Intermittent perfusion of ischemic myocardium. Possible mechanisms of protective effects on mechanical function in isolated rat heart.
Intermittent perfusion of ischemic myocardium. Possible mechanisms of protective effects on mechanical function in isolated rat heart.
复制标题
缺血心肌的间歇灌注。
DOI：
10.1161/01.cir.82.2.536
复制
发表时间：
1990
期刊：
影响因子：
37.8
通讯作者：
Neely,JR
中科院分区：
文献类型：
--
作者：
Tani,M;Neely,JR
缺血期间冠状动脉血流的间歇性恢复可减少心肌损伤并改善功能恢复。在离体大鼠心脏上研究了间歇灌流保护作用的机制。心室功能评估为发展的压力（左心室收缩压减去舒张末期压）和心率的乘积。通过再灌注结束时的产物除以缺血前的产物来计算功能恢复。持续性全脑缺血40分钟后，细胞内Na+（Nai）从11 μ mol/g干重增加到74 μ mol/g干重。在30分钟的再灌注过程中，这些心脏摄取了大量的45 Ca 2+（10 μ mol/g干重），仅恢复了缺血前功能的24%，并且左心室舒张末期压增加（48 mm Hg）。当40分钟的缺血时间被中断，在10分钟的间隔，间歇灌注（三个周期的3分钟）与氧合或低氧缓冲液，钠增加到只有12或17 mumol/g干重，和再灌注导致低得多的45 Ca 2+摄取（0.5和0.5 mumol/g干重，分别）。功能恢复为缺血前值的100%。当不含葡萄糖的低氧缓冲液用于间歇灌注时，Nai增加至50 mumol/g干重，ATP耗尽，再灌注导致功能恢复减少（76%）和45 Ca 2+摄取适度增加（2.1 mumol/g干重）。通过从间歇灌注期间使用的含氧或低氧缓冲液中去除K+，评估Na（+）-K+泵活性在维持低Nai中的作用。在这些条件下，Nai上升到64或102 μ mol/g干重，45 Ca 2+摄取增加到4.4或9.4 μ mol/g干重，功能恢复差。缺血期间Nai与再灌注Ca ~（2+）超载（r = 0.87）或功能恢复受损（r = 0.96）之间存在高度显著的相关性。这些结果表明，通过维持Na（+）-K+泵活性来防止Nai增加与通过Na+/Ca 2+交换减少Ca 2+过载有关。
Intermittent restoration of coronary flow during ischemia reduced myocardial damage and improved recovery of function. The mechanisms of the protective effects of intermittent perfusion were investigated in isolated rat hearts. Ventricular function was assessed as the product of developed pressure (left ventricular systolic pressure minus end-diastolic pressure) and heart rate. Recovery of function was calculated by division of the product at the end of reperfusion by that before ischemia. After 40 minutes of sustained global ischemia, intracellular Na+ (Nai) increased from 11 to 74 mumol/g dry wt. During 30 minutes of reperfusion, these hearts took up a large amount of 45Ca2+ (10 mumol/g dry wt), recovered only 24% of preischemic function, and had an increased left ventricular end-diastolic pressure (48 mm Hg). When the 40-minute period of ischemia was interrupted at 10-minute intervals by intermittent perfusion (three periods of 3 minutes) with either oxygenated or hypoxemic buffer, Nai increased to only 12 or 17 mumol/g dry wt, and reperfusion resulted in much lower 45Ca2+ uptake (0.5 and 0.5 mumol/g dry wt, respectively). Recovery of function was 100% of the preischemic value. When hypoxemic buffer without glucose was used for intermittent perfusion, Nai increased to 50 mumol/g dry wt, ATP was depleted, and reperfusion resulted in reduced recovery of function (76%) and moderately increased 45Ca2+ uptake (2.1 mumol/g dry wt). The role of Na(+)-K+ pump activity in maintaining low Nai was assessed by removing K+ from oxygenated or hypoxemic buffers used during intermittent perfusion. Under these conditions, Nai rose to 64 or 102 mumol/g dry wt, 45Ca2+ uptake increased to 4.4 or 9.4 mumol/g dry wt, and recovery of function was poor. There was a highly significant correlation between Nai during ischemia and reperfusion Ca2+ overload (r = 0.87) or impaired recovery of function (r = 0.96). These results indicate that prevention of an increase in Nai by maintenance of Na(+)-K+ pump activity is associated with a reduction of Ca2+ overload through Na+/Ca2+ exchange.
登录
查看更多内容
HLA-DRw 决定簇的单克隆抗体。
影响因子：
--
作者：
Frances M. Brodsky;P. Parham;W. Bodmer
通讯作者：
W. Bodmer
关于发作性睡病：I. 家族性发作性睡病
DOI：
--
发表时间：
1942
期刊：
影响因子：
--
作者：
E. Krabbe;G. Magnussen
通讯作者：
G. Magnussen
发作性睡病的遗传方面。
DOI：
--
发表时间：
1960
期刊：
影响因子：
--
作者：
Yoss Re;Daly Dd
通讯作者：
Daly Dd
DR2——阴性发作性睡病
DOI：
10.1016/s0140-6736(86)90188-1
发表时间：
1986
期刊：
The Lancet
影响因子：
--
作者：
A. Andreas;S. Scholz;E. Keller;E. Albert;B. Roth;S. Nevsimalova;K. Šonka;P. Docekal;E. Ivašková;H. Schulz;P. Geisler
通讯作者：
P. Geisler
HLA-DR2 和发作性睡病：并非所有发作性睡病-猝倒症患者都是 DR2。
影响因子：
2.7
作者：
C. Guilleminault;Carl Grumer
通讯作者：
Carl Grumer