Mentz P, Pawelski K E, Giessler C, Mest H J, Mannes F, Rotzoll S
Department of Pharmacology and Toxicology, Martin Luther University Halle-Wittenberg, GDR.
Biomed Biochim Acta. 1988;47(10-11):S244-7.
Cardiac tissue from different parts of hearts from guinea pigs and rabbits have the capacity to rapidly synthesize prostacyclin (PGI2). Auricles show a higher PGI2-formation than ventricles. Addition of the endoperoxide PGH2 markedly enhanced the myocardial PGI2-biosynthesis. Furthermore many cardiotonic drugs induced a significant rise, but eicosanoids or cyclooxygenase inhibitors a marked reduction of the cardiac PGI2-formation. Acute pressure overload by graduated aortic stenosis, ischemia by coronary ligation or pacing with high frequency reduced the cardiac contractility. After aortic stenosis the myocardial PGI2-biosynthesis is lowered, but increased after coronary ligation or pacing. Under these conditions indomethacin, PGE1, iloprost, verapamil and trapidil markedly reduced the PGI2-biosynthesis and exert a protective effect in regard to cardiac damage. The results indicate that pathophysiological changes significantly influence the PGI2-biosynthesis of the heart. The drug induced inhibition of the myocardial PGI2-formation parallels a cardioprotective effect of these substances.
豚鼠和兔子心脏不同部位的心肌组织具有快速合成前列环素（PGI2）的能力。心房的PGI2生成量高于心室。添加内过氧化物PGH2可显著增强心肌PGI2的生物合成。此外，许多强心药物可导致显著升高，但类花生酸或环氧化酶抑制剂可使心脏PGI2生成量显著降低。通过渐进性主动脉狭窄造成的急性压力超负荷、冠状动脉结扎引起的缺血或高频起搏会降低心脏收缩力。主动脉狭窄后心肌PGI2生物合成降低，但冠状动脉结扎或起搏后增加。在这些情况下，吲哚美辛、PGE1、伊洛前列素、维拉帕米和曲匹地尔可显著降低PGI2生物合成，并对心脏损伤发挥保护作用。结果表明，病理生理变化会显著影响心脏的PGI2生物合成。药物诱导的心肌PGI2生成抑制与这些物质的心脏保护作用平行。
