the resistance/viscosity ratio. RESULTS: Volume replacement with Haemaccel (n=10), compared to blood (n=10), was followed by increased cardiac output and portal venous inflow (37.1 +/- 9.0 and 3.1 +/- 0.5 vs 25.9 +/- 6.8 and 2.2 +/- 0.9 ml x min(-1) x 100 g bw(-1), respectively; P<0.05), decreased viscosity (2.8 +/- 1.3 vs 3.7 +/- 1.3, respectively; P<0.01) and decreased peripheral and splanchnic arteriolar resistance (3.8 +/- 1.1 and 40.9 +/- 7.6 vs 5.2 +/- 1.7 and 61.1 +/- 29.5 mmHg x ml(-1) x min x 100 g bw, respectively; P<0.05). No significant differences between the groups were observed in vascular hindrance and cardiac output distribution. CONCLUSION: Volume replacement with Haemaccel, compared to blood, induced increase in systemic and splanchnic blood flows, reflecting mainly changes in viscosity and not in blood vessel geometry. These results suggest no significant difference in overall activation of autoregulation process between volume restitution with blood or Haemaccel.

  • Systemic and splanchnic hemodynamics following hemorrhage and volume restitution with Haemaccel in portal hypertensive rats: the effect of propranolol.
    Journal of gastroenterology and hepatology, 2001
    Co-Authors: Nir Hilzenrat, Arie Arish, A Yaari, Emanuel Sikuler
    Abstract:

    Background and Aims: Recently, we found in a portal hypertensive rat model that hemorrhage and volume restitution with Haemaccel, a low viscosity plasma expander, induced an increase in cardiac output and portal venous inflow. The present study was conducted to evaluate whether pretreatment with propranolol will attenuate these hyperdynamic changes. Methods: Portal hypertension was induced by portal vein constriction. Treatment was initiated 14–21 days later. Propranolol (30 mg/kg per day) or water were administered for 7 days via a gastric gavage. Under ketamine anesthesia, 18 h after the last given dose, blood was withdrawn at a constant rate of 0.3 mL/min for 15 min followed by a 15-min stabilization. Haemaccel was infused at the same rate and volume used for withdrawal. Hemodynamic measurements were performed after volume restitution in both groups by using radioactive microspheres. Results: Eight rats were studied in each group. In the propranolol-treated animals, portal venous inflow was decreased (2.4 ± 0.8 vs 3.8 ± 0.7 mL/min per 100 g bodyweight; P < 0.01), while splanchnic arteriolar and porto-collateral resistance were increased (52.8 ± 21.0 vs 32.8 ± 13.0 and 6.0 ± 1.4 vs 4.1 ± 0.7 mmHg × min × 100 g bodyweight/mL; P < 0.05, respectively). Cardiac output, mean arterial pressure, heart rate, total peripheral resistance and portal pressure were not significantly different between the two groups. Conclusion: In this model, pretreatment with propranolol prevented the increase in portal venous inflow, which occurs following hemorrhage and volume restitution with Haemaccel. Although caution should be taken in extrapolating data from animal models to humans, our results suggest that volume replacement during a portal hypertensive-related bleeding episode may be safer in a patient treated with non-selective β-adrenoreceptor antagonists.

  • acute hemodynamic changes following hemorrhage and volume restitution using a low viscosity plasma expander in anesthetized portal hypertensive rats
    Journal of Hepatology, 1999
    Co-Authors: Nir Hilzenrat, Arie Arish, A Yaari, Emanuel Sikuler
    Abstract:

    Abstract Background/Aim: The aim of this study was to examine, in a portal hypertensive rat model, the hemodynamic changes following hemorrhage and volume restitution with blood and Haemaccel (a low viscosity, volume expander). Methods: Portal hypertension was induced by portal vein constriction. Under ketamine anesthesia, blood was withdrawn at a constant rate of 0.3 ml/min, for 15 min followed by 15 min of stabilization. The shed blood or Haemaccel was infused at the same rate and volume used for withdrawal. Hemodynamic measurements were performed using radioactive microspheres. Blood viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as the resistance/viscosity ratio. Results: Twelve rats were studied in each group. During blood withdrawal, significant reductions in arterial pressure and portal pressure were observed. Volume replacement with blood was accompanied by increased mean arterial pressure and portal pressure to baseline. Arterial pressure following volume replacement with Haemaccel was lower and portal pressure was higher than baseline (128±16 and 17.1±3.9 vs 146±13 and 15.9±3.0 mmHg, respectively; p vs 28.9±3 and 2.9±0.8 ml · min −1 · 100 g bw −1 , respectively; p vs 35.7±3.4% and 4.0±1.3, respectively; p vs 5.0±1.4 and 43.9±12.7 mmHg · ml −1 · min · 100 g bw, respectively; p Conclusion: In this model, volume replacement with Haemaccel induced an increase in cardiac output and portal venous inflow, thus preventing the reduction in portal pressure which might be expected when viscosity is reduced.

Arie Arish - One of the best experts on this subject based on the ideXlab platform.

  • Blood viscosity, hemodynamics and vascular hindrance in a rat model of acute controlled bleeding and volume restitution with blood or Haemaccel.
    Acta anaesthesiologica Scandinavica, 2001
    Co-Authors: Nir Hilzenrat, Arie Arish, A Yaari, Y Almog, Emanuel Sikuler
    Abstract:

    BACKGROUND: Hemorrhage and volume restitution with commercially available solutions is followed by reduced blood viscosity. Consequent hemodynamic changes may arise not only from the reduced viscosity itself but also from changes in vascular geometry induced by autoregulation processes. Vascular hindrance reflects the contribution of vascular geometry to flow. Our aim was to explore the possible effects of blood volume restitution with Haemaccel or blood, on regional blood flow and vascular geometry. METHODS: Under ketamine anesthesia, blood was withdrawn at a rate of 0.3 ml/min for 15 min followed by 15 min of stabilization. The shed blood or Haemaccel was infused at the same rate and volume as used for withdrawal. Hemodynamic measurements were performed using radioactive microspheres. Blood viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as the resistance/viscosity ratio. RESULTS: Volume replacement with Haemaccel (n=10), compared to blood (n=10), was followed by increased cardiac output and portal venous inflow (37.1 +/- 9.0 and 3.1 +/- 0.5 vs 25.9 +/- 6.8 and 2.2 +/- 0.9 ml x min(-1) x 100 g bw(-1), respectively; P

  • blood viscosity hemodynamics and vascular hindrance in a rat model of acute controlled bleeding and volume restitution with blood or Haemaccel
    Acta Anaesthesiologica Scandinavica, 2001
    Co-Authors: Nir Hilzenrat, Arie Arish, A Yaari, Y Almog, Emanuel Sikuler
    Abstract:

    BACKGROUND: Hemorrhage and volume restitution with commercially available solutions is followed by reduced blood viscosity. Consequent hemodynamic changes may arise not only from the reduced viscosity itself but also from changes in vascular geometry induced by autoregulation processes. Vascular hindrance reflects the contribution of vascular geometry to flow. Our aim was to explore the possible effects of blood volume restitution with Haemaccel or blood, on regional blood flow and vascular geometry. METHODS: Under ketamine anesthesia, blood was withdrawn at a rate of 0.3 ml/min for 15 min followed by 15 min of stabilization. The shed blood or Haemaccel was infused at the same rate and volume as used for withdrawal. Hemodynamic measurements were performed using radioactive microspheres. Blood viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as the resistance/viscosity ratio. RESULTS: Volume replacement with Haemaccel (n=10), compared to blood (n=10), was followed by increased cardiac output and portal venous inflow (37.1 +/- 9.0 and 3.1 +/- 0.5 vs 25.9 +/- 6.8 and 2.2 +/- 0.9 ml x min(-1) x 100 g bw(-1), respectively; P<0.05), decreased viscosity (2.8 +/- 1.3 vs 3.7 +/- 1.3, respectively; P<0.01) and decreased peripheral and splanchnic arteriolar resistance (3.8 +/- 1.1 and 40.9 +/- 7.6 vs 5.2 +/- 1.7 and 61.1 +/- 29.5 mmHg x ml(-1) x min x 100 g bw, respectively; P<0.05). No significant differences between the groups were observed in vascular hindrance and cardiac output distribution. CONCLUSION: Volume replacement with Haemaccel, compared to blood, induced increase in systemic and splanchnic blood flows, reflecting mainly changes in viscosity and not in blood vessel geometry. These results suggest no significant difference in overall activation of autoregulation process between volume restitution with blood or Haemaccel.

  • Systemic and splanchnic hemodynamics following hemorrhage and volume restitution with Haemaccel in portal hypertensive rats: the effect of propranolol.
    Journal of gastroenterology and hepatology, 2001
    Co-Authors: Nir Hilzenrat, Arie Arish, A Yaari, Emanuel Sikuler
    Abstract:

    Background and Aims: Recently, we found in a portal hypertensive rat model that hemorrhage and volume restitution with Haemaccel, a low viscosity plasma expander, induced an increase in cardiac output and portal venous inflow. The present study was conducted to evaluate whether pretreatment with propranolol will attenuate these hyperdynamic changes. Methods: Portal hypertension was induced by portal vein constriction. Treatment was initiated 14–21 days later. Propranolol (30 mg/kg per day) or water were administered for 7 days via a gastric gavage. Under ketamine anesthesia, 18 h after the last given dose, blood was withdrawn at a constant rate of 0.3 mL/min for 15 min followed by a 15-min stabilization. Haemaccel was infused at the same rate and volume used for withdrawal. Hemodynamic measurements were performed after volume restitution in both groups by using radioactive microspheres. Results: Eight rats were studied in each group. In the propranolol-treated animals, portal venous inflow was decreased (2.4 ± 0.8 vs 3.8 ± 0.7 mL/min per 100 g bodyweight; P < 0.01), while splanchnic arteriolar and porto-collateral resistance were increased (52.8 ± 21.0 vs 32.8 ± 13.0 and 6.0 ± 1.4 vs 4.1 ± 0.7 mmHg × min × 100 g bodyweight/mL; P < 0.05, respectively). Cardiac output, mean arterial pressure, heart rate, total peripheral resistance and portal pressure were not significantly different between the two groups. Conclusion: In this model, pretreatment with propranolol prevented the increase in portal venous inflow, which occurs following hemorrhage and volume restitution with Haemaccel. Although caution should be taken in extrapolating data from animal models to humans, our results suggest that volume replacement during a portal hypertensive-related bleeding episode may be safer in a patient treated with non-selective β-adrenoreceptor antagonists.

  • acute hemodynamic changes following hemorrhage and volume restitution using a low viscosity plasma expander in anesthetized portal hypertensive rats
    Journal of Hepatology, 1999
    Co-Authors: Nir Hilzenrat, Arie Arish, A Yaari, Emanuel Sikuler
    Abstract:

    Abstract Background/Aim: The aim of this study was to examine, in a portal hypertensive rat model, the hemodynamic changes following hemorrhage and volume restitution with blood and Haemaccel (a low viscosity, volume expander). Methods: Portal hypertension was induced by portal vein constriction. Under ketamine anesthesia, blood was withdrawn at a constant rate of 0.3 ml/min, for 15 min followed by 15 min of stabilization. The shed blood or Haemaccel was infused at the same rate and volume used for withdrawal. Hemodynamic measurements were performed using radioactive microspheres. Blood viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as the resistance/viscosity ratio. Results: Twelve rats were studied in each group. During blood withdrawal, significant reductions in arterial pressure and portal pressure were observed. Volume replacement with blood was accompanied by increased mean arterial pressure and portal pressure to baseline. Arterial pressure following volume replacement with Haemaccel was lower and portal pressure was higher than baseline (128±16 and 17.1±3.9 vs 146±13 and 15.9±3.0 mmHg, respectively; p vs 28.9±3 and 2.9±0.8 ml · min −1 · 100 g bw −1 , respectively; p vs 35.7±3.4% and 4.0±1.3, respectively; p vs 5.0±1.4 and 43.9±12.7 mmHg · ml −1 · min · 100 g bw, respectively; p Conclusion: In this model, volume replacement with Haemaccel induced an increase in cardiac output and portal venous inflow, thus preventing the reduction in portal pressure which might be expected when viscosity is reduced.

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  • Blood viscosity, hemodynamics and vascular hindrance in a rat model of acute controlled bleeding and volume restitution with blood or Haemaccel.
    Acta anaesthesiologica Scandinavica, 2001
    Co-Authors: Nir Hilzenrat, Arie Arish, A Yaari, Y Almog, Emanuel Sikuler
    Abstract:

    BACKGROUND: Hemorrhage and volume restitution with commercially available solutions is followed by reduced blood viscosity. Consequent hemodynamic changes may arise not only from the reduced viscosity itself but also from changes in vascular geometry induced by autoregulation processes. Vascular hindrance reflects the contribution of vascular geometry to flow. Our aim was to explore the possible effects of blood volume restitution with Haemaccel or blood, on regional blood flow and vascular geometry. METHODS: Under ketamine anesthesia, blood was withdrawn at a rate of 0.3 ml/min for 15 min followed by 15 min of stabilization. The shed blood or Haemaccel was infused at the same rate and volume as used for withdrawal. Hemodynamic measurements were performed using radioactive microspheres. Blood viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as the resistance/viscosity ratio. RESULTS: Volume replacement with Haemaccel (n=10), compared to blood (n=10), was followed by increased cardiac output and portal venous inflow (37.1 +/- 9.0 and 3.1 +/- 0.5 vs 25.9 +/- 6.8 and 2.2 +/- 0.9 ml x min(-1) x 100 g bw(-1), respectively; P

  • blood viscosity hemodynamics and vascular hindrance in a rat model of acute controlled bleeding and volume restitution with blood or Haemaccel
    Acta Anaesthesiologica Scandinavica, 2001
    Co-Authors: Nir Hilzenrat, Arie Arish, A Yaari, Y Almog, Emanuel Sikuler
    Abstract:

    BACKGROUND: Hemorrhage and volume restitution with commercially available solutions is followed by reduced blood viscosity. Consequent hemodynamic changes may arise not only from the reduced viscosity itself but also from changes in vascular geometry induced by autoregulation processes. Vascular hindrance reflects the contribution of vascular geometry to flow. Our aim was to explore the possible effects of blood volume restitution with Haemaccel or blood, on regional blood flow and vascular geometry. METHODS: Under ketamine anesthesia, blood was withdrawn at a rate of 0.3 ml/min for 15 min followed by 15 min of stabilization. The shed blood or Haemaccel was infused at the same rate and volume as used for withdrawal. Hemodynamic measurements were performed using radioactive microspheres. Blood viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as the resistance/viscosity ratio. RESULTS: Volume replacement with Haemaccel (n=10), compared to blood (n=10), was followed by increased cardiac output and portal venous inflow (37.1 +/- 9.0 and 3.1 +/- 0.5 vs 25.9 +/- 6.8 and 2.2 +/- 0.9 ml x min(-1) x 100 g bw(-1), respectively; P<0.05), decreased viscosity (2.8 +/- 1.3 vs 3.7 +/- 1.3, respectively; P<0.01) and decreased peripheral and splanchnic arteriolar resistance (3.8 +/- 1.1 and 40.9 +/- 7.6 vs 5.2 +/- 1.7 and 61.1 +/- 29.5 mmHg x ml(-1) x min x 100 g bw, respectively; P<0.05). No significant differences between the groups were observed in vascular hindrance and cardiac output distribution. CONCLUSION: Volume replacement with Haemaccel, compared to blood, induced increase in systemic and splanchnic blood flows, reflecting mainly changes in viscosity and not in blood vessel geometry. These results suggest no significant difference in overall activation of autoregulation process between volume restitution with blood or Haemaccel.