The opiate antagonist, naloxone, which is associated with prolonged survival in animal models of shock, has been demonstrated to increase arterial pressure and cardiac output. It is possible that the increase in cardiac output is due to a decrease in volume in the total capacitance vasculature and a subsequent increase in venous return. Because the influence of naloxone on the capacitance vasculature is unknown, the present study was undertaken to determine the influence of naloxone on intravascular volume in the total capacitance circulation. In 31 anesthetized dogs, blood from the vena cavae was drained into an extracorporeal reservoir and returned to the right atrium at a constant rate so that changes in total intravascular volume could be measured as reciprocal changes in reservoir volume. In five animals, naloxone infusion (2 mg/ml·min for 20 min) was associated with a decrease in total capacitance volume of 121 ± 30 ml (P<0.05). To determine regional volume effects, naloxone was infused in 11 animals in which the splanchnic and extrasplanchnic vasculatures were separately perfused and drained: total and splanchnic volume decreased 64 ± 13 ml (P<0.05) and 126 ± 17 ml (P<0.0001), respectively, and extrasplanchnic volume increased 62 ± 13 ml (P<0.001). After ganglionic blockade with mecamylamine (n = 3), total volume decreased 89 ± 16 ml (P<0.05), splanchnic volume did not change, and extrasplanchnic volume decreased 91 ± 32 ml (P<0.05). In another five animals, naloxone was infused during diversion of the splanchnic venous outflow to a nonrecirculating extracorporeal reservoir: total volume decreased 122 ± 33 ml (P<0.05), splanchnic volume did not change, and extrasplanchnic volume decreased 101 ± 16 ml (P<0.01). When the splanchnic venous effluent was reinfused without naloxone administration (n = 4), total volume decreased 43 ± 5 ml (P<0.05), splanchnic volume decreased 113 ± 14 ml (P<0.05), and extrasplanchnic volume increased 68 ± 10 ml (P<0.05). Thus, naloxone is associated with a decrease in total capacitance volume, which is due entirely to a decrease in splanchnic volume. The splanchnic volume decrement would appear to be mediated through neurogenic and hormonal influences. In an animal not on bypass, it would be expected that naloxone would be associated with a decrease in total capacitance volume and subsequent increases in venous return and cardiac output.
ASJC Scopus subject areas