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犬肺C纤维和快速适应性感受器传入纤维对肺充血和水肿的反应。

Responses of pulmonary C-fibre and rapidly adapting receptor afferents to pulmonary congestion and edema in dogs.

作者信息

Ravi K, Kappagoda C T

机构信息

Division of Cardiology, University of Alberta, Edmonton, Canada.

出版信息

Can J Physiol Pharmacol. 1992 Jan;70(1):68-76. doi: 10.1139/y92-010.

Abstract

The effects of cardiogenic and noncardiogenic pulmonary edema on the activities of rapidly adapting receptors (RARs) and pulmonary C-fibre receptors were investigated in dogs anaesthetized with chloralose. Cardiogenic pulmonary edema was produced by elevating the mean left atrial pressure by 25 mmHg (1 mmHg = 133.32 Pa) above the control value for a period of 45 min, by partial obstruction of the mitral valve. Noncardiogenic pulmonary edema was produced by injecting alloxan (100 mg/kg) intravenously. The effect of the latter was examined on RARs alone. Cardiogenic edema activated RARs (n = 8) and the activity was greatest during the first few minutes after elevation of mean left atrial pressure. The pulmonary C-fibre receptors (n = 6) were also activated by cardiogenic edema, but these responses were variable. Noncardiogenic pulmonary edema also activated RAR (n = 6), and this response was maintained during the entire recording period (20 min). The extravascular lung water (%), measured 15 min (n = 5) and 45 min (n = 5) after the elevation of the mean left atrial pressure, was significantly elevated above control values. However, these two values were not significantly different from each other. The extravascular lung water increased significantly after the injection of alloxan also (n = 5). These results show that during pulmonary edema, there is significant stimulation of the RARs and the pulmonary C-fibre receptors. It is suggested that the reflex respiratory responses observed in pulmonary edema may be due to the activation of both the RARs and the pulmonary C-fibre receptors.

摘要

在用氯醛糖麻醉的犬中,研究了心源性和非心源性肺水肿对快速适应感受器(RARs)和肺C纤维感受器活性的影响。通过二尖瓣部分梗阻,使平均左心房压力比对照值升高25 mmHg(1 mmHg = 133.32 Pa)并持续45分钟,从而产生心源性肺水肿。通过静脉注射四氧嘧啶(100 mg/kg)产生非心源性肺水肿。仅研究了后者对RARs的影响。心源性水肿激活了RARs(n = 8),且在平均左心房压力升高后的最初几分钟内活性最大。肺C纤维感受器(n = 6)也被心源性水肿激活,但这些反应存在变异。非心源性肺水肿也激活了RAR(n = 6),且在整个记录期(20分钟)内该反应持续存在。在平均左心房压力升高后15分钟(n = 5)和45分钟(n = 5)测量的血管外肺水(%)显著高于对照值。然而,这两个值彼此之间无显著差异。注射四氧嘧啶后血管外肺水也显著增加(n = 5)。这些结果表明,在肺水肿期间,RARs和肺C纤维感受器受到显著刺激。提示在肺水肿中观察到的反射性呼吸反应可能是由于RARs和肺C纤维感受器均被激活。

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