Pascual J, Sterin-Borda L, Wald M, Borda E S
Cefaprin--Conicet, Buenos Aires, Argentina.
Prostaglandins Leukot Essent Fatty Acids. 1988 Jul;33(1):53-9. doi: 10.1016/0952-3278(88)90123-8.
The biological properties of Thromboxane B2 (TXB2) on isolated rat heart were studied. Its actions were compared with U-46619 a Thromboxane A2 mimetic compound and with isoproterenol. TXB2 induced a concentration-dependent increase in contractility, that was non-competitively antagonized by propranolol. In addition TXB2 inhibited Na+ + K+-ATPase activity at the same concentrations that influenced the mechanical activity. Inhibition of beta-adrenoceptors efficiently blocked the inhibitory action of TXB2 upon Na+ + K+-ATPase-activity. Isoproterenol simulated the positive inotropic effect and the inhibitory action of TXB2 on Na+ + K+-ATPase-activity. In contrast, U-46619 did not alter the basal dF/dt, neither the enzyme activity. The foregoing results suggest that TXB2 resembles the biological effect of catecholamines-inducing stimulation of myocardial contractility and inhibition of Na+ + K+-ATPase activity.
研究了血栓素B2(TXB2)对离体大鼠心脏的生物学特性。将其作用与血栓素A2模拟化合物U-46619以及异丙肾上腺素进行了比较。TXB2诱导收缩力呈浓度依赖性增加,普萘洛尔对其有非竞争性拮抗作用。此外,TXB2在影响机械活性的相同浓度下抑制Na+ + K+-ATP酶活性。β-肾上腺素能受体的抑制有效地阻断了TXB2对Na+ + K+-ATP酶活性的抑制作用。异丙肾上腺素模拟了TXB2的正性肌力作用及其对Na+ + K+-ATP酶活性的抑制作用。相比之下,U-46619既不改变基础dF/dt,也不改变酶活性。上述结果表明,TXB2类似于儿茶酚胺的生物学效应,可诱导心肌收缩力增强并抑制Na+ + K+-ATP酶活性。