Abstract
Introduction Metabolic syndrome (MetS) is associated with inactivation of coronary endothelial small/intermediate (SK Ca /IK Ca ) conductance calcium-activated potassium channels and dysregulation of coronary arteriolar endothelial function in animals and humans. We investigated the effects of cardioplegia-ischemia/reperfusion (I/R) and NS309 pretreatment on the in-vitro coronary arteriolar responses to endothelium-dependent vasodilators substance P and ADP in pigs with or without MetS. Case description The MetS pigs were developed by feeding with a hyper-caloric, fat/cholesterol diet and the control animals fed with a regular diet for 12 weeks (n=8/group). Coronary arterioles (90-180 micrometers in diameter) were dissected from the harvested left ventricle tissue sample of pigs with and without MetS. The changes in diameter were measured with video microscopy. Microvessel was perfused in the presence or absence of selective SK Ca /IK Ca activator NS309 (10 -5 M). The in-vitro coronary arterioles were then subjected to 60 minutes of cardioplegia-hypoxia (15°C) and 60 minutes of re-oxygenation. Results and Conclusions At the end of reperfusion, the microvessel was treated with the endothelium-dependent vasodilators substance P and ADP. The relaxation responses to the substance P and ADP after cardioplegia-I/R were significantly decreased in MetS vessels versus control (Lean), respectively (P Ca /IK Ca activator NS309 (10 -5 M) significantly improved the recovery of coronary endothelial function showing increased response to substance P and ADP as compared with no pretreatment alone (P Take home message This study demonstrates that cardioplegic-ischemia/reperfusion impairs endothelial function and inactivation of endothelial SK Ca /IK Ca channels of the coronary microcirculation in the setting of metabolic syndrome.
Published Version
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