Key result
Anterior hypothalamic stimulation boosts cardiac output fraction to muscle by ~51% to ~146% in primates.
Why the study?
The study aimed to investigate hypothalamic control of regional organ blood flow distribution in unanesthetized rhesus monkeys, including mechanisms of skeletal muscle vasodilatation.
Does not support clinical hypothalamic stimulation; leaves open central control of regional perfusion for future human studies.
Regional organ blood flow and resistance changes evoked after 10 minutes of electrical stimulation of pressor areas in the anterior hypothalamus were studied in six unanesthetized, restrained rhesus monkeys. Five other monkeys served as controls. The regional changes produced by stimulus intensities which did not affect systemic arterial pressure, central venous pressure, cardiac output, or pulse rate were similar to those produced by the stimulations at higher levels which significantly increased the levels of these variables. With both low and high levels of stimulation the fractions of cardiac output to skeletal muscle and chest wall were increased 51 and 146% at the expense of the output to the kidneys, skin, stomach, spleen, pancreas, mesentery, and thyroid which decreased 38 to 79%. In each of two monkeys tested, the marked rise in blood flow and vasodilatation of skeletal muscle was only slightly affected by atropine. Therefore, there is at least some hypothalamic control over skeletal muscular vasodilatation in the unanesthetized monkey that is not cholinergically mediated.
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Ralph P. Forsyth (1970) studied this question. Electrical stimulation of pressor areas in the anterior hypothalamus vs. Control monkeys was evaluated on Regional organ blood flow and resistance changes. Electrical stimulation of the anterior hypothalamus in unanesthetized rhesus monkeys increased cardiac output fractions to skeletal muscle and chest wall by 51-146% at the expense of other organs.
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