氟烷会削弱内皮源性一氧化氮对血流动力学的影响。

Halothane impairs the hemodynamic influence of endothelium-derived nitric oxide.

作者信息

Sigmon D H, Florentino-Pineda I, Van Dyke R A, Beierwaltes W H

机构信息

Department of Medicine, Henry Ford Hospital, Detroit, Michigan 48202-2689.

出版信息

Anesthesiology. 1995 Jan;82(1):135-43. doi: 10.1097/00000542-199501000-00018.

DOI:10.1097/00000542-199501000-00018

PMID:7832295

Abstract

BACKGROUND

The endogenous vasodilator endothelium-derived nitric oxide (EDNO) contributes to the regulation of vascular tone and organ perfusion. It has been suggested that some volatile anesthetics may diminish the influence of EDNO and thereby decrease regional blood flow.

METHODS

Radioactive microspheres were used to determine regional hemodynamics in rats. The authors tested the hypothesis that halothane inhibits EDNO and, therefore, should diminish the response to nitric oxide synthesis inhibition by NW-nitro-L-arginine methyl ester (L-NAME) compared with either conscious or barbiturate-anesthetized rats.

RESULTS

NW-nitro-L-arginine methyl ester decreased blood flow to the brain by 23% (P < 0.005) in conscious rats to a level similar to that seen with either anesthetic agent. In both conscious and barbiturate-anesthetized rats, L-NAME increased blood pressure (BP) by 24 +/- 2 (P < 0.001) and 20 +/- 1 (P < 0.001) mmHg and total peripheral resistance (TPR) by 132% (P < 0.001) and 105% (P < 0.001), respectively. In contrast, during halothane anesthesia, both the pressor response (only 7 +/- 1 mmHg) and the increase in TPR (only 22%) were greatly diminished (P < 0.001). NW-nitro-L-arginine methyl ester decreased cardiac output (CO) by 47% (P < 0.001) and heart rate (HR) by 28% (P < 0.001) in conscious rats. In barbiturate-anesthetized rats, L-NAME decreased CO by 38% (P < 0.005) and HR by 13% (P < 0.001). In halothane-anesthetized rats, L-NAME changed neither CO nor HR. Thus halothane anesthesia largely eliminated the systemic response to EDNO synthesis inhibition. In conscious rats, L-NAME decreased blood flow to the heart (30%) and kidneys (47%). In barbiturate-anesthetized rats, L-NAME did not alter blood flow to the heart but decreased renal blood flow by 35% (P < 0.005). In halothane-anesthetized rats, L-NAME did not alter blood flow to either the heart or the kidneys. Overall, halothane blunted or blocked the systemic and regional hemodynamic responses to EDNO synthesis inhibition seen in conscious and barbiturate-anesthetized rats.

CONCLUSIONS

Halothane anesthesia greatly diminished or eliminated all systemic and regional hemodynamic responses to L-NAME. These data indicate that halothane anesthesia inhibits EDNO-mediated regulation of systemic and organ hemodynamics.

摘要

背景

内源性血管舒张因子内皮源性一氧化氮（EDNO）有助于调节血管张力和器官灌注。有人提出，一些挥发性麻醉剂可能会削弱EDNO的作用，从而减少局部血流。

方法

采用放射性微球测定大鼠局部血流动力学。作者检验了以下假设：与清醒或巴比妥类麻醉大鼠相比，氟烷抑制EDNO，因此应减弱对Nω-硝基-L-精氨酸甲酯（L-NAME）抑制一氧化氮合成的反应。

结果

在清醒大鼠中，L-NAME使脑血流量减少23%（P<0.005），降至与任何一种麻醉剂作用下相似的水平。在清醒和巴比妥类麻醉大鼠中，L-NAME分别使血压（BP）升高24±2（P<0.001）和20±1（P<0.001）mmHg，使总外周阻力（TPR）升高132%（P<0.001）和105%（P<0.001）。相比之下，在氟烷麻醉期间，升压反应（仅7±1 mmHg）和TPR的升高（仅22%）均显著减弱（P<0.001）。在清醒大鼠中，L-NAME使心输出量（CO）减少47%（P<0.001），使心率（HR）减少28%（P<0.001）。在巴比妥类麻醉大鼠中，L-NAME使CO减少38%（P<0.005），使HR减少13%（P<0.001）。在氟烷麻醉大鼠中，L-NAME对CO和HR均无影响。因此，氟烷麻醉在很大程度上消除了对EDNO合成抑制的全身反应。在清醒大鼠中，L-NAME使心脏血流量减少30%，肾脏血流量减少47%。在巴比妥类麻醉大鼠中，L-NAME未改变心脏血流量，但使肾血流量减少35%（P<0.005）。在氟烷麻醉大鼠中，L-NAME对心脏或肾脏血流量均无影响。总体而言，氟烷减弱或阻断了清醒和巴比妥类麻醉大鼠中对EDNO合成抑制的全身和局部血流动力学反应。