Rieker R P, Lee J C, Downing S E
Yale J Biol Med. 1975 Nov;48(5):353-60.
This study was designed to investigate changes in cardiac performance during hypoglycemia produced by the administration of insulin in the newborn piglet. With heart rate, aortic pressure, and aortic flow held constant, the treated group demonstrated a pronounced positive inotropic response manifested by an increase of dP/dt max to 138% of control values. Central nervous system function and beta adrenergic activity were excluded from the preparation by ligation of the brachiocephalic vessels and administration of practolol. For reasons discussed, it is unlikely that the findings can be ascribed to glucagon contamination. Therefore, the increase in contractility presumably resulted from a direct effect of insulin upon the myocardium. Clinical and laboratory data suggest that the resistance of the neonate to hypoxia is modified by glycogen stores. Insulin is known to increase glycogen synthesis, and this effect might be expected to augment myocardial resistance to hypoxia. Under the conditions of these experiments, however, pretreatment with insulin had no demonstrable influence on the rate of deterioration of cardiac function during hypoxia. The mechanism of cardiac stimulation by insulin is unknown but may involve calcium fluxes.
本研究旨在调查新生仔猪注射胰岛素诱发低血糖期间心脏功能的变化。在心率、主动脉压力和主动脉血流量保持恒定的情况下,治疗组表现出明显的正性肌力反应,表现为dP/dt max增加至对照值的138%。通过结扎头臂血管和给予心得宁,排除了中枢神经系统功能和β肾上腺素能活性的影响。出于所讨论的原因,这些发现不太可能归因于胰高血糖素污染。因此,收缩力的增加可能是胰岛素对心肌直接作用的结果。临床和实验室数据表明,新生儿对缺氧的耐受性受糖原储备的影响。已知胰岛素可增加糖原合成,预期这种作用可能增强心肌对缺氧的耐受性。然而,在这些实验条件下,胰岛素预处理对缺氧期间心脏功能恶化的速率没有明显影响。胰岛素刺激心脏的机制尚不清楚,但可能涉及钙通量。