Osmotic shock:: modulation of contractile function, pHi, and ischemic damage in perfused guinea pig heart
Osmotic shock:: modulation of contractile function, pHi, and ischemic damage in perfused guinea pig heart
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DOI：
10.1152/ajpheart.1999.276.4.h1236
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发表时间：
1999-04-01
影响因子：
4.8
通讯作者：
Clarke, K
中科院分区：
文献类型：
--
作者：
Befroy, DE;Powell, T;Clarke, K
To determine the contribution of changes in extracellular osmolarity to ischemic injury, isolated guinea pig hearts were perfused with hyposmotic (220 mosM) or hyperosmotic (380 mosM) buffer. P-31 NMR spectroscopy was used to follow changes in intracellular pH (pH(i)) and energetics. Hyposmotic buffer decreased myocardial developed pressure by 30 +/- 2% and pH(i) by 0.02 +/- 0.01 unit, whereas hyperosmotic buffer increased myocardial developed pressure by 34 +/- 1% and pH(i) by 0.14 +/- 0.01 unit. All hearts recovered to control values on restoration of isosmotic (300 mosM) buffer. The hyperosmolar-induced intracellular alkalosis and developed pressure increase were not prevented by inhibition of Na+/H+ exchange with use of 1 mu M HOE-642 but were abolished with use of bicarbonate-free buffers. After 20 min of total global ischemia, hearts perfused with hyposmotic buffer showed significantly greater recoveries of developed pressure, phosphocreatine, and ATP than control hearts, but hearts perfused with hyperosmotic buffer did not recover after ischemia. In conclusion, buffer osmolarities between 220 and 380 mosM alter myocardial pH(i) and developed pressure but are not deleterious during perfusion. However, buffer osmolarity significantly alters the extent of myocardial ischemic injury.
