Key result
Simvastatin (10 µMol) significantly attenuated ischemia/reperfusion-induced myocardial injury and oxidative stress in both normal and hyperhomocysteinemic isolated rat hearts.
Why the study?
Does simvastatin reduce myocardial injury in hyperhomocysteinemic rat hearts subjected to ischemia/reperfusion?
Does simvastatin reduce myocardial injury in hyperhomocysteinemic rat hearts subjected to ischemia/reperfusion?
p-value: p=<0.05
Simvastatin protects against ischemia/reperfusion injury in hyperhomocysteinemic rat hearts, likely through the reduction of oxidative stress.
Does not support clinical use; hypothesis-generating for simvastatin cardioprotection in hyperhomocysteinemic ischemia/reperfusion.
The present study investigated the probable role of simvastatin, 3-hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitor, in abrogated cardioprotection in hyperhomocysteinemic (Hhcy) rat hearts. Isolated Langendorff's perfused normal and Hhcy rat hearts were subjected to 30-min global ischemia (I) followed by 120-min reperfusion (R). Assessment of myocardial damage was done by measuring infarct size and analyzing the release of lactate dehydrogenase (LDH) and creatine kinase (CK-MB) in coronary effluent. In addition, the oxidative stress in the heart was assessed by measuring lipid peroxidation and superoxide anion generation. I/R produced myocardial injury in normal and Hhcy rat hearts by increasing myocardial infarct size, LDH and CK in coronary effluent and oxidative stress. Hhcy rat hearts showed enhanced myocardial injury and high oxidative stress as compared to normal hearts. Treatment with Simvastatin (10 μMol) afforded cardioprotection against I/R-induced myocardial injury in normal and hyperhomocysteinemic rat hearts as assessed in terms of reductions in myocardial infarct size, LDH and CK levels in coronary effluent and oxidative stress. The reductions in the high degree of oxidative stress may be responsible for the observed cardioprotection afforded by simvastatin against I/R-induced myocardial injury in normal and hyperhomocysteinemic rat hearts.
No takes yet. Share an insight, caveat, or question.
Rohilla et al. (2012) studied Myocardial ischemia/reperfusion injury with hyperhomocysteinemia. Simvastatin vs. Ischemia/reperfusion control without simvastatin was evaluated on Myocardial infarct size and release of lactate dehydrogenase (LDH) and creatine kinase (CK) (p=<0.05). Simvastatin (10 µMol) significantly attenuated ischemia/reperfusion-induced myocardial injury and oxidative stress in both normal and hyperhomocysteinemic isolated rat hearts.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: