Fig. 3. Chemical structure of ketamine.

Source: Modified from Goodman and Gilman's (2001) The Pharmacological Basis ofTherapeutics, 10th Ed. (Hardman, J.G. and Limbird, L.E., eds.), McGraw-Hill, New York, NY.

DPDPE, [d-Pen25]-enkephalin; DADLE, [d-Ala2, d-Leu5]-enkephalin; NorBNI, nor-binaltorphimine; DSLET, [d-Ser2, Leu5, Thr6]-enkephalin

0, no change; +, increased; ++, more increased; +++, most increased; -, decreased; - -, more decreased; - - -, most decreased.

4.4. Ketamine

Ketamine is a phencyclidine derivative (Fig. 3) that causes intense analgesia and dissociative anesthesia. Patients who receive ketamine can obtain a cataleptic state with open eyes or ocular nystagmus. The typical routes for ketamine administration include intravenous (1-2 mg/kg), intramuscular (3-6 mg/kg), or oral (5-6 mg/kg). In general, the effects of ketamine on the central nervous system are considered caused by interactions with multiple receptors, including N-methyl-d-asparate, monoaminergic, opioid, or muscarinic receptors.

Potential side effects of ketamine include the stimulation of the central sympathetic nervous system and thus an increase in circulating epinephrine and norepinephrine. In patients for whom maintenance of myocardial contractility and systemic vascular resistance is vital (i.e., because of hypovolemia, trauma, and shock), ketamine may better stimulate the cardiovascular system to maintain cardiac output and blood pressure; ketamine acts to cause an increase in heart rate, blood pressure, cardiac output, and myocardial oxygen consumption.

Fig. 4. Chemical structure of propofol.

It should be noted that pulmonary artery pressure may also become increased after the administration of ketamine. Another important side effect attributed to ketamine administration is bronchodilation; thus, patients with, or at risk for, broncho-spasm may benefit from ketamine induction. In contrast, in patients with depleted catecholamine stores, ketamine may cause a serious depression of myocardial function (42); thus, its use may be contraindicated in patients with coronary artery disease, subaortic stenosis, or increased intracranial pressures.

4.5. Propofol

Propofol (1% solution) is a 2,6-diisopropylphenol (Fig. 4) that is typically administered intravenously for sedation or induction of anesthesia. Importantly, intravenous injections of propofol (1.5-2 mg/kg) are associated with rapid (30-60 s) loss of consciousness; hence, this has obvious clinical advantages. A maintenance infusion of propofol is typically achieved with 100-200 ^g/kg/min iv. Additional advantages of propofol include clear awakening, small cumulative effects, and decreased incidence of nausea and vomiting.

Propofol is considered also to interact with GABA receptors and activate them in a similar fashion as barbiturates. Likewise, activation of GABA receptors by propofol increases the con

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