Bittner H B, Chen E P, Geiger M I, Kendall S W, Guice K S, Van Trigt P
Department of General and Cardiothoracic Surgery, Duke University Medical Center, Durham, North Carolina, USA.
J Crit Care. 1996 Mar;11(1):43-9. doi: 10.1016/s0883-9441(96)90019-2.
Nitric 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.
In 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).
Right 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).
The 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.
一氧化氮（NO）是血管张力、血压和血流的主要调节因子，在与血流动力学改变相关的疾病状态中起重要作用。然而，NO与脑死亡（BD）影响的关系尚未得到评估。
对17只杂种犬（体重23至31千克），在基线（0分钟）以及BD后120、240和360分钟时，进行右心房血清中亚硝酸盐和L-精氨酸的测量以及离体组织中亚硝酸盐提取的NO检测。心脏安装了微压计、跨音速流量探头和超声尺寸换能器，以确定收缩功能，并通过傅里叶分析来分析肺血管系统的血流特征。通过硬膜下放置球囊充气诱导脑死亡，并经神经病理学验证。结果以平均值和平均标准误差（±SEM）表示（P <.05，配对t检验）。
BD后右心室和左心室功能分别显著恶化（P <.001），下降了37%（±10）和22%（±7）。BD后6小时内，肺血管阻力、全身血管阻力以及肺阻抗均显著下降。搏动性血流（一种强力的NO释放刺激物）显著转变为更稳定的血流。BD后心肌NO提取值保持不变，血清L-精氨酸从12.84μg/L（±0.60）降至11.77μg/L（±0.55）。
与BD相关的肺血管阻力、全身血管阻力、肺阻抗和心功能的下降与NO途径的主要变化无关。NO可能在BD后的早期变化中不发挥关键作用。
