Smith P, Heath D, Padula F
Thorax. 1978 Feb;33(1):31-42. doi: 10.1136/thx.33.1.31.
Six female Wistar albino rats were exposed to the hypoxia of a simulated altitude of 5500 m, three for a period of one week and three for a month. They developed ultrastructural changes in the pulmonary trunk consisting of evaginations of muscle cells of its media through gaps in the internal elastic lamina to press into the underlying endothelial cells. Such evaginations were usually devoid of myofilaments and organelles. Some appeared so electron-lucent as to be unrecognisable as muscle apart from the unequivocal connection with the parent smooth muscle cells. Elsewhere we have demonstrated that muscular evaginations in normal pulmonary blood vessels are an artefact brought about by collapse of lung tissue and that they can be avoided by distending the lung. Hence in the present investigation, in which the pulmonary trunk was fixed in distension, the evaginations are interpreted as indicating contraction of the muscle cells able to overcome the distending force. We interpret them as evidence of constriction of muscle cells in the media of the pulmonary trunk in response to hypoxia.
六只雌性Wistar白化大鼠暴露于模拟海拔5500米的低氧环境中,三只暴露一周,三只暴露一个月。它们的肺动脉干出现了超微结构变化,表现为中膜肌细胞通过内弹性膜的间隙向外突出,压迫下方的内皮细胞。这种突出通常没有肌丝和细胞器。有些突出在电子显微镜下显得非常透亮,除了与母平滑肌细胞有明确的连接外,难以辨认出是肌肉组织。我们在其他研究中已经证明,正常肺血管中的肌肉突出是肺组织塌陷导致的人为假象,通过扩张肺可以避免这种情况。因此,在本研究中,肺动脉干是在扩张状态下固定的,这些突出被解释为表明肌细胞能够克服扩张力而发生收缩。我们将其解释为肺动脉干中膜肌细胞对低氧作出收缩反应的证据。