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1 Medical Physiology and Biochemistry, Faculty of Medicine, University of Stellenbosch, and 2 Medical Research Council Experimental Biology Programme, Tygerberg 7505, Republic of South Africa
To
determine whether nitric oxide (NO) is involved in classic
preconditioning (PC), the effect of NO donors as well as inhibition of
the L-arginine-NO-cGMP pathway were evaluated on
1) the functional recovery during reperfusion of ischemic
rat hearts and 2) cyclic nucleotides during both the PC
protocol and sustained ischemia. Tissue cyclic nucleotides were
manipulated with NO donors
[S-nitroso-N-penicillamine (SNAP), sodium
nitroprusside (SNP), or L-arginine] and inhibitors of nitric oxide synthase
(N
-nitro-L-arginine methyl ester
or N-nitro-L-arginine) or guanylyl cyclase
(1H-[1,2,4]oxadiazolol-[4,3-a]quinoxaline-1-one).
Pharmacological elevation in tissue cGMP levels by SNAP or SNP before
sustained ischemia elicited functional improvement during reperfusion
comparable to that by PC. Administration of inhibitors before and
during the PC protocol partially attenuated functional recovery,
whereas they had no effect when given after the ischemic PC protocol
and before sustained ischemia only, indicating a role for NO as a trigger but not as a mediator. Ischemic PC, SNAP, or SNP caused a
significant increase in cGMP and a reduction in cAMP levels after 25 min of sustained ischemia that may contribute to the protection
obtained. The results obtained suggest a role for NO (and cGMP) as a
trigger in classic PC.
adenosine 3',5'-cyclic monophosphate; guanosine 3',5'-cyclic monophosphate; nitric oxide donors; guanylyl cyclase inhibition; nitric oxide synthase inhibition
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