Effects of Hypovolemic Shock and Reperfusion on Liver Blood Flow in the Dog.

Kinoshita, Gen; Washizu, Makoto; Motoyoshi, Shigekatsu; Breznock, Eugene M.

doi:10.1292/jvms.57.703

Cited by 8 publications

(5 citation statements)

References 18 publications

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“…10). The HABR, the hydrodynamic interaction between the portal venous and hepatic arterial blood flow, tends to maintain liver blood flow under conditions of low mesenteric blood flow (8,11). It is believed that constantly produced adenosine in the Mall space is washed out by the portal venous blood flow under normal conditions (12).…”

mentioning

confidence: 99%

Effects of systemic arterial hypoperfusion on splanchnic hemodynamics and hepatic arterial buffer response in pigs

Jakob¹,

Tenhunen²,

Laitinen³

et al. 2001

American Journal of Physiology-Gastrointestinal and Liver Physi

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The hepatic arterial buffer response (HABR) tends to maintain liver blood flow under conditions of low mesenteric perfusion. We hypothesized that systemic hypoperfusion impairs the HABR. In 12 pigs, aortic blood flow was reduced by cardiac tamponade to 50 ml. kg(-1). min(-1) for 1 h (short-term tamponade) and further to 30 ml. kg(-1). min(-1) for another hour (prolonged tamponade). Twelve pigs without tamponade served as controls. Portal venous blood flow decreased from 17 +/- 3 (baseline) to 6 +/- 4 ml. kg(-1). min(-1) (prolonged tamponade; P = 0.012) and did not change in controls, whereas hepatic arterial blood flow decreased from 2 +/- 1 (baseline) to 1 +/- 1 ml. kg(-1). min(-1) (prolonged tamponade; P = 0.050) and increased from 2 +/- 1 to 4 +/- 2 ml. kg(-1). min(-1) in controls (P = 0.002). The change in hepatic arterial conductance (DeltaC(ha)) during acute portal vein occlusion decreased from 0.1 +/- 0.05 (baseline) to 0 +/- 0.01 ml. kg(-1). min(-1). mmHg(-1) (prolonged tamponade; P = 0.043). In controls, DeltaC(ha) did not change. Hepatic lactate extraction decreased, but hepatic release of glutathione S-transferase A did not change during cardiac tamponade. In conclusion, during low systemic perfusion, the HABR is exhausted and hepatic function is impaired without signs of cellular damage.

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confidence: 99%

Effects of systemic arterial hypoperfusion on splanchnic hemodynamics and hepatic arterial buffer response in pigs

Jakob¹,

Tenhunen²,

Laitinen³

et al. 2001

American Journal of Physiology-Gastrointestinal and Liver Physi

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Section: Discussionmentioning

confidence: 99%

“…The liver is supplied with approximately 30% of the total cardiac output, 20% of which goes through the hepatic artery and 80% through the portal vein [24], [25]. Both avenues of blood flow depend significantly on the systemic arterial blood pressure [24]. However, once hepatic blood flow decreases following hemorrhagic shock, hypovolemia triggers a corrective response that includes lowering of the resistance in the hepatic artery and the release of endogenous vasodilating substances such as prostaglandins, adenosine, and glucagon [24].…”

Section: Discussionmentioning

confidence: 99%

“…Both avenues of blood flow depend significantly on the systemic arterial blood pressure [24]. However, once hepatic blood flow decreases following hemorrhagic shock, hypovolemia triggers a corrective response that includes lowering of the resistance in the hepatic artery and the release of endogenous vasodilating substances such as prostaglandins, adenosine, and glucagon [24]. The average oxygen saturation in the portal vein was 74.5% [26], which was significantly lower than that in the hepatic artery [26].…”

Section: Discussionmentioning

confidence: 99%

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The Effect of p38 Mitogen-Activated Protein Kinase Activation on Inflammatory Liver Damage following Hemorrhagic Shock in Rats

2012

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Hemorrhagic shock is a frequent cause of liver failure and often leads to a fatal outcome. Several studies have revealed that p38 MAPK is a key mediator in hemorrhagic damage of the primary organs through the activation of proinflammatory cytokines such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β. However, the precise role of these factors in liver damage following hemorrhagic shock is unclear. In this study, we used FR167653, a specific inhibitor of p38 MAPK phosphorylation, to examine the role of p38 MAPK in liver damage occurring up to 5 hours after a hemorrhagic episode in a rat model. Activation of p38 MAPK in the liver as well as an increase in hepatic mRNA expression and serum concentrations of TNF-α and IL-1β occurred during the early phase after hemorrhage. Increased serum levels of hepatic enzymes, as well as histological damage and activated neutrophil accumulation in the liver, were observed in the late phase following hemorrhagic shock. FR167653 inhibited the inflammation-related hepatic injury following hemorrhagic shock. Bacterial lipopolysaccharide (LPS) derived from the gut appeared to have little effects on the hepatic damage. These results demonstrate that p38 MAPK activation is induced by hepatic ischemia during hemorrhagic shock and plays an important role both in the hepatic expression of proinflammatory cytokines and in the development of inflammation-related liver damage.

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“…17 Even though portal-arterialized ALT grafting helped reduce the serum bilirubin level in congenitally hyperbilirubinemic Gunn rats, the graft histologic findings in another experiment showed biliary congestion and duct proliferation due to ligation of the bile duct. 12 The graft in the portal vein-arterialized model still cannot be kept histologically normal even with complete bile drainage. All grafts stopped producing bile 1 week after grafting.…”

Section: Discussionmentioning

confidence: 99%

Rat auxiliary liver transplantation without portal vein reconstruction: Comparison with the portal vein‐arterialized model

et al. 2001

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Auxiliary liver transplantation (ALT) has been reintroduced in clinical cases recently and is now believed to be a viable alternative to orthotopic liver transplantation. To provide a simple rat ALT model for studying the physiological and immunological aspects of the ALT graft, a new ALT was performed, and the comparison between this new model and the portal arterialized one that was reported by other investigators was carried out. At first, we confirmed that liver could tolerate the deprivation of its portal flow well, using a portosystemic shunted rat model. The new rat ALT model, in which the ALT graft obtained its blood inflow only from the hepatic artery, was then performed. Our results demonstrated that 50% of the hepatic artery-alone ALT graft showed almost normal structure histologically at 1 month after grafting, with bile secretion preserved. By contrast, only 8% 1-month graft survival was noted in the portal arterialized group, and all grafts stopped bile secretion 1 week after operation. In conclusion, with arterial blood supply alone, the ALT graft survived and demonstrated normal bile secretion function for more than 1 month. Portal vein arterialization is not an appropriate way to establish the graft's blood supply if no pressure adjustment measures were taken in advance.

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Effects of Hypovolemic Shock and Reperfusion on Liver Blood Flow in the Dog.

Cited by 8 publications

References 18 publications

Effects of systemic arterial hypoperfusion on splanchnic hemodynamics and hepatic arterial buffer response in pigs

Effects of systemic arterial hypoperfusion on splanchnic hemodynamics and hepatic arterial buffer response in pigs

The Effect of p38 Mitogen-Activated Protein Kinase Activation on Inflammatory Liver Damage following Hemorrhagic Shock in Rats

Rat auxiliary liver transplantation without portal vein reconstruction: Comparison with the portal vein‐arterialized model

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