PATHOPHYSIOLOGIC EFFECTS OF SPONTANEOUS CA2+ RELEASE IN THE HEART

自发的、非同步的心肌钙振荡，一直以来 归因于肌浆钙依赖的钙释放 网状结构(SR)，并表现出周期性，这取决于 细胞钙负荷。在薄的切除心肌中，不均匀的 由自发振荡相位引起的收缩运动调制了 激光束穿过薄的切除的心肌，产生强烈的 散射光的起伏(SLIF)。在目前的项目中，我们 633 nm激光后向散射强度涨落的测量 离体鼠和兔心脏的心外膜表面。这个 通过提高细胞内水平的动作来增加SLIF的频率 钙。SILF通过去除细胞外钙而被消除 乙二醇双(β-氨基乙醚)-N，N，N‘，N’-四乙酸乙酯和 兰诺定阻断肌浆网钙释放。斯利夫没有随行 任何体表心电图仪均未被消除144毫米 胞外钾。在基线以下的兔心组织中没有滑膜 条件，但可由钙负荷使用零钾引发 还有哇巴因。因此，SLIF监测由 完整心脏的细胞内钙振荡。延迟恢复 心肌缺血后的收缩功能可能是由于增加 钙负荷。为了检验这一潜在的机制，我们在 离体房室阻断大鼠心脏60min内及之后 在30℃时出现缺血，再灌流后出现压力升高。 小幅回升，但随后突然下跌。伴随着这一增长的是 舒张末压力升至37+/-5毫米汞柱，SILF增加四倍， 至基线的252%+/-58%。在另一系列心脏初始再灌流中 添加0.08 mM的钙，防止了细长的上升，改善了 形成压力(对照的74+/-3%)和较低的细胞钙(5.9+/-3vs 10.3+/-1.4微摩尔/克干重)。因此，在再灌流期间，延迟收缩 康复可以部分归因于钙的不良影响。 可以通过当时发生的增加的滑移量来索引的载荷。

Spontaneous, asynchronous, myocardial calcium oscillations, have been attributed to calcium-dependent calcium release form the sarcoplasmic reticulum (SR) and exhibit a periodicity which depends upon the extent of cell calcium loading. In thin excised cardiac muscle the inhomogeneous contractile motion caused by the spontaneous oscillations phase modulates a laser beam passed through thin excised cardiac muscle, producing intensely fluctuations in the scattered light (SLIF). In the present project we measured intensity fluctuations of 633 nm laser light backscattered from the epicardial surface of isolated, perfused rat and rabbit hearts. The frequency of SLIF was increased by maneuvers that raise intracellular calcium. SLIF were abolished by removal of extracellular calcium with ethylene glycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid and by blockade of SR calcium release by ryanodine. SLIF were not accompanied by any surface electrocardiogram and were not abolished by 144 mM extracellular potassium. SLIF were absent in rabbit hearts under base-line conditions but could be provoked by calcium loading using zero potassium and ouabain. Thus, SLIF monitors the microscopic motion caused by intracellular calcium oscillations in the intact heart. Delayed recovery of contractile function after myocardial ischemia may be due to increased calcium loading. To examine this potential mechanism, SLIF were studied in isolated atrioventricularly blocked rat hearts during and after 60 min of ischemia at 30 degrees C. After reperfusion developed pressure evidenced a small recovery but then fell abruptly. This was accompanied by an increase in end-diastolic pressure to 37+/-5 mm Hg and a fourfold increase in SLIF, to 252+/-58% of baseline. In another series of hearts initial reperfusion with calcium of 0.08 mM prevented the SLIF rise and resulted in improved developed pressure (74+/-3% of control), and lower cell calcium (5.9+/-3 vs 10.3+/-1.4 micromol/g dry wt). Thus, during reperfusion delayed contractile recovery can be attributed, in part, to an adverse effect of calcium loading which can be indexed by increased SLIF occurring at that time.