NO介导肺动脉高压及其调节

Nitric Oxide-Mediated Pulmonary Hypertension and Its Control

目的：研究NOS、O2-·和Ca2+在犬高动力型肺动脉高压形成中的意义，控讨O2-·、［Ca2+]i在L一精氨酸→NO通路上的调节作用。方法：6只高动力型肺动脉高压模型犬，检测肺组织NOS活性，丙二醛（MDA）含量及总钙含量。结果：与正常比较，肺高压时，肺组织NOS活性较正常明显降低（P＜0.01），MDA、[Ca2+]i；含量明显升高（P＜0.05），肺组织NOS与平均肺动脉压（MPAP）、肺血管阻力（PVR）、[Ca2+]i及MDA呈明显负相关。结论：NO作用减弱在肺高压形成中与限速酶NOS活性降低密切相关,O2·和[Ca2+]；共同介导肺高压过程。

Objective: To investigae the mplication of mtric oxide synthase(N0S) [ Ca2 + ] i content and oxygen the radical level in the developmnt of hyperkinetic Pulmonary hypertension (PH). Methods: The model of hnperkinetic PH was built in 6 canines with pulmonary - systemic vessel anastomsis. The followign indices were analyzed: (1) activity of NOS, [ Ca2+ ], content and MDA capacity in lung tissue, (2) mean pulmonary arterial Pressure(MPAP), mean systemic atrerial pressure(MSAP) and Pulmonary capillary wedge presare(FCWP) by Swan Ganz catheter, Cardiac output (CO) with resistance methood, pulmonary vascular resistance (PVR) calculated, based on them. Resuitsbo: Comed with the controls, the activity of NOS in the Pulmonary tissur was markedly decreased (P < 0. 01 ) and the levels of MDA and [ Ca2+ ], were chaly elevated, showing an obvious negaive relationship among NOS MPAP' PVR' [ Ca2+ ], and MDA. Conclusion: The total Ca2+ conent and MDA capacity in the lung tissue might also assist to develop PH.