Key result
FR167653 improves LVDP recovery by ~59% and reduces TNFalpha production in ischemic-reperfused rat hearts.
Why the study?
Does FR167653 improve myocardial protection and inhibit cytokine production in an ischemic-reperfused rat heart model?
Population
Isolated, Langendorff-perfused Lewis rat hearts subjected to 30 min of 37 degrees C ischemia followed by…
Comparison
FR167653 administered before ischemia and during… vs Untreated control group subjected to…
Design
Preclinical
Follow-up
1 hour after beginning of reperfusion
Authors
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Supports cytokine-targeted protection in preclinical ischemia-reperfusion; leaves open clinical translation of p38 inhibitors.
Does FR167653 improve myocardial protection and inhibit cytokine production in an ischemic-reperfused rat heart model?
Absolute Event Rate: 130% vs 82%
p-value: p=0.002
FR167653 demonstrates positive inotropic and antiapoptotic effects, reducing TNFalpha production and p38 MAPK activation in a rat model of myocardial ischemia-reperfusion injury.
Alexey N. Aleshin (2004) studied Ischemia-reperfusion injury (n=80). FR167653 vs. Untreated was evaluated on Recovery of cardiac contractile function (LVDP in mmHg) (p=0.002). FR167653 administration in ischemic-reperfused rat hearts significantly improved recovery of left ventricular developed pressure (130 vs 82 mmHg, P=0.002) and reduced TNFalpha production.
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