The influence of hypoxia/reoxygenation on production and release of nitric oxide from cultured newborn rat cardiomyocytes
Wei, L.; Zhu, H.
Zhonghua Yi Xue Za Zhi 76(9): 697-699
1996
ISSN/ISBN: 0376-2491 PMID: 9275556 Document Number: 458512
To study the influence of hypoxia/reoxygenation on the production and release of nitric oxide (NO), lactate dehydrogenase (LDH) and creatine kinase (CPK) from cultured newborn rat cardiomyocytes. The rats were divided into four groups: control, hypoxia/reoxy-genation, heat shock pretreated, dexamethasone pretreated. After 3 hours of hypoxia and 30 minutes of reoxygenation, the content of NO in the supernatent of cardiomyocytes increased significantly (P < 0.05), which was accompanied by an increase in the release of LDH and CPK (P < 0.001, P < 0.001 respectively). When pretreated by the heat shock (exposed to 42 degrees C for 1 hour and then allowed to recover for 24 hours) or by applying dexamethasone at the onset of hypoxia, the production and release of NO, LDH, CPK decreased markedly (P < 0.05). Excessive release of NO may play an important role in the reperfusion injury of cardiomyocytes. Heat shock seems to provide protection for cardiomyocytes from hypoxia/reoxygenation injury. The mechanism may be related to the inhibition of excessive release of No from the cardiomyocytes.