[The influence of hypoxia/reoxygenation on production and release of nitric oxide from cultured newborn rat cardiomyocytes].
OBJECTIVE
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.


METHODS
The rats were divided into four groups: control, hypoxia/reoxy-genation, heat shock pretreated, dexamethasone pretreated.


RESULTS
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).


CONCLUSIONS
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.
Wei
L
L
Department of Cardiothoracic Surgery, Renji Hospital, Shanghai.
Zhu
H
H
D000818:Animals; D000831:Animals, Newborn; D015687:Cell Hypoxia; D002478:Cells, Cultured; D003402:Creatine Kinase / Q000378:metabolism; D018869:Heat-Shock Response / Q000502:physiology*; D006979:Hyperthermia, Induced; D007770:L-Lactate Dehydrogenase / Q000378:metabolism*; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism*; D010101:Oxygen Consumption; D051381:Rats
D009569:Nitric Oxide; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase