Grisk A, Hoffmann U, Möritz K U
Institute of Pharmacology and Toxicology, Ernst Moritz Arndt University, Greifswald, GDR.
Biomed Biochim Acta. 1988;47(7):681-8.
We compared the potential beta-receptor blocker, B 24/76 i.e. 1-(2,4-dichlorophenoxy)-3[2-3,4-dimethoxyphenyl)ethanolamino]-prop an-2-ol, which is characterized by beta 1-adrenoceptor blocking and beta 2-adrenoceptor stimulating properties with propranolol. The studies were performed using an experimental model of isoproterenol-induced heart hypertrophy in rats. A correlation of the blood pressure was neither found in the development nor in the attempt to suppress the development of heart hypertrophy with the two beta-receptor blockers. Both beta-blockers influenced the development of hypertrophy to a different, but not reproducible extent. It was possible to suppress the increased ornithine decarboxylase activity with both beta-blockers in hypertrophied hearts, but there was no effect on the heart mass. Neither propranolol nor B 24/76 could stop the changes in the characteristic myosin isoenzyme pattern of the hypertrophied rat heart. Thus, the investigations did not provide any evidence that the beta-receptor blockers propranolol and B 24/76 have the potency to prevent isoproterenol from producing heart hypertrophy.
我们比较了潜在的β受体阻滞剂B 24/76，即1-(2,4-二氯苯氧基)-3-[2-(3,4-二甲氧基苯基)乙醇氨基]-丙-2-醇，其具有β1-肾上腺素能受体阻断和β2-肾上腺素能受体刺激特性，并与普萘洛尔进行了比较。研究使用异丙肾上腺素诱导大鼠心脏肥大的实验模型进行。在心脏肥大的发展过程中以及用这两种β受体阻滞剂抑制心脏肥大发展的尝试中，均未发现血压与心脏肥大之间存在相关性。两种β受体阻滞剂对肥大发展的影响程度不同，但不可重复。两种β受体阻滞剂都能抑制肥大心脏中鸟氨酸脱羧酶活性的增加，但对心脏重量没有影响。普萘洛尔和B 24/76都不能阻止肥大大鼠心脏特征性肌球蛋白同工酶模式的变化。因此，这些研究没有提供任何证据表明β受体阻滞剂普萘洛尔和B 24/76有能力阻止异丙肾上腺素导致心脏肥大。
