February 15, 1996Circulation
Role of Activation of Protein Kinase C in the Infarct SizeLimiting Effect of Ischemic Preconditioning Through Activation of Ecto-5′-nucleotidase
Why the study?
Does ischemic preconditioning reduce infarct size through activation of protein kinase C and ecto-5'-nucleotidase in a canine heart model?
Population
Canine heart model of ischemia-reperfusion injury
Comparison
Ischemic preconditioning with or without protein… vs Control group (no ischemic preconditioning)
Design
Preclinical
Follow-up
6 hours of reperfusion
Authors
Discussion
Loading...
Member takes
Implication
Supports PKC mediation of preconditioning in canine models; leaves open translation to human cardioprotection and requires clinical trials.
Structured PICO
Does ischemic preconditioning reduce infarct size through activation of protein kinase C and ecto-5'-nucleotidase in a canine heart model?
P
Population
Canine heart model of ischemia-reperfusion injury
I
Intervention
Ischemic preconditioning (four 5-minute coronary artery occlusions with alternating 5-minute reperfusions) with or without protein kinase C inhibitors (polymyxin B and GF109203X) or methoxamine
C
Comparator
Control group (no ischemic preconditioning)
O
Outcome
Infarct size normalized by the risk area after 90 minutes of occlusion and 6 hours of reperfusionsurrogate
Ischemic preconditioning limits myocardial infarct size through a mechanism involving the activation of protein kinase C and ecto-5'-nucleotidase.
Cite This Study
Kitakaze et al. (1996) studied this question.