ISSN:
1435-1803
Keywords:
Key words Reperfusion injury – Oxygen paradox – Hypercontracture – Calcium – SIN-1C
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract Previous studies have shown that SIN-1C (N-morpholinoiminoacetonitrile) can protect ischemic-reperfused myocardium. The aim of the present study was to analyse on the cellular level the mechanism by which SIN-1C may exert this effect. To simulate ischemia-reperfusion, isolated adult rat cardiomyocytes were incubated at pH 6.4 under anoxia and reoxygenated at pH 7.4 in presence or absence of SIN-1C. Reoxygenation was started when intracellular Ca2+ (measured with fura-2) had increased to ≥10–5 mol/L and pHi (BCECF) decreased to 6.6. Development of hypercontracture was determined microscopically. In the control group reoxygenation provoked oscillations of cytosolic Ca2+ (60.9±9.6 min–1 at 5 min of reoxygenation) accompanied by development of hypercontracture (to 77.2±3.8% of end-ischemic cell length). When SIN-1C was added upon reoxygenation, Ca2+ oscillations were markedly reduced (27.0±4.5 min–1, p〈0.001) and hypercontracture virtually abolished (90.6±2.0% of end-ischemic cell length, p〈0.001). SIN-1C did not influence the recovery of pHi during reoxygenation. The results indicate that SIN-1C protects cardiomyocytes against reoxygenation-induced hypercontracture by its ability to suppress oscillations of intracellular Ca2+ during the early phase of reoxygenation.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s003950050198
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