Grover Robert F, Reeves John T, Will Donald H, Blount S Gilbert
J Appl Physiol (1985). 1963 May 1;18(3):567-574. doi: 10.1152/jappl.1963.18.3.567.
Each of ten steers taken for 9 weeks to 12,700 ft. (Mt. Evans, Colorado) showed a marked increase in pulmonary artery (PA) pressure. Three animals had PA pressures above 90 mm Hg and one developed right heart failure. The bovine species is remarkable for the severe pulmonary hypertension which develops during chronic hypoxia rather than for an excessive PA pressure response to acute hypoxia. The rate at which the pulmonary hypertension developed at 12,700 ft. was extremely rapid compared to that at 10,000 ft. Therefore, not only the duration of the hypoxic stimulus but also its severity determine the response. The severity of the stimulus was augmented by the absence of a sustained increase in ventilation at high altitude. The pressure rise with acute hypoxia during the control period at low altitude and the dramatic fall in PA pressure when oxygen was administered at high altitude provided evidence for hypoxia-induced pulmonary vasoconstriction as an important mechanism in bovine pulmonary hypertension.
十头被带到海拔12700英尺（科罗拉多州埃文斯山）长达9周的小牛，每头的肺动脉（PA）压力都显著升高。三头动物的肺动脉压力超过90毫米汞柱，一头出现了右心衰竭。牛类在慢性缺氧期间会出现严重的肺动脉高压，这一点很显著，而不是对急性缺氧有过度的肺动脉压力反应。与在10000英尺时相比，在12700英尺处肺动脉高压发展的速度极快。因此，不仅缺氧刺激的持续时间，而且其严重程度都决定了反应。由于在高海拔地区通气没有持续增加，刺激的严重程度进一步加剧。低海拔对照期急性缺氧时的压力升高以及高海拔吸氧时肺动脉压力的急剧下降，为缺氧诱导的肺血管收缩是牛肺动脉高压的重要机制提供了证据。
