Relation of Cyclic Nucleotide Ratios to Ischemic and Reperfusion Injury in Nitric Oxide–Donor Treated Rat Hearts

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Abstract
Nitric oxide (NO) donors given during ischemia possibly protect the myocardium by increasing tissue cyclic guanosine monophosphate (cGMP) and decreasing cytosolic Ca 2+ levels. However, NO donors also elevate ischemic cyclic adenosine monophosphate (cAMP) levels, which exacerbates ischemic-reperfusion injury. The authors propose that suppression of this NO donor–induced increase in cAMP would improve the cardioprotective properties of these compounds. Langendorff perfused rat hearts were treated with sodium nitroprusside (SNP, 0.1 m M) or glyceryl trinitrate (GTN, 1.0 μM) and/or adenylyl cyclase (SQ, 50 μM) or guanylyl cyclase (ODQ, 30–300 μM) inhibitors during 40-min low-flow (0.2 ml/min) ischemia. Control reperfusion rate-pressure product (RPP) recoveries were 47 ± 3% (n = 9) and improved to 59 ± 1% (n = 11) (p