Maron M B, Rickaby D A, Dawson C A
J Appl Physiol Respir Environ Exerc Physiol. 1980 Jul;49(1):66-72. doi: 10.1152/jappl.1980.49.1.66.
In this study, we investigated the possibility that the adrenal gland contributes to nicotine-induced pulmonary hypertension using a canine left lower lung lobe (LLL) preparation that was pump-perfused with mixed venous blood at constant flow and outflow pressure. Main pulmonary artery, left atrial, and LLL arterial pressures were monitored to assess the responses of the animal's intact right lung and isolated LLL. With the adrenal venous return intact, injection of 10-26 micrograms/kg nicotine into the left ventricle or ascending aorta resulted in a 42% increase in LLL arterial pressure and a 70% increase in the pulmonary arterial-left atrial pressure gradient (Ppa-Pla). When the adrenal venous return was interrupted, the increases in LLL arterial pressure and Ppa-Pla were reduced to 6 and 10%, respectively. The LLL response could be eliminated by alpha-adrenergic receptor blockade, suggesting that adrenal catecholamines may contribute to the pulmonary hypertension induced by nicotine infusion.
在本研究中,我们利用犬左下肺叶(LLL)制备物进行了研究,该制备物以恒定流量和流出压力用混合静脉血进行泵灌注,以探究肾上腺是否参与尼古丁诱导的肺动脉高压。监测主肺动脉、左心房和LLL动脉压力,以评估动物完整右肺和孤立LLL的反应。在肾上腺静脉回流完整的情况下,向左心室或升主动脉注射10 - 26微克/千克尼古丁会导致LLL动脉压力增加42%,肺动脉-左心房压力梯度(Ppa - Pla)增加70%。当肾上腺静脉回流中断时,LLL动脉压力和Ppa - Pla的增加分别降至6%和10%。LLL反应可通过α-肾上腺素能受体阻断消除,这表明肾上腺儿茶酚胺可能参与尼古丁输注诱导的肺动脉高压。