Erdmann E, Schwinger R H, Beuckelmann D, Böhm M
Klinik III für Innere Medizin, Universität zu Köln.
Z Kardiol. 1996;85 Suppl 6:123-28.
Intracellular calcium homoeostasis is greatly altered in heart failure. This does not seem to be due to altered calcium influx through L-type calcium channels but rather due to altered calcium uptake mechanisms of the sarcoplasmic reticulum. Recently, a negative force-frequency behaviour of the human myocardium has been detected in hearts from patients with severe heart failure. In the myocardium from these patients, SR-Ca(2+)-ATPase activity was decreased. The same defect has been reported in human isolated cardiac myocytes. A disturbed calcium release from the SR may also contribute to this finding of the inverse force-frequency-relationship in the failing myocardium. The altered intracellular calcium handling is connected with the diastolic and systolic failure of the myocardium. Mg++ and Na(+)-channel modulators are able to restore the positive force-frequency-relationship even in severely failing myocardium.
心力衰竭时细胞内钙稳态会发生显著改变。这似乎并非由于通过L型钙通道的钙内流改变,而是由于肌浆网钙摄取机制的改变。最近,在严重心力衰竭患者的心脏中检测到了人心肌的负力-频率行为。在这些患者的心肌中,肌浆网钙-ATP酶(SR-Ca(2+)-ATPase)活性降低。在人离体心肌细胞中也报道了同样的缺陷。肌浆网钙释放紊乱也可能导致衰竭心肌中这种反向力-频率关系的发现。细胞内钙处理的改变与心肌舒张和收缩功能衰竭有关。镁离子和钠离子通道调节剂即使在严重衰竭的心肌中也能够恢复正向力-频率关系。