Smith D M, Sugden P H
Biochem J. 1987 Apr 15;243(2):473-9. doi: 10.1042/bj2430473.
A modified anterogradely perfused rat heart preparation is described in which all the cardiac output passes through the coronary circulation. Such a preparation develops hypertensive aortic pressures. Hypertensive aortic pressures or insulin stimulate the rate of cardiac protein synthesis and inhibit the rate of protein degradation. Aortic pressure and insulin may be important in the regulation of cardiac nitrogen balance in vivo. By abolishing cardiac prostaglandin synthesis with 4-biphenylacetate, we were able to investigate the possible involvement of prostaglandins in the modulation of protein turnover by pressure overload or insulin. There was no evidence of any involvement. However, insulin stimulated and cycloheximide inhibited cardiac prostaglandin synthesis. These findings are consonant with an enzyme involved in prostaglandin synthesis being short-lived and prostaglandin synthesis being rapidly influenced by activators and inhibitors of protein synthesis and degradation.
本文描述了一种改良的经主动脉顺行灌注大鼠心脏标本，其中所有心输出量均通过冠状动脉循环。这种标本会产生高血压性主动脉压力。高血压性主动脉压力或胰岛素可刺激心脏蛋白质合成速率并抑制蛋白质降解速率。主动脉压力和胰岛素可能在体内心脏氮平衡的调节中起重要作用。通过用4-联苯乙酸消除心脏前列腺素合成，我们能够研究前列腺素在压力超负荷或胰岛素调节蛋白质周转中可能的参与情况。没有证据表明有任何参与。然而，胰岛素刺激而环己酰亚胺抑制心脏前列腺素合成。这些发现与参与前列腺素合成的一种酶寿命短暂以及前列腺素合成受蛋白质合成和降解的激活剂和抑制剂快速影响是一致的。
