Background: Inhibition of leukocyte adhesion can reduce myocardialinfarct size in animals.
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Significance: These findings may provide new insights in myocardialinfarct healing and repair.
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Thrombolytic therapy has been documented to reduce acute myocardialinfarct size.
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Similar results were obtained for incidence rates of myocardialinfarct.
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In contrast, propranolol and diltiazem did not show such protective effects on myocardialinfarct size.
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The acute administration of atorvastatin has been reported to reduce myocardialinfarct size in animal studies.
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These elements may be potentials tools to improve cardiac function in a swine myocardialinfarct model.
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In 12 sheep, infarct deformation was prevented by Marlex mesh placed over the anticipated myocardialinfarct.
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Results: Both ischemic and remifentanil post-conditioning reduced the myocardialinfarct size relative to the control group in both models.
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Also, the usefulness of image analysis as an objective method for the measurement of myocardialinfarct area is evaluated.
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In the present study we investigated the effect of short-term estrogen on myocardialinfarct size in oophorectomized female rabbits.
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Conclusions: The myocardialinfarct size-limiting effect of preconditioning did not correlate with the degree of myocardial stunning accompanying preconditioning.
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IPC displayed cardioprotection as evidenced by improved post-ischemic contractile recovery, decreased myocardialinfarct size and reduced number of apoptotic cardiomyocytes.
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The goal of this study was to compare the effects of these techniques in an experimental model of myocardialinfarct.
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We previously demonstrated that several epoxyeicosatrienoic acids (EETs) produce reductions in myocardialinfarct size in rats and dogs.
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The primary end point was coronary flow at the end of PCI procedure, and secondary end points included myocardialinfarct size.