Coronary Flow
During contraction of the ventricular myocardium (systole), the subendocardial coronary vessels (the vessels that enter the myocardium) are compressed due to the high intraventricular pressures. However, the epicardial coronary vessels (the vessels that run along the outer surface of the heart) remain patent. Because of this, blood flow in the subendocardium stops. As a result most myocardial perfusion occurs during heart relaxation (diastole) when the subendocardial coronary vessels are patent and under low pressure. This contributes to the filling difficulties of the coronary arteries. Compression remains the same. Failure of oxygen delivery caused by a decrease in blood flow in front of increased oxygen demand of the heart results in tissue ischemia, a condition of oxygen deficiency. Brief ischemia is associated with intense chest pain, known as angina. Severe ischemia can cause the heart muscle to die from hypoxia, such as during a myocardial infarction. Chronic moderate ischemia causes contraction of the heart to weaken, known as myocardial hibernation.
In addition to metabolism, the coronary circulation possesses unique pharmacologic characteristics. Prominent among these is its reactivity to adrenergic stimulation. The majority of vasculature in the body constricts to norepinephrine, a sympathetic neurotransmitter the body uses to increase blood pressure. In the coronary circulation, norepinephrine elicits vasodilation, due to the predominance of beta-adrenergic receptors in the coronary circulation. Agonists of alpha-receptors, such as phenylephrine, elicit very little constriction in the coronary circulation.
Read more about this topic: Coronary Circulation
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