Roles of Endogenous Prostacyclin and Thromboxane A2 in the Ischemic Canine Heart

Intracoronary Administration of a Thromboxane A2 Synthase Inhibitor Relieves Acetyicholine-Induced Coronary Spasm.

“…In previous reports, TXA2 synthase inhibitors have shown potential for reducing infarct size and in the treatment of angina pectoris, 25,26 but the administration of the TXA2 synthase inhibitor was systemic in the majority of the previous reports. Selective, intracoronary injection of a TXA2 synthase inhibitor has not been reported until now when we have shown that intracoronary TXA2 synthase inhibitor relieved coronary artery spasms induced by intracoronary injection of ACh.…”

Beneficial effect of beraprost, a prostacyclin‐mimetic agent, on post‐hypoxic recovery of cardiac function and metabolism in rabbit isolated hearts

“…As described earlier, prostacyclin has physiologically antagonistic effects to thromboxane A2 on platelet aggregation (Hamberg et al, 1975;Schrbr et al, 1981b). Inhibition of thromboxane A2 production or blocking its receptor during ischaemia has been demonstrated to protect the myocardium against ischaemia/reperfusion injury as evidenced by prevention of an increase in lactate release from the heart, limitation of cardiac risk area and decrease in reperfusion-induced arrhythmias (Sakai et al, 1982;Thiemermann & Schrbr, 1984;Grover et al, 1988;1990;Mehta et al, 1990;Lesenefsky et al, 1990). Furthermore, several investigators have found that treatment with iloprost, a prostacyclinmimetic agent, improved myocardial metabolism during ischaemia and resulted in an enhanced recovery of cardiac function (Van Glist et al, 1983;Giessen et al, 1986;Pissarek et al, 1987;Chiariello et al, 1988;Ferrari et al, 1988).…”

“…Furthermore, it has been shown that thromboxane A2 antagonists and inhibition of thromboxane A2 synthesis are capable of reducing myocardial infarct size and inhibiting lactate release (Sakai et al, 1982;Grover et al, 1988). These results suggest that prostacyclin is a possible cardioprotective agent against oxygen deficiency-induced derangements in cardiac function and myocardial metabolism.…”

“…De Deckere et al (1977), Sakai et al (1982), and Karmazyn & Dhalla (1983) have demonstrated that prostacyclin and thromboxane A2 are the major metabolites of eicosanoids produced in the heart during oxygen-deprived perfusion. Prostacyclin has been shown to be a potent vasodilator and a platelet antiaggregatory agent (Moncada et al, 1976).…”

Assessment of Prostacyclin and Thromboxane A₂ Release during Reperfusion after Global Ischemia Induced by Crystalloid Cardioplegia – Comparison between Warm and Cold Ischemia

“…As a consequence, it is suggested that thromboxane A2 (TxA:) may be released and affect the coronary circulation during reper fusion as in regional ischemia [5,6] with its effects as coronary vasoconstriction and platelet aggregation. On the other hand, pre vious experimental studies showed that prostacyclin (PGI:) is released into coronary vasuclature following ischemia [7,8] and re cent works have also shown that regional ischemia is accompanied by both PGI: and TxA: releases [9,10]. In the relationship between these eicosanoids.…”