摘要
本文用白三烯(leukotrienes,LT)合成抑制剂乙胺嗪和前列腺素(prostaglandins,PG)合成抑制剂消炎痛,分别或同时阻断LT,PG的生成,以探讨LT和PG在不同种大鼠慢性缺氧性肺血管反应中的作用。结果显示:乙胺嗪可以阻断Wistar大鼠慢性缺氧性肺动脉高压形成,(?)pa由慢性缺氧时3.2±0.04kPa降到2.4±0.05kPa,PVR从76271±3274dyn·s·cm^(-5)下降为35948±3182dyn·s·cm^(-5)(P<0.05)。右心室肥厚也明显地减轻,RV/LV+S慢性缺氧时0.36±0.01,用药后减少到0.26±0.01(P<0.05)。消炎痛在Wistar大鼠缺氧性肺动脉高压形成中有增强作用,使慢性缺氧时的(?)pa 3.2±0.04kPa上升到3.7±0.07kPa,PVR由76271±3274dyn·s·cm^(-5)增加到93780±4264dyn·s·cm^(-5)(P<0.05)。Hilltop大鼠对缺氧更敏感,慢性缺氧性肺动脉高压和右心室肥厚均较Wistar大鼠明显。(?)pa分别为4.0±0.17kPa对3.2±0.04kPa,RV/LV+S分别为0.39±0.23对0.36±0.01(P<0.05)。乙胺嗪并不能完全阻止Hilltop大鼠缺氧性肺动脉高压形成,用药后(?)pa为3.3±0.12kPa,明显低于慢性缺氧时4.0±0.17kPa,但仍显著高于常压对照组的2.3±0.03kPa。消炎痛对其缺氧性肺动脉高压和右心室肥厚无明显影响。结果提示:两种大鼠对缺氧反应性的差异可能同LT的介导作用和扩管性PG的调节作用的差别有关。
The effect of diethylcarbamazine (DEC), an inhibitor of leukotrienes (LTS) synthesis or indomethacin, an inhibitor of prostaglandins (PGs) synthesis was investigated in chronic hypoxic pulmonary hypertension and reactivity of pulmonary vessels in different strains of rats. The results showed that in Wistar rats, DEC could prevent chronic hypoxic pulmonary hypertension and right ventricular hypertrophy. (?)pa and PVR were reduced, (?)pa from 3.2±0.04kPa to 2.4±0.05kPa; PVR from 76271±3274 dyno·s·cm^(-5) to 35948±3182 dyn·s·cm^(-5) respectively (P<0.05), and RV/LV+S decreased from 0.36±0.01 to 0.26±0.01 (P<0.05). Whereas indomethacin could intensify chronic hypoxic pulmonary hypertension. Chronic hypoxia increased (?)pa and PVR were augmented, Ppa from 3.2±0.04 kPa to 3.7±0.07 kPa; PVR from 76271±3274 dyn·s·cm^(-5) to 93780±4264 dyn·s·cm^(-5), respectively (P<0.05). In Hilltop rats with high responsiveness to hypoxia, no effects on chronic hypoxic pulmonary hypertension and right ventricular hypertrophy were noted with indomethacin treatment and DEC could partially inhibit pulmonary hypertension, (?)pa decreased remarkably to 3.3±0.12 kPa after DEC treatment, but remained higher than that in normoxic group. It suggested that the difterence of pulmonary response to hypoxia in two strains of rats might be related to the different role of either LTs' modulator or PGs' regulator.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1991年第4期368-372,共5页
Chinese Journal of Pathophysiology
基金
国家自然科学基金
