[Effects of nitric oxide on cardioprotection prior to ischemia-reperfusion].
This study aimed at evaluating the role of nitric oxide (NO) when generated 24 h prior to ischemia-reperfusion. Three groups were studied in an isolated buffer-perfused heart model: Control (saline = 3.3 mL/kg, n = 10), the precursor of NO, L-arginine, (500 mg/kg, n = 10) and an inhibitor of NO synthase, L-NAME, (10 mg/kg, n = 9). All groups were injected intraperitoneally 24 h before heart extraction. Nitrites, nitrates (an index of nitric oxide release) and cardiac troponine I were assayed. During the reperfusion period, there was a low release of nitric oxide and cardiac troponine I associated with improved recovery of post-ischemic myocardial function. These results indicate that in this model, the pre-treatment improved myocardial function and thus, NO could play a role as a trigger and not as a mediator of cardioprotection.
Davani
S
S
Laboratoire de Pharmacologie, CHU Jean Minjoz, Besançon, France.
Yan
Y
Y
Bouhaddi
M
M
Chocron
S
S
Muret
P
P
Etievent
J P
JP
Kantelip
J P
JP
D000818:Animals; D008297:Male; D023421:Models, Animal; D009569:Nitric Oxide / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*; D019210:Troponin I / Q000378:metabolism*
D019210:Troponin I; D009569:Nitric Oxide