Delayed 24 hours Nomega-nitro-L-arginine methyl ester injection induces pharmacological cardioprotection against reperfusion injury

Previous studies indicate that adenosine supplementation or nitric oxide synthase (NOS) inhibition during reperfusion exert protective effects against myocardial ischemia-reperfusion (I/R) injury. We wanted to test the hypothesis that NOS inhibition before I/R also protects the myocardium against fu...

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Bibliographic Details
Published in:Cellular and Molecular Biology 2007-01, Vol.52 Suppl, p.OL868-73
Main Authors: Davani, Siamak, Vergely, C., Royer, B., Bouhaddi, Malika, Reyssie, Hervé, Rochette, Luc, Kantelip, Jean Pierre
Format: Article
Language:English
Subjects:
Adenosine
Animals
Arginine
Blood Pressure
Cardiotonic Agents
Disease Models, Animal
Enzyme Inhibitors
Human health and pathology
Life Sciences
Myocardial Ischemia
Myocardial Reperfusion Injury
Nitrates
Nitric Oxide Synthase
Nitrites
Perfusion
Rats
Regional Blood Flow
Theophylline
Time Factors
Troponin I
Ventricular Function, Left
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Summary:Previous studies indicate that adenosine supplementation or nitric oxide synthase (NOS) inhibition during reperfusion exert protective effects against myocardial ischemia-reperfusion (I/R) injury. We wanted to test the hypothesis that NOS inhibition before I/R also protects the myocardium against further injury and aimed to determine the involvement of adenosine receptors in a perfused rat heart model. Rats were injected with 10 mg/kg of L-NAME (N(omega)-nitro-L-arginine methyl ester) or L-NAME + SPT (8-(p-sulfophenyl)-theophylline)--an adenosine antagonist - at 2 x 25 mg/kg or with a saline buffer, 24 hrs prior to heart excision. The hearts, perfused retrogradely were subjected to 60 min of global ischemia followed by 120 min reperfusion. L-NAME decreased NOx (nitrite and nitrate) production (16.2 +/- 3.2 vs. 7.0 +/- 1.8 micromol/L; P
ISSN:0145-5680
1165-158X