Norepinephrine

Norepinephrine, administered to a normotensive adult either subcutaneously or by slow intravenous injection, constricts most blood vessels. Venules as well as arterioles are constricted. As a consequence, there is a net increase in the total peripheral resistance.

The effects of norepinephrine on cardiac function are complex because of the dynamic interaction of the direct effects of norepinephrine on the heart and the initiation of powerful cardiac reflexes. The baroreceptor reflexes are discussed in detail in Chapter 9.

Important considerations are as follows: (1) The direct effect of norepinephrine on the heart is stimulatory. (2) The reflex initiated is inhibitory, that is, opposite to the direct effect. (3) The reflex varies with the level of sympathetic and parasympathetic activity just before the initiation of the reflex. (4) The distribution of sympathetic and parasympathetic nerves is not uniform in the heart.

The net effect of norepinephrine administration on heart rate and ventricular contractile force therefore varies with the dose of norepinephrine, the physical activity of the subject, any prior cardiovascular and baro-receptor pathology, and the presence of other drugs that may alter reflexes.

In a normal resting subject who is receiving no drugs, there is a moderate parasympathetic tone to the heart, and sympathetic activity is relatively low. The ventricular muscle receives little, if any, parasympathetic innervation. As the blood pressure rises in response to norepinephrine, the baroreceptor reflex is activated, parasympathetic impulses (which are inhibitory) to the heart increase in frequency, and what little sympathetic outflow there is may be reduced. Heart rate is slowed so much that the direct effect of norepinephrine to increase the rate is masked and there is a net decrease in rate. Under the conditions described, however, the impact of the reflex on the ventricles is very slight because there is no parasympathetic innervation and the preexisting level of sympathetic activity is already low. A further decrease in sympathetic activity therefore would have little further effect on contractility in this subject. Thus, a decrease in heart rate and an increase in stroke volume will occur, and cardiac output will change very little.

The reflex nature of the bradycardia induced by parenterally administered norepinephrine can readily be demonstrated by administration of atropine, a choli-noreceptor antagonist. Atropine abolishes the compensatory vagal reflexes. Under conditions of vagal blockade, the direct cardiac stimulatory effects of nor-epinephrine are unmasked. There is marked tachycardia, an increase in stroke volume, and as a consequence, a marked increase in cardiac output (Fig. 10.4).

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