Organ-Specific Efficacy of Postischemic Empagliflozin in Acute Stroke and Myocardial Infarction Using Preclinical Models
Abstract
Background: Empagliflozin, a sodium-glucose cotransporter 2 inhibitor, has demonstrated cardioprotective and neuroprotective effects in preclinical myocardial infarction (MI) and ischemic stroke settings by reducing acute myocardial and cerebral infarction sizes. However, the optimal administration for acute protection remains unclear. Particularly, empagliflozin effects when administered after ischemia onset but before reperfusion have not been systematically evaluated for acute MI and stroke models.
Methods: Sprague-Dawley rats underwent either middle cerebral artery occlusion/reperfusion to induce acute ischemic stroke (n=25), or left coronary artery occlusion/reperfusion to induce acute MI (n=29). Empagliflozin (20 mg/kg) or saline was administered 10 minutes after ischemia onset. Outcomes included brain/heart injury sizes and cardiac hemodynamics were quantified after 3 hours of reperfusion.
Results: In the stroke model, postocclusion empagliflozin administration significantly reduced cerebral total infarct volume compared with controls (80.83±16.59 versus 164.10±26.23 mm3, P=0.014), corresponding to ≈50% reduction in the infarct volume percentage, while edema was unchanged. In the MI model, empagliflozin did not reduce myocardial infarct size, ischemic risk area, or no-reflow zone when given after occlusion/before reperfusion.
Conclusions: Our findings highlight that empagliflozin, when administered after ischemia onset but before reperfusion, provides robust…
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