Shen H, Mirsalimi S M, Weiler J E, Julian R J, O'Brien P J
Department of Pathology, Ontario Veterinary College, University of Guelph, Ontario, Canada.
Am J Vet Res. 1991 Sep;52(9):1527-30.
Recent studies indicate that in animals with marked cardiac hypertrophy, there is depressed function of Ca2+ sequestration by myocardial sarcoplasmic reticulum (SR) because of down regulation of the Ca(2+)-ATPase gene. However, in several animal models we have observed enhancement of myocardial Ca2+ sequestration in response to chronic cardiac stimulation. We tested the hypothesis that in animals with mild cardiac hypertrophy, there is enhanced Ca(2+)-cycling activity by the SR Ca2+ pump and Ca(2+)-release channel. Because creatine kinase activity is consistently decreased in cardiomyopathy, we also determined whether enhanced Ca2+ cycling was accompanied by down regulation or inhibition of the creatine kinase system. Mild cardiac hypertrophy was induced by volume overload; 2% salt was added to the diet of 2-week-old turkey poults for 4 weeks. Compared with age-matched controls, volume overload resulted in 14.3% increase in heart weight and 21.5% increase in heart-to-body weight ratios. The hypertrophied heart had approximately 20% increased activities of the SR Ca2+ pump and the SR Ca2+ channel. Net Ca2+ transport was increased by 16.5%. Compared with controls and in contrast to several other myocardial enzymes, creatine kinase activity was diminished in the hypertrophied hearts by 23% and creatine content was decreased by 8%. Differences between groups were not detected for lactate dehydrogenase, aspartate transaminase, and alanine transaminase. We concluded that an early adaptation of the myocardium undergoing hypertrophy in compensatory response to functional overload is an enhancement of Ca2+ cycling activity by the Ca2+ pump and Ca2+ channel of the SR.(ABSTRACT TRUNCATED AT 250 WORDS)
最近的研究表明，在有明显心脏肥大的动物中，由于Ca(2+)-ATP酶基因下调，心肌肌浆网（SR）对Ca2+的摄取功能受到抑制。然而，在我们所观察的几种动物模型中，慢性心脏刺激可使心肌Ca2+摄取增强。我们验证了这样一个假说：在轻度心脏肥大的动物中，SR的Ca2+泵和Ca2+释放通道的Ca(2+)循环活性增强。由于心肌病时肌酸激酶活性持续降低，我们还确定增强的Ca2+循环是否伴有肌酸激酶系统的下调或抑制。通过容量负荷诱导轻度心脏肥大；在2周龄火鸡幼雏的饲料中添加2%的盐，持续4周。与年龄匹配的对照组相比，容量负荷使心脏重量增加了14.3%，心脏与体重的比值增加了21.5%。肥大心脏的SR Ca2+泵和SR Ca2+通道的活性增加了约20%。净Ca2+转运增加了16.5%。与对照组相比，且与其他几种心肌酶不同，肥大心脏中的肌酸激酶活性降低了23%，肌酸含量降低了8%。乳酸脱氢酶、天冬氨酸转氨酶和丙氨酸转氨酶在各组之间未检测到差异。我们得出结论，心肌在对功能负荷的代偿性反应中发生肥大的早期适应性变化是SR的Ca2+泵和Ca2+通道的Ca2+循环活性增强。（摘要截短至250字）
