• H B Bittner, E P Chen, M I Geiger, S W Kendall, K S Guice, and P Van Trigt.
• Department of General and Cardiothoracic Surgery, Duke University Medical Center, Durham, North Carolina, USA.
• J Crit Care. 1996 Mar 1; 11 (1): 43-9.

PurposeNitric oxide (NO) is a major regulator of vascular tone, blood pressure, and blood flow, and plays a significant role in disease states associated with hemodynamic alterations. However, the role of NO in association with the effects of brain death (BD) has not yet been evaluated.MethodsIn 17 mongrel dogs (23 to 31 kg), right atrial serum measurements of nitrite and L-arginine as well as NO ex vivo tissue nitrite extraction were performed at baseline (0), and 120, 240, and 360 minutes after BD. The hearts were instrumented with micromanometers, transonic flow probes, and ultrasonic dimension transducers to determine systolic function and to analyze the pulmonary vasculature flow characteristics by Fourier analysis. Brain death was induced by inflation of a subdurally placed balloon and validated neuropathologically. The results are expressed as mean and standard error of the mean (+/- SEM) (P < .05, paired t-test).ResultsRight and left ventricular function deteriorated significantly (P < .001) by 37% (+/- 10) and 22% (+/- 7) respectively following BD. Pulmonary and systemic vascular resistance 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 remained unchanged after BD and serum L-arginine decreased from 12.84 mu g/L (+/- 0.60) to 11.77 mu g/L (+/- 0.55).ConclusionsThe decreases in pulmonary and systemic vascular resistance, pulmonary impedance, and cardiac function associated with BD are not related to major changes in the NO pathway. NO may not play a key role in the early changes after BD.

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