The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Daniel L Traber - One of the best experts on this subject based on the ideXlab platform.
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pyridoxalated hemoglobin polyoxyethylene conjugate reverses Hyperdynamic Circulation in septic sheep
Journal of Applied Physiology, 1998Co-Authors: Hans G Bone, Paul J Schenarts, Roy Mcguire, Lillian D Traber, Stefanie R Fischer, Daniel L TraberAbstract:We investigated the effects of modified hemoglobin on regional blood flow and function of different organs during Hyperdynamic sepsis. Fourteen sheep were surgically prepared for the study. After a...
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oxalated pyridoxalated hemoglobin polyoxyethylene conjugate normalizes the Hyperdynamic Circulation in septic sheep
Critical Care Medicine, 1997Co-Authors: Hans G Bone, Paul J Schenarts, Michael Booke, Roy Mcguire, Donald Harper, Lillian D Traber, Daniel L TraberAbstract:Objectives Excessive production of nitric oxide significantly contributes to the Hyperdynamic state associated with sepsis. The ability of hemoglobin to scavenge nitric oxide may therefore be beneficial in the treatment of sepsis. In this study, we determined the effects of different doses of the modified human pyridoxalated hemoglobin polyoxyethylene conjugate in an ovine model of Hyperdynamic sepsis. Design Prospective, experimental study. Setting Large animal research laboratory at a university medical center. Interventions Sheep (n = 23) were surgically prepared for chronic study. After a 5-day recovery period, all animals received a continuous infusion of live Pseudomonas aeruginosa (2.5 x 106 colony-forming units/min) for the next 48 hrs. After 24 hrs of sepsis, the animals were divided into four groups: a) six sheep were used as controls and received a bolus of 200-mL vehicle; b) three sheep received a bolus of 50 mg/kg hemoglobin; c) six sheep received 100 mg/kg of hemoglobin; d) six sheep received 200 mg/kg of hemoglobin. Measurements and Main Results All animals that survived the first 24 hrs of sepsis (n = 21) developed a Hyperdynamic Circulation. All three doses of hemoglobin reversed this Hyperdynamic state by increasing mean arterial pressure and systemic vascular resistance while decreasing cardiac index. Pulmonary arterial pressure increased after hemoglobin infusion. Increased pulmonary arterial pressure did not affect arterial oxygen saturation nor result in the development of pulmonary edema. Infusion of hemoglobin also caused a 30-fold increase in endothelin-1 plasma concentrations and significantly decreased nitrate and nitrite plasma concentrations. Conclusions The infusion of low doses of pyridoxalated hemoglobin polyoxyethylene conjugate in septic sheep reverses the Hyperdynamic circulatory state. An increase in pulmonary arterial pressure was the only observed hemodynamic side effect; changes in the structure or function of other organ systems, or their biochemical correlates were not investigated in this study. In addition to a possible nitric oxide scavenging effect, pyridoxalated hemoglobin polyoxyethylene may affect the nitric oxide synthase and endothelin systems. (Crit Care Med 1997; 25:1010-1018)
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use of nitric oxide synthase inhibitors to reverse Hyperdynamic Circulation and mof
1995Co-Authors: Michael Booke, L D Traber, Daniel L TraberAbstract:Sepsis is the leading cause of morbidity and mortality in critically ill patients [1], The number of cases of this lethal syndrome is increasing as more patients are immunosuppressed, treated with invasive techniques, and bacteria have become refractory to antibiotics [2, 3]. In the US, more than 400000 cases of sepsis are reported each year, and 50% of these patients die during their course of illness [1]. Death occurs mostly within 24 h after diagnosis and is the result of persistent hypotension.
Hans G Bone - One of the best experts on this subject based on the ideXlab platform.
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pyridoxalated hemoglobin polyoxyethylene conjugate reverses Hyperdynamic Circulation in septic sheep
Journal of Applied Physiology, 1998Co-Authors: Hans G Bone, Paul J Schenarts, Roy Mcguire, Lillian D Traber, Stefanie R Fischer, Daniel L TraberAbstract:We investigated the effects of modified hemoglobin on regional blood flow and function of different organs during Hyperdynamic sepsis. Fourteen sheep were surgically prepared for the study. After a...
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oxalated pyridoxalated hemoglobin polyoxyethylene conjugate normalizes the Hyperdynamic Circulation in septic sheep
Critical Care Medicine, 1997Co-Authors: Hans G Bone, Paul J Schenarts, Michael Booke, Roy Mcguire, Donald Harper, Lillian D Traber, Daniel L TraberAbstract:Objectives Excessive production of nitric oxide significantly contributes to the Hyperdynamic state associated with sepsis. The ability of hemoglobin to scavenge nitric oxide may therefore be beneficial in the treatment of sepsis. In this study, we determined the effects of different doses of the modified human pyridoxalated hemoglobin polyoxyethylene conjugate in an ovine model of Hyperdynamic sepsis. Design Prospective, experimental study. Setting Large animal research laboratory at a university medical center. Interventions Sheep (n = 23) were surgically prepared for chronic study. After a 5-day recovery period, all animals received a continuous infusion of live Pseudomonas aeruginosa (2.5 x 106 colony-forming units/min) for the next 48 hrs. After 24 hrs of sepsis, the animals were divided into four groups: a) six sheep were used as controls and received a bolus of 200-mL vehicle; b) three sheep received a bolus of 50 mg/kg hemoglobin; c) six sheep received 100 mg/kg of hemoglobin; d) six sheep received 200 mg/kg of hemoglobin. Measurements and Main Results All animals that survived the first 24 hrs of sepsis (n = 21) developed a Hyperdynamic Circulation. All three doses of hemoglobin reversed this Hyperdynamic state by increasing mean arterial pressure and systemic vascular resistance while decreasing cardiac index. Pulmonary arterial pressure increased after hemoglobin infusion. Increased pulmonary arterial pressure did not affect arterial oxygen saturation nor result in the development of pulmonary edema. Infusion of hemoglobin also caused a 30-fold increase in endothelin-1 plasma concentrations and significantly decreased nitrate and nitrite plasma concentrations. Conclusions The infusion of low doses of pyridoxalated hemoglobin polyoxyethylene conjugate in septic sheep reverses the Hyperdynamic circulatory state. An increase in pulmonary arterial pressure was the only observed hemodynamic side effect; changes in the structure or function of other organ systems, or their biochemical correlates were not investigated in this study. In addition to a possible nitric oxide scavenging effect, pyridoxalated hemoglobin polyoxyethylene may affect the nitric oxide synthase and endothelin systems. (Crit Care Med 1997; 25:1010-1018)
Roberto J. Groszmann - One of the best experts on this subject based on the ideXlab platform.
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the Hyperdynamic Circulation of chronic liver diseases from the patient to the molecule
Hepatology, 2006Co-Authors: Yasuko Iwakiri, Roberto J. GroszmannAbstract:The Hyperdynamic circulatory syndrome observed in chronic liver diseases is a great example of research that originated from clinical observations and progressed in the last 50 years from the patient to the experimental laboratory. Our knowledge has evolved from the patient to the molecule, using experimental models that serve as a source for understanding the complex pathophysiological mechanisms that govern this complex syndrome. We now know that progressive vasodilatation is central to the detrimental effects observed in multiple organs. Although nitric oxide has been shown to be the primary vasodilator molecule in these effects, other molecules also participate in the complex mechanisms of vasodilatation. This review summarizes three major areas: first, clinical observation in patients; second, experimental models used to study the Hyperdynamic circulatory syndrome; and third, the vasodilator molecules that play roles in vascular abnormalities observed in portal hypertension. (Hepatology 2006;43:S121–S131.)
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the Hyperdynamic Circulation of chronic liver diseases from the patient to the molecule
Hepatology, 2006Co-Authors: Yasuko Iwakiri, Roberto J. GroszmannAbstract:The Hyperdynamic circulatory syndrome observed in chronic liver diseases is a great example of research that originated from clinical observations and progressed in the last 50 years from the patient to the experimental laboratory. Our knowledge has evolved from the patient to the molecule, using experimental models that serve as a source for understanding the complex pathophysiological mechanisms that govern this complex syndrome. We now know that progressive vasodilatation is central to the detrimental effects observed in multiple organs. Although nitric oxide has been shown to be the primary vasodilator molecule in these effects, other molecules also participate in the complex mechanisms of vasodilatation. This review summarizes three major areas: first, clinical observation in patients; second, experimental models used to study the Hyperdynamic circulatory syndrome; and third, the vasodilator molecules that play roles in vascular abnormalities observed in portal hypertension.
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mice with targeted deletion of enos develop Hyperdynamic Circulation associated with portal hypertension
American Journal of Physiology-gastrointestinal and Liver Physiology, 2002Co-Authors: Yasuko Iwakiri, Roberto J. Groszmann, Gregory W Cadelina, William C SessaAbstract:Systemic vasodilation is the initiating event of the Hyperdynamic circulatory state, being most likely triggered by increased levels of vasodilators, primarily nitric oxide (NO). Endothelial NO syn...
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tumor necrosis factor α a major contributor to the Hyperdynamic Circulation in prehepatic portal hypertensive rats
Gastroenterology, 1995Co-Authors: Juan Carlos Lopeztalavera, William W Merrill, Roberto J. GroszmannAbstract:Abstract Background/Aims: Portal hypertension is often accompanied by a Hyperdynamic circulatory syndrome. Tumor necrosis factor (TNF) α causes vasodilatation and a Hyperdynamic state in mammals by activating nitric oxide synthesis. The aim of this study was to investigate whether TNF-α plays a role in developing the Hyperdynamic syndrome in portal hypertension. Methods: Portal-hypertensive rats, induced by partial ligation of the portal vein (PVL), were used. In experiment 1, rats that underwent PVL were treated with polyclonal anti-mouse TNF-α or placebo intravenously the same day of the PVL operation and 24 hours before hemodynamic studies. Hemodynamic studies were performed 5 days after PVL. In experiment 2, rats that underwent PVL received anti-TNF-α or placebo intravenously 3 days and 24 hours before hemodynamics as in experiment 1. Hemodynamics were performed 14 days after the PVL operation. TNF-α blood levels were measured using a bioassay. Results: Anti-TNF-α treatment induced a significant increase in mean arterial pressure, heart rate, and systemic vascular resistance and a significant decrease in cardiac index, portal pressure, and TNF-α levels in comparison with placebo animals. No significant effects were observed in sham rats. Conclusions:Anti-TNF-α treatment in rats that underwent PVL significantly blunts the development of the Hyperdynamic Circulation and reduces portal pressure. TNF-α may play a role in the hemodynamic abnormalities of portal hypertension.
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liver pancreas and biliary tract tumor necrosis factor a major contributor to the Hyperdynamic Circulation in prehepatic portal hypertensive rats
1995Co-Authors: Juan Carlos Lopeztalavera, William W Merrill, Roberto J. GroszmannAbstract:Background/Aims: Portal hypertension is often accompanied by a Hyperdynamic circulatory syndrome. Tumor necrosis factor (TNF) (~ causes vasodilatation and a Hyperdynamic state in mammals by activating nitric oxide synthesis. The aim of this study was to investigate whether TNF-~ plays a role in developing the Hyperdynamic syndrome in portal hypertension. Methods: Portal-hypertensive rats, induced by partial ligation of the portal vein (PVL), were used. In experiment 1, rats that underwent PVL were treated with polyclonal anti-mouse TNF-~ or placebo intravenously the same day of the PVL operation and 24 hours before hemodynamic studies. Hemodynamic studies were performed 5 days after PVL. In experiment 2, rats that underwent PVL received anti-TNF-¢ or placebo intravenously 3 days and 24 hours before hemodynamics as in experiment 1. Hemodynamics were performed 14 days after the PVL operation. TNF-~ blood levels were measured using a bioassay. Results: Anti-TNF-~ treatment induced a significant increase in mean arterial pressure, heart rate, and systemic vascular resistance and a significant decrease in cardiac index, portal pressure, and TNF-(~ levels in comparison with placebo animals. No significant effects were observed in sham rats. Conclusions: Anti-TNF-~ treatment in rats that underwent PVL significantly blunts the development of the Hyperdynamic Circulation and reduces portal pressure. TNFmay play a role in the hemodynamic abnormalities of portal hypertension,
Roy Mcguire - One of the best experts on this subject based on the ideXlab platform.
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pyridoxalated hemoglobin polyoxyethylene conjugate reverses Hyperdynamic Circulation in septic sheep
Journal of Applied Physiology, 1998Co-Authors: Hans G Bone, Paul J Schenarts, Roy Mcguire, Lillian D Traber, Stefanie R Fischer, Daniel L TraberAbstract:We investigated the effects of modified hemoglobin on regional blood flow and function of different organs during Hyperdynamic sepsis. Fourteen sheep were surgically prepared for the study. After a...
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oxalated pyridoxalated hemoglobin polyoxyethylene conjugate normalizes the Hyperdynamic Circulation in septic sheep
Critical Care Medicine, 1997Co-Authors: Hans G Bone, Paul J Schenarts, Michael Booke, Roy Mcguire, Donald Harper, Lillian D Traber, Daniel L TraberAbstract:Objectives Excessive production of nitric oxide significantly contributes to the Hyperdynamic state associated with sepsis. The ability of hemoglobin to scavenge nitric oxide may therefore be beneficial in the treatment of sepsis. In this study, we determined the effects of different doses of the modified human pyridoxalated hemoglobin polyoxyethylene conjugate in an ovine model of Hyperdynamic sepsis. Design Prospective, experimental study. Setting Large animal research laboratory at a university medical center. Interventions Sheep (n = 23) were surgically prepared for chronic study. After a 5-day recovery period, all animals received a continuous infusion of live Pseudomonas aeruginosa (2.5 x 106 colony-forming units/min) for the next 48 hrs. After 24 hrs of sepsis, the animals were divided into four groups: a) six sheep were used as controls and received a bolus of 200-mL vehicle; b) three sheep received a bolus of 50 mg/kg hemoglobin; c) six sheep received 100 mg/kg of hemoglobin; d) six sheep received 200 mg/kg of hemoglobin. Measurements and Main Results All animals that survived the first 24 hrs of sepsis (n = 21) developed a Hyperdynamic Circulation. All three doses of hemoglobin reversed this Hyperdynamic state by increasing mean arterial pressure and systemic vascular resistance while decreasing cardiac index. Pulmonary arterial pressure increased after hemoglobin infusion. Increased pulmonary arterial pressure did not affect arterial oxygen saturation nor result in the development of pulmonary edema. Infusion of hemoglobin also caused a 30-fold increase in endothelin-1 plasma concentrations and significantly decreased nitrate and nitrite plasma concentrations. Conclusions The infusion of low doses of pyridoxalated hemoglobin polyoxyethylene conjugate in septic sheep reverses the Hyperdynamic circulatory state. An increase in pulmonary arterial pressure was the only observed hemodynamic side effect; changes in the structure or function of other organ systems, or their biochemical correlates were not investigated in this study. In addition to a possible nitric oxide scavenging effect, pyridoxalated hemoglobin polyoxyethylene may affect the nitric oxide synthase and endothelin systems. (Crit Care Med 1997; 25:1010-1018)
Paul J Schenarts - One of the best experts on this subject based on the ideXlab platform.
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pyridoxalated hemoglobin polyoxyethylene conjugate reverses Hyperdynamic Circulation in septic sheep
Journal of Applied Physiology, 1998Co-Authors: Hans G Bone, Paul J Schenarts, Roy Mcguire, Lillian D Traber, Stefanie R Fischer, Daniel L TraberAbstract:We investigated the effects of modified hemoglobin on regional blood flow and function of different organs during Hyperdynamic sepsis. Fourteen sheep were surgically prepared for the study. After a...
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oxalated pyridoxalated hemoglobin polyoxyethylene conjugate normalizes the Hyperdynamic Circulation in septic sheep
Critical Care Medicine, 1997Co-Authors: Hans G Bone, Paul J Schenarts, Michael Booke, Roy Mcguire, Donald Harper, Lillian D Traber, Daniel L TraberAbstract:Objectives Excessive production of nitric oxide significantly contributes to the Hyperdynamic state associated with sepsis. The ability of hemoglobin to scavenge nitric oxide may therefore be beneficial in the treatment of sepsis. In this study, we determined the effects of different doses of the modified human pyridoxalated hemoglobin polyoxyethylene conjugate in an ovine model of Hyperdynamic sepsis. Design Prospective, experimental study. Setting Large animal research laboratory at a university medical center. Interventions Sheep (n = 23) were surgically prepared for chronic study. After a 5-day recovery period, all animals received a continuous infusion of live Pseudomonas aeruginosa (2.5 x 106 colony-forming units/min) for the next 48 hrs. After 24 hrs of sepsis, the animals were divided into four groups: a) six sheep were used as controls and received a bolus of 200-mL vehicle; b) three sheep received a bolus of 50 mg/kg hemoglobin; c) six sheep received 100 mg/kg of hemoglobin; d) six sheep received 200 mg/kg of hemoglobin. Measurements and Main Results All animals that survived the first 24 hrs of sepsis (n = 21) developed a Hyperdynamic Circulation. All three doses of hemoglobin reversed this Hyperdynamic state by increasing mean arterial pressure and systemic vascular resistance while decreasing cardiac index. Pulmonary arterial pressure increased after hemoglobin infusion. Increased pulmonary arterial pressure did not affect arterial oxygen saturation nor result in the development of pulmonary edema. Infusion of hemoglobin also caused a 30-fold increase in endothelin-1 plasma concentrations and significantly decreased nitrate and nitrite plasma concentrations. Conclusions The infusion of low doses of pyridoxalated hemoglobin polyoxyethylene conjugate in septic sheep reverses the Hyperdynamic circulatory state. An increase in pulmonary arterial pressure was the only observed hemodynamic side effect; changes in the structure or function of other organ systems, or their biochemical correlates were not investigated in this study. In addition to a possible nitric oxide scavenging effect, pyridoxalated hemoglobin polyoxyethylene may affect the nitric oxide synthase and endothelin systems. (Crit Care Med 1997; 25:1010-1018)