Effects of Acute Normovolemic Hemodilution on Splanchnic Oxygenation and on Hepatic Histology and Metabolism in Anesthetized Pigs.
Noldge, Gabriele F. E. M.D. *; Priebe, Hans-Joachim M.D. +; Bohle, Wolfram M.D. ++; Buttler, Klaus Jurgen [S]; Geiger, Klaus M.D. [P]
74(5):908-918, May 1991.
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Perioperative hemodilution (HD) has become an accepted means of reducing transfusion requirements. Therefore, the effects of limited (decrease in hematocrit [Hct] from 30 to 20%, "HD1'') and severe (decrease in Hct from 20 to 14%, "HD2'') acute normovolemic HD with 6% hydroxyethyl starch on splanchnic blood flows (electro-magnetic flow probes), O2 uptakes and deliveries, surface O2 tensions (PO2) (Clark-type electrode), hepatic metabolism (organic acids), and hepatic histology (liver biopsies) were studied in nine pigs anesthetized and paralyzed with ketamine/flunitrazepam and pancuronium. HD1 caused significant (P < 0.05) increases in cardiac output and all splanchnic flows. Only hepatic arterial blood flow increased twice as much as did cardiac output. Except for hepatic arterial O2 delivery, all splanchnic O2 deliveries decreased. Splanchnic O2 extractions increased, and O2 uptakes remained unchanged. There were no changes in mean surface PO2 values or in surface PO2, histograms of liver and small intestine; in portal or hepatic venous pH; and in hepatic uptake of pyruvate and lactate. In contrast, during HD2 (despite further increases in flows and O2 extractions) portal and hepatic venous pH decreased; mean surface PO2 of liver and small intestine decreased; and the liver surface PO2 histogram showed broadening and a shift to the left. However, hepatic uptake of lactate and pyruvate, and splanchnic O2 uptake remained unchanged, and histologic examination did not reveal significant cell injury. These data indicate that in this experimental model limited acute normovolemic HD was well tolerated by the splanchnic organs. After severe HD, gross liver function remained intact, but there was evidence that compensatory mechanisms (increases in flows and O2 extractions) were no longer fully able to counteract the decrease in-splanchnic O2 delivery.
(C) 1991 American Society of Anesthesiologists, Inc.