急性肺泡缺氧对大鼠活体肺微循环的影响  

Effects of acute alveaolar hypoxia on pulmonary microcirculation in rats in vivo

作　　者：皮业庆[1] 王迪浔[1] 

机构地区：[1]同济医科大学病理生理教研室

出　　处：《中国病理生理杂志》1992年第2期118-121,共4页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金委员会青年基金

摘　　要：本实验采用胸壁开窗术及显微录像电视系统,活体内观察了Wistar大鼠(n=60)在急性肺泡缺氧时(FiO_2=0.1,3 min)肺表面微循环的变化。结果如下:急性肺泡缺氧时,(1).肺细动脉内径(ID)明显缩小,A_1组(ID≥60μm)平均减少18.00%,A_2组(40～59μm)减少15.10%,A_3组(20～39μm)减少0.59%(与缺氧前比较P<0.001),肺细静脉内径(20～100μm)缩小12.43%(P<0.001),提示这两类肺微血管都有收缩,但细静脉收缩程度轻于细动脉;(2).细动脉(平均ID为55μm)内平均血流速度由0.27±0.02cm/s减慢至0.18±0.01cm/s,平均血流量由0.04±0.005ml/min减少至0.02±0.002ml/min(P<0.001);(3).肺动脉平均压由2.84±0.06kPa上升到3.33±0.07kPa(P<0.001)。本实验结果提示,肺泡缺氧既引起肺细动脉收缩,也诱发肺细静脉的收缩反应,二者都参与缺氧性肺动脉高压的形成。Abstract Making a 'thoracic window' on the right thoracic wall of an animal, changes of the surface pulmonary microcirculation in Wistar rats (n=60) in vivo were observed during acute alveaolar hypoxia (Fi=0.1,3minutes), by using intravital microscopic-video recording TV system. The data showed that: (1). Internal diameter (ID) of pulmonary arterioles (20-90μm) decreased markedly, ID of group Al (≥60μm), A2 (40-59μm), and A3 (20-39μm), were decreased by 18.00%, 15.10%, and 9,59%, respectively, and ID of venules (20-100um) were decreased by 12.43% during hypoxia (P<0.001 compared with values before hypoxia), indicating that constriction of both kinds of pulmonary microvessels was induced by hypoxia; (2). The mean flow velocity and flow volume in the pulmonary arteriole (ID=55μm) were decreased from 0.27±0.02 cm/s to 0.18±0.01cm/s, and from O.04±0.005ml/min to 0.02±0.002ml/min, respectively (P<0.001); (3). Mean pulmonary arterial pressure (Ppa) was elevated from 2.84±0.06 kPa to 3.33±0.07 kPa (P<0.001). These results suggest that the constriction of both pulmonary arterioles and venules was involved in hypoxia and which induced the formation of pulmonary hypertension in hypoxia.

关 键 词：缺氧症 微循环 肺循环 HPV 

分 类 号：R563[医药卫生—呼吸系统]