Janssens S P, Thompson B T, Spence C R, Hales C A
Department of Medicine, Massachusetts General Hospital, Boston 02114.
J Appl Physiol (1985). 1994 Sep;77(3):1101-7. doi: 10.1152/jappl.1994.77.3.1101.
Chronic hypoxic pulmonary hypertension involves both vasoconstriction and vascular remodeling. Spontaneously hypertensive rats (SHR) have an increased systemic vascular resistance and a greater responsiveness to constricting stimuli. We hypothesized that, in contrast to age-matched normotensive Wistar-Kyoto rats (WKY), SHR also display spontaneous pulmonary hypertension in normoxia and increased vascular response to acute and chronic hypoxia. Baseline mean pulmonary arterial pressure (PAP) and total pulmonary resistance (TPR) were higher in SHR than in WKY. With acute hypoxia (10% O2 for 15 min), PAP increased to the same extent in SHR and WKY and cardiac output (CO) was unchanged in WKY but increased in SHR. Thus, the rise in PAP in the SHR might be accounted for by the rise in CO, as TPR did not rise, but not that in the WKY, as TPR increased. After 12 days in hypoxia (10% O2), mean arterial pressure was unchanged in WKY but decreased significantly in SHR without a change in CO. PAP increased by 59% in SHR and 54% in WKY when the rats were taken from the hypoxic chamber for 1 h. Acute hypoxic challenge caused a further increase in PAP only in WKY. Medial wall thickness of alveolar duct and terminal bronchial vessels was similar in WKY and SHR after chronic hypoxia. We conclude that SHR exhibit mild baseline pulmonary hypertension in normoxia and that chronic hypoxia does not produce a disproportionate increase in SHR pulmonary vascular remodeling and pulmonary hypertension.
慢性缺氧性肺动脉高压涉及血管收缩和血管重塑。自发性高血压大鼠（SHR）的全身血管阻力增加，对收缩刺激的反应性更强。我们假设，与年龄匹配的正常血压Wistar-Kyoto大鼠（WKY）相比，SHR在常氧状态下也表现出自发性肺动脉高压，并且对急性和慢性缺氧的血管反应增强。SHR的基线平均肺动脉压（PAP）和总肺阻力（TPR）高于WKY。急性缺氧（10%氧气，持续15分钟）时，SHR和WKY的PAP升高幅度相同，WKY的心输出量（CO）不变，而SHR的心输出量增加。因此，SHR中PAP的升高可能是由于CO的升高，因为TPR没有升高，而WKY中PAP的升高并非如此，因为TPR升高了。在缺氧（10%氧气）12天后，WKY的平均动脉压不变，而SHR的平均动脉压显著下降，CO无变化。当大鼠从缺氧舱中取出1小时后，SHR的PAP升高了59%，WKY的PAP升高了54%。急性缺氧刺激仅使WKY的PAP进一步升高。慢性缺氧后，WKY和SHR的肺泡导管和终末支气管血管的中膜厚度相似。我们得出结论，SHR在常氧状态下表现出轻度的基线肺动脉高压，慢性缺氧不会使SHR的肺血管重塑和肺动脉高压出现不成比例的增加。
