Route of endotoxin delivery; effects on canine mesenteric hemodynamics

Brungardt, JM; Reynolds, DG; Swan, KG

doi:10.1152/ajplegacy.1972.223.3.565

Cited by 12 publications

(2 citation statements)

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“…The endotoxic canine model of splanchnic ischemia used in this study represents a common clinical scenario of enteric hypoxia in critically ill septic patients [13,14], as endotoxin administration through the portal vein accelerates direct, severe hemodynamic alterations in the abdominal viscera [15]. In all experimental animals, early after lipopolysaccharide administration all intestinal hemodynamic parameters (i.e., superior mesenteric artery blood flow, gut mucosal microcirculation, intramural pH) exhibited a statistically significant decline.…”

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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“…The relationship of this work to endotoxin shock in other species including man remains obscure. In dogs, although the acute response to endotoxin administration involves outflow block of the liver which is not seen in cats (Greenway & Stark, 1971), a severe maintained vasoconstriction of the intestine develops over 60 min (Brungardt, Reynolds & Swan, 1972;Hinshaw, 1968;Kux, Holmes, Hinshaw & Massion, 1971 ;Lillehei, Dietzman & Movsas, 1967;Rayner, McLean & Grim, 1960). Mesenteric vasoconstriction does not appear to occur in sub-human primates (Brobmann, Ulano, Hinshaw & Jacobson, 1970;Wyler, Forsyth, Nies, Neutze & Melmon, 1969) but there have been some reports of haemorrhagic necrosis of the small intestine in man (Horton, Murthy & Seal, 1968).…”

Section: Discussionmentioning

confidence: 99%

Further observations on mesenteric vasoconstriction, survival and the clotting defect after endotoxin administration

Cohen¹,

Greenway²,

Innes³

et al. 1973

British J Pharmacology

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Summary1. The initial response after endotoxin administration (3 mg/kg) in cats involved pulmonary vasoconstriction. This was not seen when endotoxin was given by slow infusion and it could be prevented after a bolus injection of endotoxin by pretreatment of the cats with aspirin (10 mg/kg). Intense mesenteric vasoconstriction occurred in all the cats. 2. The mesenteric vasoconstriction was a specific response of the mesenteric blood vessels. At the time the mesenteric bed constricted, the renal bed dilated, the hepatic arterial bed remained unchanged and the smooth muscle of the intestinal wall relaxed. 3. Arterial blood from cats with a fully developed mesenteric vasoconstriction after endotoxin administration was perfused through a normal intestine. No immediate vasoconstriction developed but the perfused intestine constricted slowly over 60 minutes. This suggests that mesenteric constriction was not due to circulating vasoconstrictor factors or the intestinal innervation, but involved a slow local mechanism within the intestine. It could not be prevented or reversed by a variety of pharmacological agents. 4. These observations suggest that endotoxin caused a unique type of mesenteric vasoconstriction in cats by a local mechanism which took up to 60 min to develop, was sufficiently potent to reduce mesenteric flow to <30% control, and was maintained until death of the cats. Blood from these animals did not clot when placed in a glass tube. 5. The mesenteric constriction and the clotting defect could be prevented by repeated administration of aminophylline and dextran solution before and after a bolus intravenous injection of endotoxin. Arterial pressure and mesenteric flow were maintained for at least 10 h in these experiments. Inadequate treatment intensified rather than reduced the intestinal mucosal damage. 6. Cats were treated with aspirin, endotoxin and the optimal regimen for prevention of the mesenteric constriction and allowed to recover from the anaesthetic agent. In this series, 63% survived indefinitely compared to 25% after aspirin and endotoxin treatment and 0% after endotoxin alone. 7. The possible mechanisms of action of aspirin and aminophylline-dextran solution are discussed. Our failure to obtain 100% survival is probably due to pulmonary damage which develops 10-24 h after endotoxin administration. This delayed pulmonary action of endotoxin is not prevented by aspirin M. M. Cohen and others treatment and it seenis unlikely that aspirin will be of any value in the treatment of the pulmonary lesion in man.

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