Experimental Study Of The Relationship Between Myocardial Protection Of Lidocaine And Nitric Oxide

Lidocaine is a commonly used anti-arrhythmic drug and local anesthetic in clinical practice. Although its exact mechanism against ischemia/reperfusion injury is unclear, lidocaine has been shown to improve energy metabolism of myocarcial tissue subjected to ischemic reperfusion, to inhabit intracellular Na⁺ and Ca²⁺ overloads and neutrophil adherence and aggregation, and to decrease myocardial infarct size.As an important cellular signaling molecular and chemical mediator, the role of nitric oxide (NO) in the myocardial ischemic reperfusion process is being a hotspot subject studied. At normal physiological conditions, NO is mainly synthesed by catalysis of the eNOS in the vascular endothelium. It has been shown that NO has a variety of functions, such as endothelium-dependent vasorelaxation, inhibition of platelet adhesion and aggregation, depression of vascular smooth muscle proliferation, reduction of neutrophil adherence and aggregation, and decrease of intracellular Ca²⁺ overload. Both insufficiency and excessiveness of NO production can aggravate myocardial ischemia/reperfusion injury.This experiment was designed to investigate the relationships between myocardial protection of lidocaine and NO. Our purpose was to further clarity the mechanism of myocardial protection of lidocaine. This study consists of the following three parts:...