Shelub I, van Grondelle A, McCullough R, Hofmeister S, Reeves J T
J Appl Physiol Respir Environ Exerc Physiol. 1984 Mar;56(3):810-5. doi: 10.1152/jappl.1984.56.3.810.
Despite numerous efforts, a reliable model of chronic embolic pulmonary hypertension has not been established. To develop such a model five conscious mongrel dogs were embolized repeatedly over 16-30 wk with Sephadex microspheres 286 +/- 70 micron in diameter. Hemodynamic and respiratory measurements were obtained just prior to each embolization. Chronic pulmonary hypertension developed in all dogs. Pulmonary hypertension was not accounted for by increased cardiac output, wedge pressure, right atrial pressure, or systemic arterial pressure. Gas exchange was little altered. Lung histological study revealed microspheres clustered within vessels. In three dogs increased pulmonary arterial pressure was sustained despite cessation of embolization for up to 5 mo. Reembolization in one of these caused further pulmonary hypertension. In two dogs acute pulmonary vasodilation by O2 breathing and administration of prostaglandin E1 reduced, but did not abolish, the increased pulmonary vascular resistance, suggesting some vascular tone was present. An embolic model of chronic pulmonary hypertension in awake dogs allows further investigation into the evolution of pulmonary hypertension.
尽管进行了大量努力，但尚未建立可靠的慢性栓塞性肺动脉高压模型。为了建立这样一个模型，对5只清醒的杂种犬在16 - 30周内反复用直径为286±70微米的葡聚糖微球进行栓塞。在每次栓塞前进行血流动力学和呼吸测量。所有犬均出现慢性肺动脉高压。肺动脉高压并非由心输出量、楔压、右心房压力或体动脉压力升高所致。气体交换几乎没有改变。肺组织学研究显示微球聚集在血管内。在3只犬中，尽管停止栓塞长达5个月，肺动脉压力仍持续升高。其中1只犬再次栓塞导致进一步的肺动脉高压。在2只犬中，通过吸氧和给予前列腺素E1进行急性肺血管舒张可降低但不能消除升高的肺血管阻力，提示存在一定的血管张力。清醒犬慢性肺动脉高压的栓塞模型有助于进一步研究肺动脉高压的演变。
