THE EFFECT OF ADENOSINE-INDUCED HYPOTENSION OF SYSTEMIC AND SPLANCHNIC HEMODYNAMICS DURING HALOTHANE OF SEVOFLURANE ANESTHESIA IN THE RAT

Background: It has been suggested that the liver may be at risk for is chemic damage during adenosine-induced hypotension. This notion, howev er, is somewhat inconsistent with the understanding that adenosine is a powerful vasodilator of the splanchnic circulation. To help clarify the effect of adenosine-induced hypotension on splanchnic hemodynamics , we studied the systemic and splanchnic hemodynamic responses to aden osine, both alone and in the presence of halothane or sevoflurane. Met hods: Systemic and splanchnic hemodynamics were determined during the infusion of adenosine in 36 rats allocated randomly to one of three st udy groups: (1) awake, (2) halothane anesthesia (1.0 MAC), or (3) sevo flurane anesthesia (1.0 MAC). Adenosine was infused at a rate sufficie nt to decrease the mean arterial pressure by 35-38% from awake control values. Cardiac output and organ blood flows were measured using the radiolabeled microsphere technique. Results: Adenosine infusion produc ed stable hypotension of rapid onset due to a reduction in systemic va scular resistance. Stroke volume increased, but cardiac output remaine d unchanged in the awake and sevoflurane groups because of a decrease in heart rate. Infusion of adenosine during halothane anesthesia incre ased cardiac output enough to compensate for the decrease in cardiac o utput due to halothane alone. In the splanchnic circulation, there was an increase in portal tributary (42%, P<0.01) and hepatic arterial(38 %, P<0.05) blood flows during adenosine infusion in awake rats. This r e suited in an overall increase in total liver blood flow (42%, P<0.01 ). Halothane anesthesia was associated with a decrease in portal tribu tary blood flow (28%, P<0.05). In contrast, sevoflurane anesthesia was associated with an increase in hepatic arterial flow (35%, P<0.05) bu t with no change in portal tributary blood flow. During halothane anes thesia, adenosine infusion increased portal tributary (90%, P<0.01) an d hepatic arterial (37%, P<0.05) blood flows, thereby increasing total liver blood flow to values similar to those in awake adenosine infuse d rats. During sevoflurane anesthesia, adenosine infusion increased po rtal tributary blood flow (48%, P<0.01), but hepatic arterial blood fl ow did not increase beyond the values observed during sevoflurane anes thesia alone. Conclusions: These findings demonstrate that adenosine i s a potent vasodilator of portal tributary and hepatic arterial vascul ature in the rat and that the splanchnic hemodynamic effects of adenos ine predominate over those of halothane and sevoflurane.