Cytosolic calcium transients from the beating mammalian heart.
Cytosolic calcium transients from the beating mammalian heart.
复制标题
来自跳动的哺乳动物心脏的胞质钙瞬变。
DOI：
10.1073/pnas.84.21.7793
复制
发表时间：
1987
影响因子：
11.1
通讯作者：
Clusin,WT
中科院分区：
文献类型：
--
作者：
Lee,HC;Smith,N;Mohabir,R;Clusin,WT
为了阐明细胞内钙离子[Ca ~（2+）]i在正常和缺血心脏生理中的作用，我们开发了一种方法，用细胞渗透性细胞内钙指示剂indo-1 AM记录兔心室心外膜表面的[Ca ~（2+）]i瞬变。在360 nm下照射心脏，并在400和550 nm下同时记录荧光。通过模拟电路计算F400/F550荧光比率，该模拟电路允许消除在单个波长处存在的小运动伪影。F400/F550信号中存在清晰的[Ca 2 +]i瞬变，并且其缓慢衰减是显著的。瞬变的缓慢衰减不是由于indo-1对[Ca 2 +]i的缓冲，因为没有相关的收缩或舒张损伤。哇巴因、肾上腺素、期外收缩后增强和乙酰胆碱可增加[Ca 2 +]i瞬变的峰值幅度。瞬变衰减的程度随着心搏间期的缩短而减小，但乙酰胆碱或咖啡因可以进一步减小瞬变的衰减。完整心脏相对于分离的肌细胞的主要优点是能够测量缺血期间[Ca 2 +]i的变化。缺血引起收缩期峰值和舒张末期[Ca 2 +]i显著增加，在前30秒内最快，90秒后接近平台值。这种[Ca 2 +]i的增加与瞬态峰的特征性加宽相关。缺血期间[Ca 2 +]i的增加与[Ca 2 +]i在介导早期电生理异常中的致病作用一致。
To elucidate the role of cytosolic calcium, [Ca2+]i, in the physiology of the normal and ischemic heart, we have developed a method for recording [Ca2+]i transients from the epicardial surface of the rabbit ventricle after arterial perfusion with the cell-permeant cytosolic calcium indicator indo-1 AM. Hearts were illuminated at 360 nm, and fluorescence was recorded simultaneously at 400 and 550 nm. The F400/F550 fluorescence ratio was calculated by an analog circuit that allowed cancelation of small movement artifacts that were present at single wavelengths. Clear [Ca2+]i transients were present in the F400/F550 signal and were remarkable for their slow decay. Slow decay of the transients was not due to buffering of [Ca2+]i by indo-1, since there was no associated impairment of contraction or relaxation. The peak amplitude of the [Ca2+]i transients was increased by ouabain, adrenaline, postextrasystolic potentiation, and acetylcholine. The extent to which the transients decayed diminished with shortening of the interbeat interval, but decay of the transients could be further diminished by acetylcholine or caffeine. A major advantage of the intact heart over isolated myocytes is the ability to measure changes in [Ca2+]i during ischemia. Ischemia produced a marked increase in both peak systolic and end-diastolic [Ca2+]i, which was most rapid during the first 30 sec, and approached a plateau value after 90 sec. This increase in [Ca2+]i was associated with a characteristic broadening of the peak of the transient. The increase in [Ca2+]i during ischemia is consistent with a proposed causative role of [Ca2+]i in mediating early electrophysiological abnormalities.