Ravi Krishnan, Kappagoda C Tissa
Department of Physiology, V.P. Chest Institute, University of Delhi, Delhi, India.
Indian J Chest Dis Allied Sci. 2008 Jan-Mar;50(1):7-18.
The essential feature of left ventricular dysfunction is an increase in left atrial pressure and pulmonary venous congestion leading to a fluid flux across the pulmonary microvasculature. Small acute increases (< 10 mmHg) in left atrial pressure enhance the extravascular fluid volume in the airways and activate the rapidly adapting receptors (RAR). With larger increases in left atrial pressure (approximately 25 mmHg) both the RAR and the C-fiber receptors in the airways and the alveoli are activated. Activation of RAR causes a reflex increase in respiratory rate, tracheal tone and mucus secretion from the airways. It appears that small increases in extravascular fluid volume of the airways also cause a reflex diuresis which is mediated by activation of neuronal nitric oxide synthase in the renal medulla. In contrast, when left atrial pressure is elevated chronically, further small increments in extravascular fluid volume of the airways no longer stimulate the RAR. The reflex diuresis is also not evident under these circumstances. However, the RAR continue to be activated by increments in left atrial pressure in excess of 25 mmHg. It is suggested that the RAR of the airways play a significant role in monitoring changes in the extravascular fluid volume of the airways and mediate the reflexes which are associated with the symptomatology of acute left ventricular dysfunction.
左心室功能障碍的基本特征是左心房压力升高和肺静脉充血，导致液体通过肺微血管流动。左心房压力的小幅急性升高（<10 mmHg）会增加气道内血管外液体量，并激活快速适应性受体（RAR）。随着左心房压力进一步升高（约25 mmHg），气道和肺泡中的RAR以及C纤维受体均被激活。RAR的激活会导致呼吸频率、气管张力和气道黏液分泌反射性增加。气道血管外液体量的小幅增加似乎也会引起反射性利尿，这是由肾髓质中神经元型一氧化氮合酶的激活介导的。相比之下，当左心房压力长期升高时，气道血管外液体量的进一步小幅增加不再刺激RAR。在这种情况下，反射性利尿也不明显。然而，左心房压力超过25 mmHg的升高仍会激活RAR。有人认为，气道的RAR在监测气道血管外液体量的变化以及介导与急性左心室功能障碍症状相关的反射方面发挥着重要作用。
