Zimmer H G, Irlbeck M, Kolbeck-Rühmkorff C K
Department of Physiology, University of Munich, Germany.
Mol Cell Biochem. 1995;147(1-2):105-14. doi: 10.1007/BF00944790.
Catecholamines and thyroid hormones have a similar influence on heart function and metabolism, but this may occur in a differential manner and to a different extent. In this study, the effects of norepinephrine (NE) and of triiodothyronine (T3) were studied in regard to the function of the left (LV) and right ventricle (RV) and to the oxidative pentose phosphate pathway (PPP). NE was applied in rats as continuous i.v. infusion (0.2 mg/kg/h) for three days. T3 was given as daily s.c. injections (0.2 mg/kg) for the same period of time. LV and RV function was measured in the closed-chest trapanal-anesthetized animals using special Millar ultraminature catheter pressure transducers. NE induced an increase in heart rate, in mean arterial pressure, and in total peripheral resistance (TPR). The cardiac RNA/DNA and the left ventricular weight/body weight ratios were increased by about 40%. These effects were prevented by simultaneous alpha- and beta-receptor blockade with prazosin and metoprolol, respectively, but not by verapamil which abolished the hemodynamic effects. RVSP was significantly elevated by NE in a dose-dependent manner. The functional effects of T3 on the LV were not as pronounced as those induced by NE. Heart rate and LV dp/dtmax were increased by T3, and this increase was prevented by concomitant beta-receptor blockade with metoprolol. In contrast to NE, T3 induced an increase in cardiac output and a concomitant decrease in TPR. The RNA/DNA ratio was elevated and cardiac hypertrophy had developed after treatment for three days with T3. These changes were not affected by beta-receptor blockade with metoprolol. RVSP was increased by T3 to a lesser extent than with NE. In metabolic terms it turned out that only NE, but not T3 had a stimulating effect on the cardiac PPP. NE increased the mRNA and activity of glucose-6-phosphate dehydrogenase (G-6-PD), the first and regulating enzyme of this pathway. However, there was no effect of T3 on G-6-PD activity nor on 6-phosphogluconate dehydrogenase activity, one of the following enzymes in the pathway within the first 5 days of T3 treatment. These results demonstrate that the functional effects of T3 were not as pronounced as or even different from those of NE, and that T3 lacked a stimulating effect on the cardiac PPP.
儿茶酚胺和甲状腺激素对心脏功能和新陈代谢有相似的影响,但这种影响可能以不同的方式且在不同程度上发生。在本研究中,研究了去甲肾上腺素(NE)和三碘甲状腺原氨酸(T3)对左心室(LV)和右心室(RV)功能以及氧化戊糖磷酸途径(PPP)的影响。NE以连续静脉输注(0.2mg/kg/h)的方式应用于大鼠,持续三天。T3在相同时间段内每日皮下注射(0.2mg/kg)。使用特殊的Millar超微型导管压力传感器在开胸经口麻醉的动物中测量LV和RV功能。NE导致心率、平均动脉压和总外周阻力(TPR)增加。心脏RNA/DNA以及左心室重量/体重比增加了约40%。这些效应分别被哌唑嗪和美托洛尔同时进行的α和β受体阻滞所阻止,但维拉帕米消除血流动力学效应时并未阻止这些效应。NE以剂量依赖性方式显著升高RVSP。T3对LV的功能影响不如NE诱导的明显。T3使心率和LV dp/dtmax增加,并且这种增加被美托洛尔同时进行的β受体阻滞所阻止。与NE相反,T3导致心输出量增加并伴随TPR降低。RNA/DNA比升高,并且在T3治疗三天后出现心脏肥大。这些变化不受美托洛尔β受体阻滞的影响。T3使RVSP升高的程度小于NE。在代谢方面,结果表明只有NE对心脏PPP有刺激作用,而T3没有。NE增加了葡萄糖-6-磷酸脱氢酶(G-6-PD)的mRNA和活性,G-6-PD是该途径的第一个调节酶。然而,在T3治疗的前5天内,T3对G-6-PD活性以及该途径中后续酶之一的6-磷酸葡萄糖酸脱氢酶活性均无影响。这些结果表明,T3的功能影响不如NE明显甚至与之不同,并且T3对心脏PPP缺乏刺激作用。