الفهرس 
Anatomy and Physiology of Cardiac MuscleOnly 14 pages are availabe for public view
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Abstract
The heart and its associated structures form an intricate system that has the primary aim of pumping blood through the lungs and around the body. For this reason, a good knowledge of the normal anatomy of the cardiovascular system is essential to understand pathology, and to manage patients with cardiovascular disease
The term, ischemia, to denote deficient blood supply to tissues due to obstruction of the arterial inflow was first used in the early nineteenth century. Ischemia-reperfusion (IR) injury is known as the tissue damage that results from the process of ischemia followed by the further insult induced by the restoration of blood supply to ischemic tissues. Reperfusion causes an inflammatory response as a result of the induction of various cytokines and chemokines and increased oxidative stress, which lead to microvascular dysfunction in the ischemic tissues and organs. The seminal observation that reperfusion following ischemia was associated with myocardial injury was made in 1960 by Jennings. Their report was based on experiments with canine hearts subjected to coronary ligation in which reperfusion appeared to accelerate the development of necrosis. Whether reperfusion is independently responsible for tissue injury, or simply hastens the demise of cells otherwise destined for necrosis, remained a matter of debate for some years. After the discovery of ischemic preconditioning, the independent effects of ischemia and reperfusion began to be unraveled from one another.
The extent of cell dysfunction, injury, and death is influenced by both the magnitude and the duration of ischemia. The discovery that short periods of IR (ischemic preconditioning) prior to the induction of lethal ischemia activates cell survival programs that limit postischemic injury. This indicates that the response to ischemia is bimodal.
Treatment of IR injury is also confounded by the fact that inhibition of IR associated inflammation might disrupt protective physiologic responses or result in immunosuppression.