IntroductionThe 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. Other investigators have observed prolonged survival with naloxone administration in various hypotensive experimental conditions including endotoxin shock (1) and hypovolemic shock (2-4). The prolonged survival may be related to increases in cardiac contractility, cardiac output, and mean arterial pressure, which have been observed after administration in hypotensive animals (1-9) or patients (10, 11). It is also possible that the increases in cardiac output and arterial pressure are due, in part, to a decrease in capacitance volume; however, capacitance volume changes have not been previously examined.Hence, the present study was undertaken in order to assess the influence of naloxone administration on the total capacitance vasculature. A venous bypass preparation was employed to determine regional and total intravascular volume changes and the extent to which these changes are mediated by direct, neurogenic, and hormonal influences.
MethodsVenous bypass preparation. 31 mongrel dogs of either sex, weighing between 11 and 18 kg (mean 14±0 kg) were anesthetized with chloralose (60-80 mg/kg iv) and urethan (600-800 mg/kg iv), intubated, and ventilated with a mixture of room air and 100% oxygen. A median sternotomy was performed and 3,000 U of sodium heparin was administered iv. The experimental preparation utilized in dogs 1-10 is illustrated in Fig. 1. The azygos vein was ligated and the superior and inferior vena cavae were cannulated with no. 32 or 34 French catheters. The total systemic venous return was drained to an overflow column and central venous pressure was adjusted by setting the height of the column at 5 cm H20 with the right atrium as a reference point. The venous return was drained from the overflow column into a 2-liter no. 2022 graduated cylinder (Corning Glass Works, Corning, NY), which had 20-ml graduations. The draihage from the overflow column into the reservoir was sufficiently rapid to prevent accumulation of blood in the overflow column. From the 2-liter graduated cylinder, blood was pumped (Travenol perfusion pump, Travenol Laboratories, Inc., Morton Grove, IL) to the right atrium via a no. 26 French catheter in the right atrial appendage at a constant rate of 350-800 ml/min (mean 579±26 ml/min, 89% of the perfusion rates were between 500 and 800 ml/min). Because blood was returned to the animal at a constant rate, it was possible to record changes in volume in the total capacitance vasculature as reciprocal changes in volume in...