Björnsson O G, Kobayashi K, Williamson J R
Eur J Clin Invest. 1987 Apr;17(2):146-55. doi: 10.1111/j.1365-2362.1987.tb02394.x.
The interaction between leukotriene D4 and adenosine or the prostacyclin analogue iloprost was studied in isolated guinea-pig hearts. Adenosine (1 X 10(-6) M) or iloprost (5 X 10(-8) M) abolished or greatly attenuated the vasoconstrictive effect of leukotriene D4 over a wide dose range of leukotriene D4 (0.01-1000 ng), and myocardial ischemia as a consequence of coronary insufficiency completely disappeared. Comparison of myocardial levels of reduced pyridine nucleotide fluorescence in hearts treated with leukotriene D4 and in hearts subjected to varying degrees of high-flow hypoxia, or the calcium agonist BAY-K 8644, revealed low levels of reduced pyridine nucleotides in the leukotriene D4-treated hearts, suggesting that leukotriene D4 directly suppressed myocardial contractility. These findings were supported by full restoration of cardiac work by the receptor antagonist FPL 55712 following leukotriene D4 treatment. It is concluded that adenosine and iloprost are potent inhibitors of leukotriene D4-induced reduction in coronary flow in guinea-pig hearts, and that myocardial ischaemia and suppressed cardiac work are prevented during leukotriene D4 study in adenosine or iloprost perfused hearts. Low levels of myocardial-reduced pyridine nucleotides during leukotriene D4 treatment and restoration of cardiac work by FPL 55712 indicate that leukotriene D4 may also have a direct suppressive effect on myocardial contractility.
在离体豚鼠心脏中研究了白三烯D4与腺苷或前列环素类似物伊洛前列素之间的相互作用。腺苷（1×10⁻⁶ M）或伊洛前列素（5×10⁻⁸ M）在白三烯D4的广泛剂量范围（0.01 - 1000 ng）内消除或极大地减弱了白三烯D4的血管收缩作用，并且冠状动脉供血不足导致的心肌缺血完全消失。比较用白三烯D4处理的心脏与经历不同程度高流量缺氧的心脏或钙激动剂BAY - K 8644处理的心脏中还原型吡啶核苷酸荧光的心肌水平，发现白三烯D4处理的心脏中还原型吡啶核苷酸水平较低，表明白三烯D4直接抑制心肌收缩力。白三烯D4处理后受体拮抗剂FPL 55712使心脏功能完全恢复，支持了这些发现。得出的结论是，腺苷和伊洛前列素是豚鼠心脏中白三烯D4诱导的冠状动脉血流减少的有效抑制剂，并且在腺苷或伊洛前列素灌注心脏的白三烯D4研究过程中可预防心肌缺血和心脏功能抑制。白三烯D4处理期间心肌还原型吡啶核苷酸水平较低以及FPL 55712使心脏功能恢复表明白三烯D4可能也对心肌收缩力有直接抑制作用。
