NITRIC-OXIDE IN BRAIN-DEATH RELATED CARDIOVASCULAR DYSFUNCTION

Purpose: Nitric oxide (NO) is a major regulator of vascular tone, bloo d pressure, and blood flow, and plays a significant role in disease st ates associated with hemodynamic alterations. However, the role of NO in association with the effects of brain death (ED) has not yet been e valuated. Methods: In 17 mongrel dogs (23 to 31 kg), right atrial seru m measurements of nitrite and L-arginine as well as NO ex vivo tissue nitrite extraction were performed at baseline (0), and 120, 240, and 3 60 minutes after BD. The hearts were instrumented with micromanometers , transonic flow probes, and ultrasonic dimension transducers to deter mine systolic function and to analyze the pulmonary vasculature flow c haracteristics by Fourier analysis. Brain death was induced by inflati on of a subdurally placed balloon and validated neuropathologically. T he results are expressed as mean and standard error of the mean (+/-SE M) (P < .05, paired t-test). Results: Right and left ventricular funct ion deteriorated significantly (P < .001) by 37% (+/-10) and 22% (+/-7 ) respectively following ED. Pulmonary and systemic vascular resistanc e as well as pulmonary impedance decreased significantly over 6 hours after BD. Pulsatile flow, a potent stimulant of NO release, converted significantly to more steady flow. Myocardial NO extraction values rem ained unchanged after BD and serum L-arginine decreased from 12.84 mu g/L (+/-0.60) to 11.77 mu g/L (+/-0.55). Conclusions: The decreases in pulmonary and systemic vascular resistance, pulmonary impedance, and cardiac function associated with BD are not related to major changes i n the NO pathway. NO may not play a key role in the early changes afte r BD. (C) 1996 by W.B. Saunders Company