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Effect of Cd36 on cardiac ischemic tolerance and adrenergic signaling in spontaneously hypertensive rats

CD36 fatty acid translocase plays a key role in supplying heart with its major energy substrate, long‐chain fatty acids (FA). Spontaneously hypertensive rat (SHR) harbors a deletion variant of Cd36 gene. We analyzed the effects of mutant Cd36 on cardiac susceptibility to ischemia‐reperfusion injury in adult SHR‐Cd36 transgenic rats with wild type Cd36 compared to age‐matched SHR controls. Using an open‐chest model of coronary artery occlusion, we found that SHR‐Cd36 showed profound ischemic arrhythmogenesis resulting in significantly increased total number of premature ventricular complexes (2623±517 vs. 849±250) in SHR controls. On the other hand, transgenic SHR showed significantly reduced infarct size (52.6±4.3% vs. 72.4±2.9% of area at risk). Similar differences were observed in isolated perfused hearts and the increased incidence of arrhythmias in transgenic SHR was abolished by reserpine suggesting the involvement of catecholamines. Furthermore, forskolin‐stimulated activity of adenylyl cyclase was increased in the SHR‐Cd36. It can be concluded that Cd36 plays an important role in modulating cardiac susceptibility to ischemia‐reperfusion injury. The proarrhythmic effect of Cd36 transgene appears to be related to increased adrenergic stimulation. Supported by grants: GAAV IAAX01110901, GAUK 429611