呼气末正压通气会使家兔呼出气体中检测到的内源性一氧化氮增加。

Positive end-expiratory pressure ventilation elicits increases in endogenously formed nitric oxide as detected in air exhaled by rabbits.

作者信息

Persson M G, Lönnqvist P A, Gustafsson L E

机构信息

Department of Physiology and Pharmacology, St. Göran's Hospital, Stockholm, Sweden.

出版信息

Anesthesiology. 1995 Apr;82(4):969-74. doi: 10.1097/00000542-199504000-00021.

DOI:10.1097/00000542-199504000-00021

PMID:7717570

Abstract

BACKGROUND

Nitric oxide (NO) formed from L-arginine is exhaled by mammals and regulates pulmonary vascular tone. Little is known about how its formation is stimulated.

METHODS

The concentration of NO in exhaled air was monitored by chemiluminescence in pentobarbital-anesthetized rabbits receiving mechanical ventilation by tracheostomy with graded positive end-expiratory pressure (PEEP).

RESULTS

Introduction of PEEP (2.5-15 cmH2O) elicited dose-dependent and reproducible increments in exhaled NO and in arterial oxygen tension (PaO2). The increase in exhaled NO exhibited a biphasic pattern, with an initial peak followed by a partial reversal during the 4-min period at each level of PEEP. Thus, at a PEEP of 10 cmH2O, exhaled NO initially increased from 19 +/- 4 to 30 +/- 5 parts per billion (ppb) (P < 0.001, n = 9) and then decreased to 27 +/- 5 ppb (P < 0.005) at the end of the 4-min observation period. Simultaneously, PaO2 increased from 75 +/- 12 mmHg in the control situation to 105 +/- 11 mmHg (P < 0.05) at a PEEP of 10 cmH2O. After bilateral vagotomy, including bilateral transection of the depressor nerves, the increase in exhaled NO in response to PEEP was significantly reduced (P < 0.01). Thus, after vagotomy, a PEEP of 10 cmH2O elicited an increase in the concentration of exhaled NO from 13 +/- 3 to 17 +/- 3 ppb (n = 7). Vagotomy did not affect the baseline concentration of NO in exhaled air. The PEEP-induced increments in PaO2 were not affected by the NO synthase inhibitor L-N omega-arginine-methylester (30 mg.kg-1 intravenously). In open-chest experiments, PEEP (10 cmH2O) induced a reduction in cardiac output from 317 +/- 36 to 235 +/- 30 ml.min-1 and an increase in exhaled NO from 23 +/- 6 to 30 +/- 7 ppb (P < 0.05, n = 5). Reduction in cardiac output from 300 +/- 67 to 223 +/- 52 ml.min-1 by partial obstruction of the pulmonary artery did not significantly increase exhaled NO (from 23 +/- 7 to 25 +/- 6, difference not significant; n = 3).

CONCLUSIONS

PEEP elicited increments in exhaled NO, perhaps by a stretch-dependent effect on the respiratory system. This finding may be attributed in part to a vagally influenced mechanism.

摘要

背景

由L-精氨酸生成的一氧化氮（NO）可被哺乳动物呼出，并调节肺血管张力。关于其生成是如何被刺激的，人们了解甚少。

方法

通过化学发光法监测经气管切开接受机械通气并给予不同水平呼气末正压（PEEP）的戊巴比妥麻醉兔呼出气体中NO的浓度。

结果

引入PEEP（2.5 - 15 cmH₂O）可引起呼出NO和动脉血氧张力（PaO₂）呈剂量依赖性且可重复的增加。呼出NO的增加呈现双相模式，在每个PEEP水平的4分钟内，先是出现一个初始峰值，随后部分回落。因此，在PEEP为10 cmH₂O时，呼出NO最初从19±4 ppb增加到30±5 ppb（P < 0.001，n = 9），然后在4分钟观察期结束时降至27±5 ppb（P < 0.005）。同时，在PEEP为10 cmH₂O时，PaO₂从对照情况下的75±12 mmHg增加到105±11 mmHg（P < 0.05）。双侧迷走神经切断术后，包括双侧减压神经切断，对PEEP的呼出NO增加反应显著降低（P < 0.01）。因此，迷走神经切断术后，10 cmH₂O的PEEP引起呼出NO浓度从13±3 ppb增加到17±3 ppb（n = 7）。迷走神经切断术不影响呼出气体中NO的基线浓度。PEEP诱导的PaO₂增加不受NO合酶抑制剂L-Nω-精氨酸甲酯（30 mg·kg⁻¹静脉注射）的影响。在开胸实验中，PEEP（10 cmH₂O）导致心输出量从317±36降至235±30 ml·min⁻¹，呼出NO从23±6增加到30±7 ppb（P < 0.05，n = 5）。通过部分阻塞肺动脉使心输出量从300±67降至223±52 ml·min⁻¹，未显著增加呼出NO（从23±7到25±6，差异不显著；n = 3）。