Temporal Relationship of Hepatocellular Dysfunction and Ischemia in Sepsis

Machiedo, George W.; Hurd, Thelma C.; Rush, Benjamin F.; Dikdan, George; McGee, John; Lysz, Thomas W.

doi:10.1001/archsurg.1988.01400280030005

Cited by 30 publications

(4 citation statements)

References 8 publications

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“…Nevertheless, the role of hepatic blood flow in the development of hepatic failure during sepsis remains a controversial issue. A number of experimental studies indicated reduced hepatic blood flow during sepsis [24], leading to the conclusion that hepatic dysfunction arises from parenchymal ischemia. On the other hand, a few clinical reports have detailed an increase in hepatic blood flow during sepsis [25,26], suggesting the responsibility of a more complex mechanism of hepatic dysfunction, although it is possible that the discrepancy in findings reflects measurements made at different stages of the septic process.…”

Section: Discussionmentioning

confidence: 99%

Influence of Enteral Nutrition‐induced Splanchnic Hyperemia on the Septic Origin of Splanchnic Ischemia

et al. 1998

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The purpose of this experimental study was to investigate whether enteral nutrition-induced postprandial intestinal hyperemia has a beneficial effect on the splanchnic ischemia due to sepsis. Fourteen dogs, after exposure to Escherichia coli endotoxin via portal vein administration were grouped according to whether they were fed enterally via a jejunostomy or given a placebo. Systemic hemodynamics; portal vein, hepatic, and superior mesenteric artery blood flow; hepatic and intestinal microcirculation; hepatic tissue PO2; intestinal pHi; and hepatic energy charge were assessed before, during, and after endotoxin infusion as well as during and after enteral or placebo feeding. All splanchnic hemodynamic parameters revealed a statistically significant decline (p = 0.001) during the endotoxin shock period relative to the baseline. After enteral feeding all parameters exhibited a statistically significant increase (p = 0.001) relative to the placebo group. The results of this study led us to suggest that enteral nutrition reverses the lipopolysaccharide infusion-induced splanchnic ischemia.

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Section: Discussionmentioning

confidence: 99%

Influence of Enteral Nutrition‐induced Splanchnic Hyperemia on the Septic Origin of Splanchnic Ischemia

et al. 1998

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“…There are both direct effects on cellular function induced by the sepsis [34,37], and also secondary effects on cell function induced by insufficient hepatic perfusion with possible reperfusion injuries after resuscitation [38,39]. These changes in cell function will affect both hepatocytes and sinusoidal cells.…”

Section: Hepatic Function In Sepsismentioning

confidence: 99%

Hyaluronan turnover in relation to infection and sepsis

Berg¹

1997

Journal of Internal Medicine

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. Berg S (University Hospital, Linköping, Sweden). Hyaluronan turnover in relation to infection and sepsis (Minisymposium: Hyaluronan). J Intern Med 1997; 242: 73–7. Sepsis is a major clinical problem in intensive care. The mortality in septic shock is high, and predominantly due to cardiovascular collapse and multiple organ dysfunction. In sepsis high levels of circulating hyaluronan have been found, correlating to disease severity and prognosis. The reason behind the increased levels could be both decreased hepatic uptake and increased peripheral synthesis. Thus, plasma hyaluronan may be a clinically useful marker of hepatic dysfunction and possibly also an indicator of the increased inflammatory and reparative activity in different organs in septic conditions.

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“…But even with increased oxygen delivery the septic liver seems to be exposed to ischemic insults [6,7], Experimental evi dence suggests that this may especially apply to nonparenchymal cells [8]. Furthermore, it has been shown that ischemia primes Kupffer cells to release increased amounts o f TNF-a after endotoxin challenge, thus augmenting the mediator response [9], Although results are conflicting, and the precise role for hepatic ischemia in sepsis remains unsettled [10][11][12], sufficient evidence has amounted to support the view that it is at least a contributing ele ment in the development o f hepatic dysfunc tion. Hence hypoperfusion may be a major etiologic factor for the subsequent progression into a systemic inflammatory response syn drome and multiple system organ failure.…”

Section: Introductionmentioning

confidence: 99%

Modulators of Nitric Oxide in Porcine Endotoxemia: Effects on Hepatic Oxygen Delivery and Consumption

Gundersen

Sætre²,

Carlsen³

et al. 1997

Eur Surg Res

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In a porcine model of endotoxemia we have studied the effects of nitric oxide (NO) on hepatic oxygen delivery and consumption. After 3 h of endotoxemia, NO biosynthesis was modulated by a bolus dose of the NO synthase inhibitor N^G-nitro-L-arginine methyl ester (L-NAME). Fifteen minutes thereafter a continuous infusion of the NO donor sodium nitroprusside (SNP) was started. Endotoxin significantly reduced hepatic oxygen delivery from 3.4 ± 0.6 to 2.2 ± 0.3 ml/kg/min at 3 h. Due to an increased extraction ratio (ER), oxygen consumption was nearly unaffected. L-NAME further diminished oxygen delivery to 1.0 ± 0.2 ml/kg/min within 15 min (p < 0.05), but despite an increase in ER from 47 to 68% (p < 0.05), oxygen consumption tended to decrease (from 1.0 to 0.7 ml/ kg/min, nonsignificant). A similar tendency was observed in a control group of 9 pigs which was treated in the same way as the study group, except for the SNP infusion. SNP induced an almost selective increase in hepatic arterial flow, with a corresponding increase in oxygen delivery to 1.8 ± 0.3 ml/kg/min (p < 0.05). At the same time ER was reduced from 68 to 42% (p < 0.05). Oxygen consumption remained unaltered. The control group exhibited no change in either oxygen delivery or consumption. The study shows that nonselective inhibition of NO synthesis is detrimental to hepatic perfusion and oxygen transport. The NO donor SNP increased oxygen delivery via a selective increase in hepatic arterial flow, but failed to influence oxygen consumption. This was probably mainly due to a massive shutdown of sinusoids, which did not reopen when flow was increased. A functioning microcirculation thus seems to be a prerequisite for the stimulation of organ blood flow to be effective.

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Temporal Relationship of Hepatocellular Dysfunction and Ischemia in Sepsis

Cited by 30 publications

References 8 publications

Influence of Enteral Nutrition‐induced Splanchnic Hyperemia on the Septic Origin of Splanchnic Ischemia

Influence of Enteral Nutrition‐induced Splanchnic Hyperemia on the Septic Origin of Splanchnic Ischemia

Hyaluronan turnover in relation to infection and sepsis

Modulators of Nitric Oxide in Porcine Endotoxemia: Effects on Hepatic Oxygen Delivery and Consumption

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