Introduction

Cardiac ischemia is the principal cause of human death worldwide and its rate is rising because of co-morbid diseases, such as diabetes and obesity and aging. Cardiac ischemia is often investigated by the occlusion of the coronary arteries and while reperfusion can salvage the ischemic heart from death rate, it can induce side effects and it is known as ischemiaâ??reperfusion (IR) injuries.

Sleep is a vital regulator of cardiovascular function, both in the anatomical state and in disease conditions. Previous cohort and case-control studies have indicated that sleep disorders are related to an increased prevalence of cardiovascular disease and even an independent risk factor for the development of that disease. Sleep disorders exert harmful effects on a variety of systems with obvious changes in the endocrine, metabolic and immune pathways that are related to unfavorable health outcomes, including diabetes, hypertension and obesity persons that are written to contribute to the improvement of cardiovascular disease.

Nitric oxide (NO) is synthesized by nitrous oxide synthase enzymes in the heart and plays a vital role in cardiac functions. Despite the evidence based highlighting the roles of an ischemia in a rise in nitric oxide production no studies have yet examined the exchanges in the nitic oxide content in the hearts of sleep deprivation rats and its contribution to ischemia reperfusion injury. Moreover, there is no evidence to addressing the effects of subdermal on basal cardiac function and the cardiac tolerance following IR injury. Therefore, the main aim of this study was explaining about the effect of subdermal on basal hemodynamic functions and tolerance to the myocardial IR injury effecting in male rats. In addition, changes in NO metabolites (NOx) following IR injury were also assessed.

The term hypoxia refers to a condition where the tissues are not appropriately oxygenated and those are usually due to interrupted coronary blood flow or a reduction in arterial blood oxygen levels are partial pressurized. With the heart being a highly oxidative organ, depending on high oxygen intake for the work of its contractile machinery, it appears obvious that cardiac cells are very sensitive to oxygen deprivation.

Conclusion

Heart hypoxia, which originates because of disproportion between the amount of oxygen supplied to the cardiac cell and the amount required by the cell, plays a critical role in the pathobiology of several cardiovascular diseases. These are including the myocardial infarction, coronary artery diseases, heart failure secondary to pulmonary disease rate and congenital heart failure diseases. In patients with coronary artery diseases and myocardial infarction, hypoxia is usually due to the formation of an atherosclerotic plaque in the wall of coronary arteries, which reduces the perfusion of myocardial tissue.