Effect of total spinal anesthesia on arterial and venous responses to dopamine and dobutamine.

To test whether acute denervation alters the vascular effects of dopamine and dobutamine, we anesthetized 16 greyhounds and placed them on total cardiopulmonary bypass (CPB). Eight dogs received total spinal anesthesia before drug testing; eight dogs were tested in the absence of total spinal anesthesia. During dopamine and dobutamine infusions, venous capacitance [determined by the volume of the CPB venous reservoir (VR)] and mean arterial pressure (MAP) were monitored. The CPB pump flows remained constant throughout our studies. Every dog received six increasing doses of both drugs. In the absence of total spinal anesthesia, both dopamine and dobutamine increased VR (decreased venous capacitance) in a dose-dependent manner. Dobutamine decreased MAP in a dose-related fashion but dopamine had no significant effect on MAP. After total spinal anesthesia, both dopamine and dobutamine produced greater dose-related increases in VR (i.e., decreases in venous capacitance) than in the absence of spinal anesthesia. Dopamine increased MAP but dobutamine had no significant effect. These data demonstrate how dopamine and dobutamine differ in their effects on the arterial circulation in the presence or absence of spinal anesthesia. The acute denervation of spinal anesthesia altered venous and arterial dose-response relationships of both drugs. Finally, our study demonstrates the effectiveness of dobutamine and, perhaps even more so, dopamine as possible alternatives to ephedrine for the pharmacologic correction of the noncardiac circulatory sequelae of spinal anesthesia.

Hemodynamic, metabolic, and morphological effects of cardiopulmonary bypass with a fluorocarbon priming solution.

Systemic perfusion, myocardial contractility, and morphological changes during and after cardiopulmonary bypass (CPB) were investigated in 22 greyhounds; Fluosol-DA 20% (FDA) and normal saline (NaCl) were compared as priming solutions for hypothermic (25 degrees C) CPB. Hemodynamic and oxygenation indices were similar in all groups. Animals with fluorocarbon primes had higher serum lactate concentrations (mean +/- standard error of the mean [SEM]) during CPB (NaCl 1.64 +/- 0.2, FDA 2.39 +/- 0.3, p less than 0.01), representing an increase over the control of 12% and 319% in the NaCl and FDA groups, respectively. After CPB, serum lactate concentration remained elevated in the FDA group, but it returned to the level of the control in the NaCl group (NaCl 1.49 +/- 0.5, FDA 2.29 +/- 1.1, p less than 0.01); increases over the control level were 7% and 302% in the NaCl and FDA groups, respectively. Myocardial contractility after CPB, expressed as dP/dt[40], was similar in the two experimental groups. Three weeks after CPB, a histological examination by light microscopy of multiple organs obtained from a separate group of 12 animals treated similarly was performed, demonstrating no significant morphological differences between animals primed with fluorocarbon or with saline. The results suggest that FDA is a satisfactory priming agent for hypothermic CPB. It adequately preserves myocardial function and causes no adverse morphological changes, but a persistent, as yet unexplained, elevation in serum lactate concentration occurs.

Inotropic response of the salvaged myocardium after acute coronary occlusion.

We determined the response of the reperfused myocardium to inotropic stimulation with dobutamine hydrochloride. The middle part of the left anterior descending coronary artery (LAD) was occluded in 15 greyhounds for 3 hours. Group 1 (N = 8) was reperfused for 3 hours in the beating, working heart. Group 2 (N = 7) was put on cardiopulmonary bypass (CPB) for 1 hour, received 500 ml of potassium cardioplegia in the aortic root and in the area of ischemia through an internal mammary-LAD graft, and the LAD was reperfused off CPB for 3 hours. After 3 hours of reperfusion, dobutamine was given at 10 micrograms/kg/min for 20 minutes. Regional myocardial function was determined with subendocardial ultrasonic crystals in the area of ischemia and in the base of the heart; segmental contractility was determined from the ratio of peak left ventricular pressure to end-systolic segment length; and global contractility was determined by the slope of the ventricular pressure wave at a developed pressure of 40 mm Hg. Measurements were made prior to LAD occlusion (control), at the end of 3 hours of reperfusion (6 hours from the beginning of occlusion), and after 20 minutes of dobutamine infusion. Dobutamine infusion improved segmental function in all animals compared with 3 hours of reperfusion. The study shows that the reperfused myocardium responds favorably to inotropic stimulation after 3 hours of occlusion and 3 hours of reperfusion, and that the contractile response both to reperfusion and to inotropic stimulation is greatly affected by the method of reperfusion.