The Experts below are selected from a list of 138 Experts worldwide ranked by ideXlab platform
Toshishige Shibamoto - One of the best experts on this subject based on the ideXlab platform.
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biphasic renal sympathetic response to Hemorrhagic Hypotension in mice
Shock, 2017Co-Authors: Tao Zhang, Mamoru Tanida, Kunitoshi Uchida, Yoshiro Suzuki, Wei Yang, Yuhichi Kuda, Yasutaka Kurata, Makoto Tominaga, Toshishige ShibamotoAbstract:ABSTRACTAim:The inhibitory responses of renal sympathetic nerve activity (RSNA) and heart rate (HR) to sustained Hemorrhagic shock occurred in anesthetized rats, but have not yet been determined in mice. Here, we investigated the responses of RSNA and HR to Hemorrhagic Hypotension in anesthetized mi
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Changes in tissue blood flow and sympathetic activities to various organs during prolonged Hemorrhagic Hypotension in monkeys.
Journal of The Autonomic Nervous System, 1996Co-Authors: Satoshi Tanaka, Toshishige Shibamoto, Yoshikazu Matsuda, Hong-gang WangAbstract:This experiment was designed to determine whether prolonged Hemorrhagic Hypotension in anesthetized monkeys produces differential control of tissue blood flow and sympathetic nerve activities to various organs (heart, kidney, liver, spleen, and hind-limb). We performed simultaneous multifiber recording of sympathetic nerve activity to the kidney (RNA), heart (CNA), spleen (SpNA), liver (HNA), and hind-limb (LNA) during sustained Hemorrhagic Hypotension at a mean blood pressure of 40 mmHg for 2 h. Immediately after bleeding, all of the sympathetic nerve activities increased significantly (Stage I) and then gradually decreased towards the prebleeding levels (Stage II). Thereafter, the secondary sympathetic excitation was observed (Stage III), followed by a gradual decrease in sympathetic activities below the prebleeding levels (Stage IV). The shed blood started to return to the animals at this final stage. Time course of changes in sympathetic nerve activities did not differ among organs innervated. However, tissue blood flow of the renal cortex, liver, skeletal muscle and spleen significantly decreased at Stage I and remained at low levels until the end of the experimental period. In contrast, blood flow of the renal medulla and heart was preserved until Stage III and Stage IV, respectively. These results indicate that although the sympathetic response to prolonged Hemorrhagic Hypotension of 40 mmHg did not differ among organs, changes in tissue blood flow were variable and blood flow to the heart and renal medulla was maintained at a steady level until a late stage of hemorrhage.
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relative contribution of renal nerve and adrenal gland to renal vascular tone during prolonged canine Hemorrhagic Hypotension
Circulatory shock, 1993Co-Authors: Sekiya Koyama, Toshishige Shibamoto, Yoshikazu Matsuda, Takashi Fujita, T Hayashi, Y Saeki, M Kawamoto, Yoshihiro YamaguchiAbstract:: This study was designed to determine roles of renal sympathetic nerve activity (RNA) and adrenal catecholamines in the changes of renal vascular resistance during prolonged Hemorrhagic shock in anesthetized dogs. In animals with intact baroreceptors, Hemorrhagic Hypotension (40 mm Hg) caused RNA to increase significantly within 1 min after bleeding, followed by a return to baseline within 10 min. Thereafter, a secondary increase in RNA occurred that was followed by a gradual decline towards the baseline level. The renal perfusion pressure (RPP) showed a progressive and significant increase until the end of the experiment. The initial increase in RNA was abolished by complete denervation of the systemic baroreceptors. The initial increase in RPP, which was observed within 10 min after bleeding in animals with intact baroreceptors, was attenuated by the denervation. In animals with bilateral adrenalectomy, RPP still showed an initial increase, but the progressive increase throughout the entire experimental period did not occur. In animals with baroreceptor denervation and bilateral adrenalectomy, RPP did not show any significant changes during the experiment. These results indicate that the initial renal vasoconstrictive response to hemorrhage is regulated by a reflex sympathetic mechanism. In contrast, a late renal vasoconstriction during Hemorrhagic Hypotension is predominantly evoked by humoral substances such as adrenal catecholamines.
Roland N Pittman - One of the best experts on this subject based on the ideXlab platform.
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early physiologic responses to Hemorrhagic Hypotension
Translational Research, 2010Co-Authors: Ivo Torres P Filho, Luciana N Torres, Roland N PittmanAbstract:The identification of early indicators of Hemorrhagic Hypotension (HH) severity may support early therapeutic approaches and bring insights into possible mechanistic implications. However, few systematic investigations of physiologic variables during early stages of hemorrhage are available. We hypothesized that, in certain subjects, early physiologic responses to blood loss are associated with the ability to survive hemorrhage levels that are lethal to subjects that do not present the same responses. Therefore, we examine the relevance of specific systemic changes during and after the bleeding phase of HH. Stepwise hemorrhage, representing prehospital situations, was performed in 44 rats, and measurements were made after each step. Heart and respiratory rates, arterial and venous blood pressures, gases, acid-base status, glucose, lactate, electrolytes, hemoglobin, O 2 saturation, tidal volume, and minute volume were measured before, during, and after bleeding 40% of the total blood volume. Fifty percent of rats survived 100min (survivors, S) or longer; others were considered nonsurvivors (NS). Our findings were as follows: (1) S and NS subjected to a similar hemorrhage challenge showed significantly different responses during nonlethal levels of bleeding; (2) survivors showed higher blood pressure and ventilation than NS; (3) although pH was lower in NS at later stages, changes in bicarbonate and base excess occurred already during the hemorrhage phase and were higher in NS; and (4) plasma K + levels and glucose extraction were higher in NS. We conclude that cardiorespiratory and metabolic responses, essential for the survival at HH, can differentiate between S and NS even before a lethal bleeding was reached.
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microvascular blood flow and oxygenation during Hemorrhagic Hypotension
Microvascular Research, 2008Co-Authors: Luciana N Torres, Roland N Pittman, Ivo Torres P FilhoAbstract:Abstract Understanding microvascular oxygen transport requires the knowledge of microvessel topology and geometry, blood flow and oxygen levels. Microvascular hemodynamic responses to Hemorrhagic Hypotension (HH) such as size-dependent vasoconstriction and blood flow reduction could lead to increased longitudinal oxygen partial pressure (PO2) gradients. However, the mesenteric microvascular PO2 has never been evaluated during HH. Therefore, we studied hemodynamic variables and PO2 distribution in 165 mesenteric microvessels from 39 anesthetized rats to investigate whether HH-induced vasoconstriction and blood flow reduction were associated with changes in longitudinal PO2 gradients. Vessels were analyzed according to their position in the network, as well as a few interstitial PO2 areas. We found that during baseline a small PO2 gradient exists, but HH is accompanied by more pronounced microvascular longitudinal PO2 gradients. Decreased blood flow did not seem to completely explain these findings, since blood flow was uniformly diminished in arterioles and venules, independent of diameter and position in the network. During HH, some microvessels presented higher PO2 than during baseline despite blood flow reduction, possibly due to a combination of systemic hyperoxia and low oxygen consumption of mesentery. The data suggest that blood flow measurements may be a poor indicator of the oxygenation status in some regions of the mesentery. The enhanced mesenteric longitudinal PO2 gradient may lead to regions with different levels of other physiologically active compounds.
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systemic responses to prolonged Hemorrhagic Hypotension
American Journal of Physiology-heart and Circulatory Physiology, 2004Co-Authors: Luciana N Torres, Ivo Torres P Filho, Wayne R Barbee, Hakam M Tiba, Kevin R Ward, Roland N PittmanAbstract:Studies are needed to provide a rigorous examination of the relevance of monitored variables during prolonged Hemorrhagic Hypotension (HH). This study was designed to investigate the parameters tha...
Csilla Csaki - One of the best experts on this subject based on the ideXlab platform.
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role of platelet activating factor in the development of endothelial dysfunction in Hemorrhagic Hypotension and retransfusion
Thrombosis Research, 1992Co-Authors: Csaba Szabo, Csilla Csaki, Zoltan Benyo, Arisztid G.b. KováchAbstract:Abstract Platelet-activating factor (PAF), an important mediator of ischemic and shock states, has been shown to prime direct and neutrophil-mediated endothelial cell injury. In the present study we investigated therefore whether PAF is involved in the development of dysfunction of the cerebrovascular endothelium in Hemorrhagic Hypotension and retransfusion in cats. In vitro responses of middle cerebral arteries prepared from control animals and from animals subjected to Hemorrhagic Hypotension with or without specific PAF antagonist WEB 2086 treatment (1 mg/kg initial bolus followed by a 0.05 mg/kg/min infusion) were studied by measuring isometric force in organ chambers containing Krebs-Henseleit solution (37°C, gassed with 95% O2– 5% CO2). Bleeding was performed in a stepwise fashion by bringing the mean arterial blood pressure to 90, 70 and 50 mmHg and maintained for 20 min at each level followed by a 20-min retransfusion. Hemorrhagic Hypotension and retransfusion caused a marked attenuation of the acetylcholine- and ATP-induced endothelium-dependent relaxations of the middle cerebral artery whereas the dilations induced by the nitric oxide donor and direct vasorelaxant SIN-1, remained unaltered. In the vessels, prepared from animals which received WEB 2086 treatment during hemorrhage and retransfusion there were more pronounced cholinergic (but not purinergic) relaxations than in the untreated animals subjected to hemorrhage. SIN-1 induced relaxations remained unaltered after WEB 2086 treatment. Our results suggest that platelet-activating factor is in part involved in the pathophysiological processes leading to the development of the endothelial dysfunction in the present model of Hemorrhagic Hypotension and retransfusion.
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role of the l arginine nitric oxide pathway in the changes in cerebrovascular reactivity following Hemorrhagic Hypotension and retransfusion
Circulatory shock, 1992Co-Authors: Csaba Szabo, Csilla Csaki, Zoltan Benyo, Martin Reivich, Arisztid G.b. KováchAbstract:Abstract We studied the involvement of the L-arginine-nitric oxide pathway in the changes in cerebrovascular reactivity following Hemorrhagic Hypotension and retransfusion. Feline middle cerebral arteries were prepared from control animals killed under anesthesia and from anesthetised animals subjected to Hemorrhagic Hypotension (stepwise bleeding to 90, 70, and 50 mmHg, maintained for 20 min at each level) followed by retransfusion (20 min). Two-mm-long vessel segments were suspended in organ chambers containing Krebs-Henseleit solution (37 degrees C, gassed with 95% O2-5% CO2) for isometric force measurements. Contractions to noradrenaline (norepinephrine), relaxations to acetylcholine, ATP, adenosine, and SIN-1, a nitric oxide donor compound, were compared in the vessels of the control and hemorrhage-subjected animals. Contractile responses to noradrenaline were significantly enhanced after hemorrhage, whereas relaxations to acetylcholine, ATP, and adenosine were significantly reduced. Relaxations to SIN-1, however, remained unchanged. L-Arginine did not cause relaxations in control vessels but relaxed the arteries after hemorrhage and retransfusion. To clarify the involvement of the L-arginine-nitric oxide pathway in these alterations, we studied the effect of exogenous application of L-arginine, the precursor of endothelium-derived relaxing factor (EDRF) and NG-nitro-L-arginine (NOLA), a competitive antagonist of the EDRF-producing enzyme on the vascular responses in vitro. Similar to the effect of Hypotension and retransfusion, NOLA enhanced the noradrenaline-induced contractions and inhibited the acetylcholine-induced and purinoceptor-mediated relaxations in the control arteries. In the control vessels in vitro, L-arginine treatment did not modify any contractile or relaxant response. At the same time, in vitro L-arginine treatment inhibited the Hemorrhagic Hypotension-induced enhancement of the contractions to noradrenaline and restored the diminished relaxations to acetylcholine (but not to ATP or adenosine). In the vessels after hemorrhage, NOLA neither further enhanced the already markedly enhanced noradrenaline-induced contractions nor further inhibited the relaxations caused by ATP and adenosine. In the case of acetylcholine, however, NOLA caused a further inhibition of the relaxations. The effect of in vivo L-Arg infusion (30 mg/kg initial bolus and 10 mg/kg/min infusion) during Hemorrhagic Hypotension and retransfusion on the in vitro vascular reactivity was similar to that of the in vitro L-arginine treatment. The present study demonstrates that even short-lasting Hemorrhagic Hypotension combined with retransfusion markedly inhibits nitric oxide-mediated, agonist-induced endothelium-dependent cerebrovascular responses. In vivo or in vitro L-arginine treatment is able to restore normal responses to some agents.(ABSTRACT TRUNCATED AT 400 WORDS)
Arisztid G.b. Kovách - One of the best experts on this subject based on the ideXlab platform.
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EFFECT OF FASTING AND Hemorrhagic Hypotension ON NICKEL CONTENT OF DIFFERENT ORGANS IN THE RAT
Homeostasis in Injury and Shock, 2013Co-Authors: Anna Gergely, Gabor M. Rubanyi, M. Bakos, Arisztid G.b. Kovách, Ö. GaálAbstract:Publisher Summary This chapter describes the effect of fasting and Hemorrhagic Hypotension on nickel content of different organs in a rat. It presents a study where the effect of 24 h fasting and 2, 5 h Hemorrhagic Hypotension on distribution of nickel in different organs of the rats was studied. The experimental animals were divided into four groups: (1) control, (2) fasted control, (3) animals exposed to 2–5 h Hemorrhagic Hypotension, and (4) fasted animals exposed to 2, 5 h Hemorrhagic Hypotension. 24h fasting caused significant decrease of Ni content in the liver, spleen, and serum, but Ni content increased in the heart and kidney. Hemorrhagic Hypotension caused elevation of Ni level not only in liver and serum but also in the kidney of fasted animals. Both fasting and shock cause significant changes in the Ni content of different organs of the rat, and fasting influences the effect of Hemorrhagic shock considerably. Endogenous Ni release from the myocardium may lead to a positive feedback loop, further damage of cardiac function, and subsequent death.
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role of platelet activating factor in the development of endothelial dysfunction in Hemorrhagic Hypotension and retransfusion
Thrombosis Research, 1992Co-Authors: Csaba Szabo, Csilla Csaki, Zoltan Benyo, Arisztid G.b. KováchAbstract:Abstract Platelet-activating factor (PAF), an important mediator of ischemic and shock states, has been shown to prime direct and neutrophil-mediated endothelial cell injury. In the present study we investigated therefore whether PAF is involved in the development of dysfunction of the cerebrovascular endothelium in Hemorrhagic Hypotension and retransfusion in cats. In vitro responses of middle cerebral arteries prepared from control animals and from animals subjected to Hemorrhagic Hypotension with or without specific PAF antagonist WEB 2086 treatment (1 mg/kg initial bolus followed by a 0.05 mg/kg/min infusion) were studied by measuring isometric force in organ chambers containing Krebs-Henseleit solution (37°C, gassed with 95% O2– 5% CO2). Bleeding was performed in a stepwise fashion by bringing the mean arterial blood pressure to 90, 70 and 50 mmHg and maintained for 20 min at each level followed by a 20-min retransfusion. Hemorrhagic Hypotension and retransfusion caused a marked attenuation of the acetylcholine- and ATP-induced endothelium-dependent relaxations of the middle cerebral artery whereas the dilations induced by the nitric oxide donor and direct vasorelaxant SIN-1, remained unaltered. In the vessels, prepared from animals which received WEB 2086 treatment during hemorrhage and retransfusion there were more pronounced cholinergic (but not purinergic) relaxations than in the untreated animals subjected to hemorrhage. SIN-1 induced relaxations remained unaltered after WEB 2086 treatment. Our results suggest that platelet-activating factor is in part involved in the pathophysiological processes leading to the development of the endothelial dysfunction in the present model of Hemorrhagic Hypotension and retransfusion.
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role of the l arginine nitric oxide pathway in the changes in cerebrovascular reactivity following Hemorrhagic Hypotension and retransfusion
Circulatory shock, 1992Co-Authors: Csaba Szabo, Csilla Csaki, Zoltan Benyo, Martin Reivich, Arisztid G.b. KováchAbstract:Abstract We studied the involvement of the L-arginine-nitric oxide pathway in the changes in cerebrovascular reactivity following Hemorrhagic Hypotension and retransfusion. Feline middle cerebral arteries were prepared from control animals killed under anesthesia and from anesthetised animals subjected to Hemorrhagic Hypotension (stepwise bleeding to 90, 70, and 50 mmHg, maintained for 20 min at each level) followed by retransfusion (20 min). Two-mm-long vessel segments were suspended in organ chambers containing Krebs-Henseleit solution (37 degrees C, gassed with 95% O2-5% CO2) for isometric force measurements. Contractions to noradrenaline (norepinephrine), relaxations to acetylcholine, ATP, adenosine, and SIN-1, a nitric oxide donor compound, were compared in the vessels of the control and hemorrhage-subjected animals. Contractile responses to noradrenaline were significantly enhanced after hemorrhage, whereas relaxations to acetylcholine, ATP, and adenosine were significantly reduced. Relaxations to SIN-1, however, remained unchanged. L-Arginine did not cause relaxations in control vessels but relaxed the arteries after hemorrhage and retransfusion. To clarify the involvement of the L-arginine-nitric oxide pathway in these alterations, we studied the effect of exogenous application of L-arginine, the precursor of endothelium-derived relaxing factor (EDRF) and NG-nitro-L-arginine (NOLA), a competitive antagonist of the EDRF-producing enzyme on the vascular responses in vitro. Similar to the effect of Hypotension and retransfusion, NOLA enhanced the noradrenaline-induced contractions and inhibited the acetylcholine-induced and purinoceptor-mediated relaxations in the control arteries. In the control vessels in vitro, L-arginine treatment did not modify any contractile or relaxant response. At the same time, in vitro L-arginine treatment inhibited the Hemorrhagic Hypotension-induced enhancement of the contractions to noradrenaline and restored the diminished relaxations to acetylcholine (but not to ATP or adenosine). In the vessels after hemorrhage, NOLA neither further enhanced the already markedly enhanced noradrenaline-induced contractions nor further inhibited the relaxations caused by ATP and adenosine. In the case of acetylcholine, however, NOLA caused a further inhibition of the relaxations. The effect of in vivo L-Arg infusion (30 mg/kg initial bolus and 10 mg/kg/min infusion) during Hemorrhagic Hypotension and retransfusion on the in vitro vascular reactivity was similar to that of the in vitro L-arginine treatment. The present study demonstrates that even short-lasting Hemorrhagic Hypotension combined with retransfusion markedly inhibits nitric oxide-mediated, agonist-induced endothelium-dependent cerebrovascular responses. In vivo or in vitro L-arginine treatment is able to restore normal responses to some agents.(ABSTRACT TRUNCATED AT 400 WORDS)
Luciana N Torres - One of the best experts on this subject based on the ideXlab platform.
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early physiologic responses to Hemorrhagic Hypotension
Translational Research, 2010Co-Authors: Ivo Torres P Filho, Luciana N Torres, Roland N PittmanAbstract:The identification of early indicators of Hemorrhagic Hypotension (HH) severity may support early therapeutic approaches and bring insights into possible mechanistic implications. However, few systematic investigations of physiologic variables during early stages of hemorrhage are available. We hypothesized that, in certain subjects, early physiologic responses to blood loss are associated with the ability to survive hemorrhage levels that are lethal to subjects that do not present the same responses. Therefore, we examine the relevance of specific systemic changes during and after the bleeding phase of HH. Stepwise hemorrhage, representing prehospital situations, was performed in 44 rats, and measurements were made after each step. Heart and respiratory rates, arterial and venous blood pressures, gases, acid-base status, glucose, lactate, electrolytes, hemoglobin, O 2 saturation, tidal volume, and minute volume were measured before, during, and after bleeding 40% of the total blood volume. Fifty percent of rats survived 100min (survivors, S) or longer; others were considered nonsurvivors (NS). Our findings were as follows: (1) S and NS subjected to a similar hemorrhage challenge showed significantly different responses during nonlethal levels of bleeding; (2) survivors showed higher blood pressure and ventilation than NS; (3) although pH was lower in NS at later stages, changes in bicarbonate and base excess occurred already during the hemorrhage phase and were higher in NS; and (4) plasma K + levels and glucose extraction were higher in NS. We conclude that cardiorespiratory and metabolic responses, essential for the survival at HH, can differentiate between S and NS even before a lethal bleeding was reached.
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microvascular blood flow and oxygenation during Hemorrhagic Hypotension
Microvascular Research, 2008Co-Authors: Luciana N Torres, Roland N Pittman, Ivo Torres P FilhoAbstract:Abstract Understanding microvascular oxygen transport requires the knowledge of microvessel topology and geometry, blood flow and oxygen levels. Microvascular hemodynamic responses to Hemorrhagic Hypotension (HH) such as size-dependent vasoconstriction and blood flow reduction could lead to increased longitudinal oxygen partial pressure (PO2) gradients. However, the mesenteric microvascular PO2 has never been evaluated during HH. Therefore, we studied hemodynamic variables and PO2 distribution in 165 mesenteric microvessels from 39 anesthetized rats to investigate whether HH-induced vasoconstriction and blood flow reduction were associated with changes in longitudinal PO2 gradients. Vessels were analyzed according to their position in the network, as well as a few interstitial PO2 areas. We found that during baseline a small PO2 gradient exists, but HH is accompanied by more pronounced microvascular longitudinal PO2 gradients. Decreased blood flow did not seem to completely explain these findings, since blood flow was uniformly diminished in arterioles and venules, independent of diameter and position in the network. During HH, some microvessels presented higher PO2 than during baseline despite blood flow reduction, possibly due to a combination of systemic hyperoxia and low oxygen consumption of mesentery. The data suggest that blood flow measurements may be a poor indicator of the oxygenation status in some regions of the mesentery. The enhanced mesenteric longitudinal PO2 gradient may lead to regions with different levels of other physiologically active compounds.
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systemic responses to prolonged Hemorrhagic Hypotension
American Journal of Physiology-heart and Circulatory Physiology, 2004Co-Authors: Luciana N Torres, Ivo Torres P Filho, Wayne R Barbee, Hakam M Tiba, Kevin R Ward, Roland N PittmanAbstract:Studies are needed to provide a rigorous examination of the relevance of monitored variables during prolonged Hemorrhagic Hypotension (HH). This study was designed to investigate the parameters tha...