Hislop A, Reid L
Br J Exp Pathol. 1977 Dec;58(6):653-62.
Pulmonary hypertension has been induced in rats by 2 weeks' exposure to hypoxia, equivalent to an altitude of approximately 5500 m, in a hypobaric chamber. The rats were removed from the chamber and allowed to recover for up to 8 weeks at atmospheric pressure. Precise quantitative microscopic techniques after injection of the pulmonary artery have been used to estimate the regression in the pulmonary artery of the structural changes associated with pulmonary hypertension. During recovery the degree of muscularization of the pulmonary arteries decreases by disappearance of muscle cells from the small arteries and a drop in arterial wall thickness of larger vessels. These changes do not seem to reflect pulmonary artery pressure directly, since right ventricular hypertrophy regresses at a faster rate. In hypertensive rats there is a "loss" of small arteries in the alveolar region and little filling of precapillary vessels. On recovery, some of the vessels fill, suggesting that encroachment on the lumen by muscle and endothelial cells has lessened. Even after 8 weeks' recovery, however, some arteries do not return, suggesting they have completely disappeared and that regions are left with relatively little perfusion. This reduction of vascular reserve presents without there being right ventricular hypertrophy.
通过在低压舱中暴露于相当于海拔约5500米的低氧环境2周，诱导大鼠发生肺动脉高压。将大鼠从舱中取出，使其在常压下恢复长达8周。在注入肺动脉后，采用精确的定量显微镜技术来评估与肺动脉高压相关的结构变化在肺动脉中的消退情况。在恢复过程中，肺动脉的肌化程度通过小动脉中肌肉细胞的消失以及较大血管动脉壁厚度的下降而降低。这些变化似乎并不直接反映肺动脉压力，因为右心室肥大消退得更快。在高血压大鼠中，肺泡区域的小动脉出现“丢失”，毛细血管前血管几乎没有充盈。恢复时，一些血管开始充盈，这表明肌肉和内皮细胞对管腔的侵犯有所减轻。然而，即使在恢复8周后，仍有一些动脉未能恢复，这表明它们已完全消失，并且某些区域的灌注相对较少。这种血管储备的减少在没有右心室肥大的情况下出现。
