Hilliker K S, Bell T G, Roth R A
Thromb Haemost. 1983 Dec 30;50(4):844-7.
Platelets are believed to be involved in the development of monocrotaline pyrrole (MCTP)-induced pulmonary hypertension. To help identify the role of the platelet, the cardiopulmonary toxicity of MCTP was examined in fawn-hooded (FH) rats, a strain with a platelet function defect. Both Sprague-Dawley (SD) and FH rats developed right ventricular hypertrophy and increased lung weights and exhibited decreased biogenic amine removal by isolated, perfused lung preparations after MCTP treatment. The responses of the FH rats were not significantly different from those of the SD rats, suggesting that platelet uptake and release of 5-hydroxytryptamine (5HT) are not the platelet functions involved in MCTP-induced pulmonary hypertension. The FH rats had an interesting strain-related difference from SD rats; isolated lungs from FH rats removed and metabolized a greater proportion of perfused 5HT than the SD rats.
血小板被认为参与了野百合碱吡咯（MCTP）诱导的肺动脉高压的发展过程。为了帮助确定血小板的作用，在一种具有血小板功能缺陷的品系——淡黄褐家鼠（FH）中检测了MCTP的心肺毒性。经MCTP处理后，斯普拉格-道利（SD）大鼠和FH大鼠均出现右心室肥大、肺重量增加，并且分离的灌注肺标本对生物胺的清除能力降低。FH大鼠的反应与SD大鼠的反应无显著差异，这表明5-羟色胺（5HT）的血小板摄取和释放并非参与MCTP诱导的肺动脉高压的血小板功能。FH大鼠与SD大鼠存在一个有趣的品系相关差异；与SD大鼠相比，FH大鼠分离的肺对灌注5HT的清除和代谢比例更高。
