Nursing Pharmacology Chapter 9: Antianginal Drugs
Coronary blood flow regulation:
Coronary blood flow is controlled by the myocardial oxygen demand and modulated by varying coronary vascular resistance considerably.
The myocardium extracts a fixed and high percentage of oxygen.
In the absence of atherosclerotic disease, intramyocardial resistance arterioles can significantly dilate.
By regulation of smooth muscle tone, intramyocardial arterioles (resistance vessels) a balance is maintained between coronary blood flow and myocardial oxygen requirement.
In healthy individuals, the large epicardial vessels are conductance vessels.
Selwyn, A.P. and Braunwald, E Ischemic Heart Disease in Harrison's Principles of Internal Medicine (Isselbacher et al., eds) McGraw-Hill, Inc., New York, 1994, p 1077.
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Control of coronary blood flow involves:
Local metabolism
Nervous system regulation.
More important of these two mechanism is local myocardial metabolism, i.e. local arterial vasodilation is regulated by myocardial requirements.
Normally, increases in coronary blood flow, even in a denervated heart, occurs in response to increased myocardial contractility and rate.
Production of local vasodilator products may be responsible.
Candidates for these vasodilatory substances include:
Adenosine
Prostaglandins
Potassium ions
Bradykinin
Hydrogen ions
Carbon dioxide
Nitric oxide
Autonomic nervous system activity can affect coronary vasculature tone.
On the parasympathetic (vagal) side: there are so few fibers terminating on the coronary vasculature that the vagal dilating effects are minimal.
Coronary vascular bed has both alpha and beta-adrenoceptors.
α-adrenergic receptor activation produces constriction, mainly in epicardial capacitance vessels when these receptors are mostly found.
Coronary vessel vasodilation is mediated by β-adrenoceptors which are mainly localized in intramuscular arteries.
Sympathetic activation probably produces more constriction than dilation and in individuals with accentuated responses to α-receptor activation may be susceptible to vasospastic myocardial ischemia
Guyton, A.C. and Hall, J.E. in Textbook of Medical Physiology, W.B. Saunders & Co., Philadephia, 1984, p 258-259.