Farrukh I S, Michael J R, Summer W R, Adkinson N F, Gurtner G H
J Appl Physiol (1985). 1985 Jan;58(1):34-44. doi: 10.1152/jappl.1985.58.1.34.
Infusion of tert-butyl hydroperoxide (t-bu-OOH) or arachidonic acid into rabbit pulmonary arteries stimulated thromboxane B2 (TxB2) production and caused pulmonary vasoconstriction. Both phenomena were blocked by cyclooxygenase inhibitors or a thromboxane synthase inhibitor. The increase in pulmonary arterial pressure caused by either t-bu-OOH or arachidonic acid infusion correlated with the concentration of TxB2 in the effluent perfusate. The concentration of TxB2 in the effluent perfusate, however, was always 10-fold greater after arachidonic acid infusion. In the rabbit pulmonary vascular bed lipoxygenase products did not appear involved in the vasoactive response to t-bu-OOH or exogenous arachidonic acid infusion. Calcium entry blockers or a calcium-free perfusate prevented the thromboxane-induced pulmonary vasoconstriction. Calmodulin inhibitors also blocked the pulmonary vasoconstriction induced by t-bu-OOH without affecting the production of TxB2 or prostacyclin. These results suggest that thromboxane causes pulmonary vasoconstriction by increasing cytosol calcium concentration.
向兔肺动脉内注入叔丁基过氧化氢（t-bu-OOH）或花生四烯酸可刺激血栓素B2（TxB2）生成并引起肺血管收缩。这两种现象均被环氧化酶抑制剂或血栓素合酶抑制剂所阻断。由注入t-bu-OOH或花生四烯酸所引起的肺动脉压力升高与流出灌注液中TxB2的浓度相关。然而，注入花生四烯酸后流出灌注液中TxB2的浓度总是高出10倍。在兔肺血管床中，脂氧合酶产物似乎未参与对t-bu-OOH或外源性花生四烯酸注入的血管活性反应。钙通道阻滞剂或无钙灌注液可防止血栓素诱导的肺血管收缩。钙调蛋白抑制剂也可阻断由t-bu-OOH诱导的肺血管收缩，而不影响TxB2或前列环素的生成。这些结果表明，血栓素通过增加胞浆钙浓度而引起肺血管收缩。
