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While barbiturates are generally considered to be CNS depressants, they can invoke all levels of CNS mood alteration from paradoxical excitement to deep coma and death. While the exact mechanisms for the CNS effects caused by barbiturates are unknown, they have been shown to inhibit the release of acetylcholine, norepinephrine, and glutamate. The barbiturates also have effects on GABA and pentobarbital has been shown to be GABA-mimetic. At high anesthetic doses, barbiturates have been demonstrated to inhibit the uptake of calcium at nerve endings.
The degree of depression produced is dependent on the dosage, route of administration, pharmacokinetics of the drug, and species treated. Additionally, effects may be altered by the age or physical condition of the patient, or the concurrent use of other drugs. The barbiturates depress the sensory cortex, lessen motor activity, and produce sedation at low dosages. Some barbiturates such as phenobarbital are useful as anticonvulsants because they tend to have sufficient motor activity depression, without causing excessive sedation. In humans, it has been shown that barbiturates reduce the rapid-eye movement (REM) stage of sleep. Barbiturates have no true intrinsic analgesic activity.
In most species, barbiturates cause a dose-dependent respiratory depression, but in some species they can cause slight respiratory stimulation. At sedative/hypnotic doses respiratory depression is similar to that during normal physiologic sleep. As doses increase, the medullary respiratory center is progressively depressed with resultant decreases in rate, depth, and volume. Respiratory arrest may occur at 4 times lower the dose that will cause cardiac arrest. These drugs must be used very cautiously in cats as they are particularly sensitive to the respiratory depressant effects of barbiturates.
Besides the cardiac arresting effects of the barbiturates at euthanatizing dosages, the barbiturates have other cardiovascular effects. In the dog, pentobarbital has been demonstrated to cause tachycardia, decreased myocardial contractility and stroke volume, and decreased mean arterial pressure and total peripheral resistance.
The barbiturates cause reduced tone and motility of the intestinal musculature, probably secondary to its central depressant action. The thiobarbiturates (thiamylal, thiopental) may, after initial depression, cause an increase in both tone and motility of the intestinal musculature. However, these effects do not appear to have much clinical significance. Administration of barbiturates reduces the sensitivity of the motor end-plate to acetylcholine, thereby slightly relaxing skeletal muscle. Because the musculature is not completely relaxed, other skeletal muscle relaxants may be necessary for surgical procedures.
There is no direct effect on the kidney by the barbiturates, but severe renal impairment may occur secondary to hypotensive effects in overdose situations. Liver function is not directly affected when used acutely, but hepatic microsomal enzyme induction is well documented with extended barbiturate (especially phenobarbital) administration. Although barbiturates reduce oxygen consumption of all tissues, no change in metabolic rate is measurable when given at sedative dosages. Basal metabolic rates may be reduced with resultant decreases in body temperature when barbiturates are given at anesthetic doses.