Special:Badtitle/NS90:Talk:Coronary Blood Flow/coronary blood flow

"There are direct and indirect effects which are stimulated by the Autonomic nervous system to the heart that control the coronary blood flow as well. Direct Effects result from stimulation of the Vagus nerve which in turn releases acetylcholine and norepinephrine and epinephrine from the sympathetic nerves of the coronary vessels. The sympathetic stimulation increases heart rate, activity as well as the metabolic rate, in turn sets off local blood flow regulators which dilate the vessels. The Vagal stimulation functions the opposite way, it slows the heart by depressing the cardiac oxygen consumption and indirectly constricting the coronary arteries. Indirect Effects are more important for normal coronary flow conditions as they result from secondary changes of the heart by increased or decreased activity which changes the coronary blood flow. "

Corrections to above: The Vagus nerve does not carry sympathetic fibers - only parasympathetic. Therefore, it does not "release norepinephrine or epinephrine from nerves of the cornary vessels." Rather, parasympathetic stimulation causes release of acetylcholine from postganglionic parasympathetic neurons in ganglia on the heart, itself. Sympathetic fibers to the heart arise from lateral horns of T1-T6 and synapse in the cervical and upper 4-5 thoracic ganglia; postganglionic fibers release norepinephrine at the heart. This speeds the heart rate and increases the force of contraction and although sympathetic stimulation of the coronary arteries (via alpha receptors) may initially constrict the cornonary vessels, the much increased oxygen consumption and production of metabolic products secondarily causes dilation of the coronary arteries. There is also direct dilation of the arteries via beta-2 adrenergic receptors. It is also not correct to say, "The Vagal stimulation functions the opposite way, it slows the heart by depressing the cardiac oxygen consumption." Vagal stimulation slows the heart by depressing the SA node. This causes a decreased heart rate which results in lower oxygen consumption by the heart. This may result in constriction of the coronary arteries as a secondary effect but the outcome is apparently different for coronary arteries in different parts of the heart and there are also marked differences in various species which makes it difficult to draw conclusions from animal research models.

Susan Heaphy Instructor of physiology The Ohio State University at Lima Lima, OH