Guazzi M D, Alimento M, Berti M, Fiorentini C, Galli C, Tamborini G
Istituto di Cardiologia, University of Milan, Italy.
Circulation. 1989 Feb;79(2):337-43. doi: 10.1161/01.cir.79.2.337.
In this study, we tested the hypothesis that hypoxic pulmonary vasoconstriction may be enhanced in systemic hypertension. The hypothesis took origin from the following two considerations: alveolar hypoxia constricts the pulmonary vessels by enhancing the Ca2+ penetration across sarcolemma of the smooth muscle cells and systemic high blood pressure is associated with an elevation of tone and reactivity of the lung vessels, which seems to depend on an excessive cytosol free Ca2+ concentration due to alterations in sodium handling and in the Na+-Ca2+ exchange system. These considerations suggest the possibility that the disorders in the biochemistry of smooth muscle contraction in hypertension facilitate the rise of cytosol Ca2+ concentration during alveolar hypoxia, thus resulting in a potentiation of the vasoconstrictor properties of this stimulus. In 43 hypertensive and 17 normotensive men, pulmonary arteriolar resistance has been evaluated during air respiration and after 15 minutes of breathing 17%, 15%, and 12% oxygen in nitrogen. Curves relating changes in pulmonary arteriolar resistance to oxygen breathing contents had similar configuration in the two populations but in hypertension were steeper and significantly shifted to the left, reflecting a lower threshold and an enhanced reactivity. This pattern was not related to differences in severity of the hypoxic stimulus, plasma catecholamine concentration, or hypocapnia and respiratory alkalosis induced by hypoxia and probably was not mediated through alpha-receptor activation. Calcium channel blockade with nifedipine was able to almost abolish both the normotensive and the hypertensive pulmonary vasoconstriction reaction. These findings support the hypothesis that hypoxic pulmonary vasoconstriction may be enhanced in systemic hypertension.
在本研究中，我们验证了系统性高血压可能增强低氧性肺血管收缩的假说。该假说源于以下两点考虑：肺泡低氧通过增强钙离子跨平滑肌细胞膜的内流来收缩肺血管，而系统性高血压与肺血管张力和反应性升高有关，这似乎取决于由于钠转运及钠钙交换系统改变导致的胞浆游离钙离子浓度过高。这些考虑提示，高血压时平滑肌收缩生化过程的紊乱可能会促进肺泡低氧时胞浆钙离子浓度升高，从而增强这种刺激的血管收缩特性。我们对43名高血压男性和17名血压正常男性在空气呼吸时以及呼吸含17%、15%和12%氧气的氮气15分钟后，评估了肺小动脉阻力。两组人群中肺小动脉阻力变化与吸氧含量的关系曲线形态相似，但高血压组的曲线更陡且明显左移，这反映出阈值更低且反应性增强。这种模式与低氧刺激的严重程度、血浆儿茶酚胺浓度或低氧引起的低碳酸血症和呼吸性碱中毒的差异无关，且可能不是通过α受体激活介导的。硝苯地平阻断钙通道几乎能够消除血压正常者和高血压者的肺血管收缩反应。这些发现支持系统性高血压可能增强低氧性肺血管收缩的假说。
