缺氧时猪肺、胸主动脉内皮细胞分泌的缩血管多肽对肺动脉平滑肌的作用

在单个肺动脉平滑肌细胞(PSMC)舒缩模型上观察了缺氧及来源于猪肺内动脉、胸主动脉内皮细胞的常氧、缺氧条件培养液对PSMC的作用。浴槽内低氧(pO_2=5.33±1.33kPa)未引起PSMC形态的显著变化(n=44)。常氧培养的肺动脉内皮细胞条件培养液(NPEC)、低氧(pO_2=2.66kPa)48小时的肺动脉内皮细胞条件培养液(HPEC)、常氧及低氧培养的胸主动脉内皮细胞条件培养液(NAEC及HAEC)均能引起PSMC的收缩,细胞表面积分别缩小了22.8%、16.4%、15.7%及20%,均较对照值有显著差异。以胰蛋白酶处理HPEC使其中多肽成份灭活后,HPEC对PSMC的收缩效应减弱(n=12,P<0.05)。不同血管来源(肺动脉或胸主动脉)、不同条件(常氧及缺氧培养)的内皮细胞条件培养液对PSMC的收缩作用无差别(P>0.05)。结果提示浴槽内轻度低氧不能引起PSMC的收缩;猪肺动脉、胸主动脉内皮细胞在培养过程中均可产生内皮衍生收缩因子(EDCFs),但缺氧不能刺激两类血管的内皮产生更多的EDCFs。

Hypoxia do not increase EDCFs release from porcine pulmonary arterial and aortic endothelial cells in culture

The effects of culture media collected from porcine pulmonary arterialendothelial cells (ECs) cultured in normoxic (NPEC), hypoxic (HPEC) conditions and fromaortic ECs (NAEC and HAEC) were tested directly on single smooth muscle cells of pul-monary artery (PSMC). Both NPEC and NAEC can induce contract of PSMC, the cellularsurface area decreased by 22.8% and 15%, respectively, and no significant difference(P>0.05) found between two groups. Hypoxia did not stimulate ECs to release endothe-lium-derived contracting factors (EDCFs), and the contracting effects of HPEC (16.4%)and HAEC (20%) were similar to that of NPEC and NAEC. These results indicated thatEDCFs released from endothelial cells of pulmonary artery and aorta can induce contrac-tion of PSMC directly and that hypoxia did not increase the release of EDCFs from ECs.