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The Hatter Institute, University College London, London WC1E 6DB, United Kingdom
Bradykinin
is an important endogenous mediator exerting acute protective effects
in the ischemic myocardium. The aims of this study were to
investigate whether exogenously administered bradykinin could evoke
delayed myocardial protection and to determine whether any protection
observed might be dependent on nitric oxide (NO) generation. Conscious
rats received bradykinin (40 µg/kg iv) or saline, preceded 15-20
min earlier by the NO synthase inhibitor N
-nitro-L-arginine methyl ester
(L-NAME, 10 mg/kg ip) or saline. Twenty-four hours
later, hearts were Langendorff perfused and subjected to 35 min of
regional ischemia and 120 min of reperfusion. Infarct size was
assessed using tetrazolium staining and expressed as a percentage of
the risk zone. Bradykinin pretreatment reduced the infarct-to-risk
ratio from 53.5 ± 3.2% to 29.1 ± 4.7% (P < 0.01). The administration of L-NAME before bradykinin
abrogated the delayed protection (infarct size 52.3 ± 5.0%) but
alone did not influence infarct size (53.5 ± 4.8%). These
results are the first to demonstrate that bradykinin can evoke a
delayed ("second window") enhancement of myocardial tolerance to
ischemia, an action that is dependent on the early generation
of NO.
infarct size; nitric oxide synthase; preconditioning
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