Why the study?
Does liver denervation increase susceptibility to hypovolemic shock in swine?
Does liver denervation increase susceptibility to hypovolemic shock in swine?
Liver denervation impairs the normal compensatory mechanism to maintain portal flow during hypovolemic shock in swine, suggesting neural mediation of splanchnic vasodilatation.
Liver denervation may heighten shock susceptibility in swine; leaves open neural mediation of portal compensation in humans.
This study tested the hypothesis that the denervated liver is more susceptible to hypovolemic shock than the normal liver. Fourteen swine, seven nondenervated and seven after liver denervation, were studied during hypovolemic shock to 50% of baseline blood pressure. Hepatic artery and portal vein flows were measured using transonic flow probes, and cardiac output and central venous pressure were measured using Swan-Ganz catheters. Hepatic artery flow fell equivalently in the two groups, from 132 +/- 71 to 94 +/- 17 ml/min in the nondenervated group compared with 149 +/- 56 to 91 +/- 55 ml/min in the denervated group. In contrast, portal flow in the denervated group (276 +/- 71 to 119 +/- 53 ml/min) fell significantly (p less than 0.001) more than in the nondenervated group (289 +/- 135 to 194 +/- 70 ml/min). The 58% reduction from baseline in portal flow in the denervated group compared with the 30% reduction in the nondenervated group suggests that the normal compensatory mechanism to maintain portal flow during hypovolemic shock is neurally mediated. It can be hypothesized that sensory afferent fibers might initiate a feedback to splanchnic vasodilatation in response to reduced portal flow. This study supports the hypothesis that the denervated liver is more susceptible to hypovolemic shock.
No takes yet. Share an insight, caveat, or question.
Henderson et al. (1992) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: