Nivatpumin T, Yipintsoi T, Penpargkul S, Scheuer J
Am J Physiol. 1975 Aug;229(2):501-5. doi: 10.1152/ajplegacy.1975.229.2.501.
To study the effects of acute uremia on the inotropic state of the rat heart, we subjected rats to bilateral nephrectomy and studied their hearts in the open chest 24 h later. Uremic rats had significantly higher systolic blood pressure than sham-operated animals. Left ventricular systolic pressure and maximum dP/dt, both during ejection and isovolumic contrations, were higher for any given end-diastolic pressure in hearts of uremic rats than in sham-operated animals. This difference in performance charcteristics was not abolished by doses of propranolol that blocked the heart rate response to isoproterenol. The administration of phenoxybenzamine during the 24 h of uremia abolished the blood pressure rise in uremic rats, but the increased contractile state persisted. Treatment of sham-operated animals with methoxamine to produce the same course of blood pressure as observed in uremic rats was also associated with an increased inotropic state. These results indicate that in the rat, acute uremia is associated with an increased inotropic state that is not mediated by beta-adrenergic mechanisms. The systolic hypertension of acute uremia is not the major cause of the increased contractility, although systolic hypertension without uremia can mimic the performance characteristics found in hearts of uremic rats.
为研究急性尿毒症对大鼠心脏变力状态的影响，我们对大鼠进行双侧肾切除术，并于24小时后在开胸状态下研究其心脏。尿毒症大鼠的收缩压显著高于假手术动物。在任何给定的舒张末期压力下，尿毒症大鼠心脏在射血期和等容收缩期的左心室收缩压和最大dP/dt均高于假手术动物。这种性能特征的差异并未被阻断心脏对异丙肾上腺素心率反应的普萘洛尔剂量所消除。在尿毒症的24小时内给予酚苄明可消除尿毒症大鼠的血压升高，但收缩状态增加仍持续存在。用甲氧明治疗假手术动物以产生与尿毒症大鼠相同的血压过程，也与变力状态增加有关。这些结果表明，在大鼠中，急性尿毒症与变力状态增加有关，且这种增加并非由β-肾上腺素能机制介导。急性尿毒症的收缩期高血压不是收缩性增加的主要原因，尽管无尿毒症的收缩期高血压可模拟尿毒症大鼠心脏的性能特征。
