Howard P, Barer G R, Thompson B, Warren P M, Abbott C J, Mungall I P
Respir Physiol. 1975 Sep;24(3):325-45. doi: 10.1016/0034-5687(75)90022-5.
Vasoconstriction occuring a unventilated or hypoxic lung was studied in dogs and cats to elucidate mechanisms which both cause and reverse it. Lungs were perfused in vivo at constant pressure or constant blood flow; alternatively blood flow and pressure were measured with minimal operative interference. Stimulus-response curves of lung vessels to hypoxia showed a large response within the physiological range of P02 values. Vasoconstriction in unventilated lung caused by bronchial occlusion sometimes matched that caused by an equal degree of ventilation hypoxia but was sometimes greater. Responses to both stimuli varied widely between animals and in one animal at different times. This could be due to variable availability of a transmitter or variable presence of vasodilator substances. Both histamine and beta-adrenoreceptor stimulants caused pulmonary vasodilatation in unventilated lung. Histamine caused pulmonary vasoconstriction and vasodilatation in different circumstances which could be blocked respectively by H1 and H2 antihistamine drugs. Potent alpha- and beta-adrenoreceptor action on pulmonary vessels was demonstrated in both species. Alpha-adrenoreceptor blocking drugs caused dilatation and beta-adrenoreceptor blocking drugs caused vasoconstriction. The possible role of histamine and catecholamines in causing or reversing hypoxic vasoconstriction or in maintaining pulmonary vascular tone is discussed.
为了阐明引起和逆转肺血管收缩的机制，研究人员在犬和猫身上对未通气或低氧肺中的血管收缩进行了研究。在体内以恒压或恒血流灌注肺；或者在最小手术干扰下测量血流和压力。肺血管对低氧的刺激-反应曲线在生理范围内的P02值时显示出较大反应。支气管阻塞引起的未通气肺血管收缩有时与同等程度通气性低氧引起的收缩相匹配，但有时更大。对这两种刺激的反应在不同动物之间以及同一动物在不同时间差异很大。这可能是由于递质的可用性不同或血管扩张物质的存在不同。组胺和β-肾上腺素能受体激动剂在未通气肺中均引起肺血管舒张。组胺在不同情况下分别引起肺血管收缩和舒张，可分别被H1和H2抗组胺药阻断。在这两个物种中均证实了α-和β-肾上腺素能受体对肺血管有强大作用。α-肾上腺素能受体阻断药引起血管舒张，β-肾上腺素能受体阻断药引起血管收缩。文中讨论了组胺和儿茶酚胺在引起或逆转低氧性血管收缩或维持肺血管张力方面的可能作用。
