- Adrenergic agonists can be categorized as direct or indirect. Direct agonists bind to the receptor, whereas indirect agonists increase endogenous neurotransmitter activity.
- The primary effect of phenylephrine is peripheral vasoconstriction with a concomitant rise in systemic vascular resistance and arterial blood pressure.
- Clonidine seems to decrease anesthetic and analgesic requirements and to provide sedation and anxiolysis.
- Dexmedetomidine is a lipophylic α-methylol derivative with a higher affinity for α2-receptors than clonidine. It has sedative, analgesic, and sympatholytic effects that blunt many of the cardiovascular responses seen during the perioperative period.
- Long-term use of these agents, particularly clonidine and dexmedetomidine, leads to supersensitization and up-regulation of receptors; with abrupt discontinuation of either drug, an acute withdrawal syndrome manifested by a hypertensive crisis can occur.
- Ephedrine is commonly used as a vasopressor during anesthesia. As such, its administration should be viewed as a temporizing measure while the cause of hypotension is determined and remedied.
- Small doses (approximately 2 mcg/kg/min) of dopamine (DA) have minimal adrenergic effects but activate dopaminergic receptors. Stimulation of these nonadrenergic receptors (specifically, DA1 receptors) vasodilates the renal vasculature and promotes diuresis.
- Favorable effects on myocardial oxygen balance are believed to make dobutamine a good choice for patients with the combination of congestive heart failure and coronary artery disease, particularly if peripheral vascular resistance is elevated. (There are some recent debates regarding this beneficial effect.)
- Labetalol lowers blood pressure without reflex tachycardia because of its combination of α- and β-effects.
- Esmolol is an ultrashort-acting selective β1-antagonist that reduces heart rate and, to a lesser extent, blood pressure.
- Discontinuation of β-blocker therapy for 24-48 hr may trigger a withdrawal syndrome characterized by hypertension, tachycardia, and angina pectoris.
Adrenergic agonists and antagonists produce their clinical effects by interacting with the adrenergic receptors (ie, adrenoceptors). The clinical effects of these drugs can be deduced from an understanding of the adrenoceptor physiology and a knowledge of which receptors each drug activates or blocks.
The term “adrenergic” originally referred to the effects of epinephrine (adrenaline), although norepinephrine (noradrenaline) is the primary neurotransmitter responsible for most of the adrenergic activity of the sympathetic nervous system. With the exception of eccrine sweat glands and some blood vessels, norepinephrine is released by postganglionic sympathetic fibers at end-organ tissues (Figure 14-1). In contrast, acetylcholine is released by preganglionic sympathetic fibers and all parasympathetic fibers.
The sympathetic nervous system. Organ innervation, receptor type, and response to stimulation. The origin of the sympathetic chain is the thoracoabdominal (T1-L3) spinal cord, in contrast to the craniosacral distribution of the parasympathetic nervous system. Another anatomic difference is the greater distance from the sympathetic ganglion to the visceral structures.
Norepinephrine is synthesized in the cytoplasm of sympathetic postganglionic nerve endings and stored in the vesicles (Figure 14-2). After release by a ...