Key result
Diabetic rat hearts did not develop ischemic contracture and had markedly suppressed hypercontracture compared with control hearts, resulting in better post-ischemic recovery.
Why the study?
Does diabetes alter ischemic contracture, hypercontracture, and post-ischemic recovery in isolated rat hearts subjected to ischemia and reperfusion?
Does diabetes alter ischemic contracture, hypercontracture, and post-ischemic recovery in isolated rat hearts subjected to ischemia and reperfusion?
In a rat model, diabetic hearts exhibited suppressed hypercontracture and no ischemic contracture, which correlated with improved post-ischemic functional recovery.
Hypothesis-generating for diabetes-mediated protection against ischemic contracture; requires human confirmation before any clinical consideration.
Objective: Previous studies suggest a relation among ischemic contracture and/or hypercontracture profiles and the functional responses in diseased hearts isolated from hypothyroid and post-infarcted animals. We therefore aimed to find out whether there is a similar relation in the diabetic hearts. Methods: Experiments were performed on Sprague-Dawley rats divided into control and diabetic groups. Diabetes was induced by streptozotocin (45 mg/kg) in citrate buffer (0.1 M, pH:4.5) into the tail vein of the rat. Isolated hearts from control and diabetic rats were subjected to 40-min ischemia followed by 40-min of reperfusion. The left ventricular end-diastolic pressure and left ventricular developed pressure were measured during the experimental protocol. Furthermore, the increase in minimal value of left ventricular pressure during ischemia and the peak value of left ventricular end-diastolic pressure measured during the first 5 min of reperfusion for each heart were evaluated as a measure of ischemic contracture and hypercontracture, respectively. Results: Ischemic contracture did not develop and hypercontracture was markedly suppressed in the diabetic hearts compared with control hearts. In addition, post-ischemic recovery was negatively correlated with hypercontracture in both groups. Conclusion: Both the non-existence of ischemic contracture and the suppressed hypercontracture results in a better post-ischemic recovery of diabetic heart. Furthermore, the relationship between hypercontracture and post-ischemic recovery suggests that the utility of hypercontracture as a predictor of the post-ischemic recovery.
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Altunkaynak et al. (2017) studied Diabetes and myocardial ischemia-reperfusion injury. Streptozotocin-induced diabetes vs. Control (non-diabetic) rats was evaluated on Ischemic contracture and hypercontracture. Diabetic rat hearts did not develop ischemic contracture and had markedly suppressed hypercontracture compared with control hearts, resulting in better post-ischemic recovery.
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