大鼠离体肺血管反应性的品系差异

The Strain Difference in Vasoreactivity in Isolated Perfused Rat Lungs

采用改进的离体肺灌流方法,比较 Wistar与 Hilltop 大鼠缺氧性肺血管收缩反应(HPV)的差异及其与前列腺素(PGs)和白三烯(LTs)的关系。结果显示:缺氧时 Hilltop 大鼠肺动脉压增值(△Ppa)(0.88±0.13kPa),高于Wistar大鼠(0.42±0.03kPa)。灌流血中加消炎痛使Hilltop大鼠△Ppa降低43.8％,Wistar大鼠变化不明显,两者之间差异消失,灌流血中加乙胺嗪抑制LTs生成后,Hilltop和Wistar大鼠△Ppa下降率分别为38.9％和37.9％。结果表明:Hilltop 大鼠的HPV 比Wistar 大鼠强与其在缺氧时产生缩血管性PGs有关。

I ne anierence in nypoxic pulmonary vasoconsmcion (HPV) oetween wistar and Hilltop rats and the role of prostaglandins (PGs) and leukotrienes (LTs) in it were studied in isolated perfused lungs. The increment of pulmonary artery pressure (APpa) in Hilltop rats was 0. 88 ± 0.13kPa during hypoxia, which was significantly higher than that in Wistar rats (0. 42±0.03kPa). Indomethacin, a PGs synthetase inhibitor, reduced the APpa in Hilltop rats by 43. 8%, but not in Wistar rats, and the difference in APpa between these two strains of rats disappeared. Diethylcarbamazine, a LTs synthesis blockor, reduced the APpa of Hilltop and Wistar rats by 38. 9% and 37. 9%, respectively. The results suggested that the difference in vasoreactivity between Hilltop and Wistar rats was mainly related to metabolic function of lung per se. LTs might play a role as an important mediator in HPV of these two strains of rats. The production and release of vasoconstrictive PGs in Hilltop rat lung during hypoxia might be one of the mechanism responsible for the stronger HPV in Hilltop rats than in Wistar rats.