Key result
Ischemic preconditioning reduced infarct size by 65% in wild-type mice compared to 40% in tissue kallikrein-deficient mice (P<0.05), demonstrating TK's critical role in cardioprotection.
Why the study?
Does tissue kallikrein mediate the cardioprotective effects of ischemic preconditioning and ramiprilat in myocardial ischemia?
Population
Littermate wild-type, tissue kallikrein-deficient, and B2 receptor-deficient mice undergoing in vivo…
Comparison
Ischemic preconditioning or ACE inhibitor… vs Ischemia-reperfusion injury without…
Design
Preclinical
Authors
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TK may mediate preconditioning cardioprotection in mice; leaves open translation to ACE inhibition or clinical ischemia strategies.
Does tissue kallikrein mediate the cardioprotective effects of ischemic preconditioning and ramiprilat in myocardial ischemia?
p-value: p=<0.05
Tissue kallikrein and the B2 receptor play a critical mechanistic role in the cardioprotection provided by ischemic preconditioning and ACE inhibition during myocardial ischemia.
Griol‐Charhbili et al. (2005) studied myocardial ischemia. Ischemic preconditioning (IPC) or ramiprilat vs. No preconditioning / TK deficiency was evaluated on Infarct size (p=<0.05). Ischemic preconditioning reduced infarct size by 65% in wild-type mice compared to 40% in tissue kallikrein-deficient mice (P<0.05), demonstrating TK's critical role in cardioprotection.
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