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Hepatic arterial and portal venous pressure, flow, and resistance changes have been measured in healthy dogs following the administration of intravenous Salmonella enteritidis endotoxin. The hepatic circulatory changes have been compared with those occurring in total body hemodynamics. Intravenous endotoxin caused an immediate fall in blood pressure, cardiac output, and central venous pressure. There was an abrupt rise in the net portal pressure which was associated with a marked fall in hepatic arterial and portal venous flows following endotoxin administration. There was a gradual reduction in the ratio of portal venous to hepatic arterial flow indicating relative maintenance of the hepatic arterial circulation during the period of endotoxin shock. Hepatic arterial flow increased from 7 to 9% of cardiac output, whereas portal venous flow fell from 15 to 11% of cardiac output following endotoxin administration. The hematocrit showed a progressive rise during the period of observation indicating acute plasma volume reduction. This finding suggests that some of the changes observed in hepatic circulation following endotoxin administration may be due to acute plasma volume reduction.
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Müller et al. (1963) studied this question.
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