Differential effects of dobutamine, dopamine, and noradrenaline on splanchnic haemodynamics and oxygenation in the pig.

Supranormal oxygen (O2) transport may benefit critically ill patients. Catecholamines are clinically employed for this purpose. However, their effects on splanchnic haemodynamics and oxygenation are now well defined. The effects of dobutamine (DOBU), dopamine (DOPA), and noradrenaline (NA) on splanchnic blood flows electromagnetic flow probes), O2 deliveries and uptakes (catheterisation of portal and hepatic veins) were studied in nine anaesthetised (ketamine/flunitrazepam), ventilated, paralysed, and laparotomised pigs. All three catecholamines (DOPA at 15 micrograms.kg-1.min-1, DOBU at 13 micrograms.kg-1.min-1, NA at 0.4 micrograms.kg-1.min-1) significantly (P < 0.05) increased cardiac output and systemic O2 delivery. Only DOPA increased small intestinal and total hepatic blood flows, and O2 deliveries, and decreased O2 extractions. The same parameters did not change during DOBU. During NA, total hepatic blood flow and O2 delivery decreased, and hepatic O2 extraction increased. During all three catecholamines, small intestinal and total hepatic O2 uptakes did not change significantly. Whereas hepatic arterial blood flow decreased during both DOPA and NE, portal venous flow increased during DOPA. These data suggest that in the experimental model used splanchnic O2 supply and O2 reserve capacity appear improved by DOPA, unaffected by DOBU, and impaired by NA.

Splanchnic hemodynamics and oxygen supply during acute normovolemic hemodilution alone and with isoflurane-induced hypotension in the anesthetized pig.

Safety of combined hemodilution and isoflurane-induced hypotension was assessed by studying their effects on splanchnic hemodynamics and oxygenation in nine anesthetized (ketamine/flunitrazepam) pigs. Acute normovolemic hemodilution (decrease in hematocrit from 29% to 15%) with 6% hydroxyethyl starch decreased (P < 0.05) O2 delivery despite increases in cardiac output and all splanchnic flows, as measured by electromagnetic flow probes. Superimposed isoflurane (1.45% end-tidal concentrations) caused marked decreases in arterial blood pressure, cardiac output, and splanchnic flows. Oxygen uptake of the liver became O2 supply dependent. A liver surface PO2 histogram (Clark-type electrode) showed 38% of PO2 values between 0 and 5 mm Hg. Hepatic lactate uptake decreased by 75%. These data suggest that depression of cardiovascular function during reduced O2-carrying capacity adversely affects hepatic perfusion, oxygenation, and function. Combined hemodilution and isoflurane-induced hypotension may not be appropriate in patients.

Effects of acute normovolemic hemodilution on splanchnic oxygenation and on hepatic histology and metabolism in anesthetized pigs.

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 (electromagnetic 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 less than 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 flow and O2 extractions) were no longer fully able to counteract the decrease in splanchnic O2 delivery.

Differences in effects of isoflurane and enflurane on splanchnic oxygenation and hepatic metabolism in the pig.

The effects of end-tidal concentrations of 1.45% isoflurane and 2.12% enflurane on splanchnic blood flow (electromagnetic flow probes), oxygen (O2) extraction and surface PO2 (Clark-type electrode), and hepatic metabolism (organic acids) were compared in an animal model relevant to humans. Eighteen laparotomized, ventilated pigs, anesthetized and paralyzed with ketamine/flunitrazepam and pancuronium, were studied. Enflurane caused significantly (P less than 0.05) greater decreases in mean arterial pressure, cardiac output, and superior mesenteric arterial, portal, and total hepatic blood flows. In addition, hepatic arterial blood flow decreased during enflurane administration but increased markedly (40%) during isoflurane administration. However, mean surface PO2 of liver and small intestine decreased to similar degrees (20%) during isoflurane and enflurane. Summary histograms of surface PO2 values were leftward shifted but did not show O2 values in the hypoxic range (0-5 mm Hg). Except for a decrease in hepatic lactate uptake during enflurane, there were no changes in either hepatic uptake or release of organic acids during anesthesia with either agent. These data show that splanchnic O2 supply is better maintained during isoflurane than during enflurane. Although this was not reflected in differences in tissue oxygenation and metabolism, decreased portal and hepatic venous O2 contents during enflurane indicate that an increase in preportal and hepatic oxygen extraction was necessary to preserve tissue oxygenation.