The relative potency of pentobarbital in suppressing the kainic acid- or the N-methyl-D-aspartic acid-induced enhancement of cGMP in cerebellar cells

The Effect of Barbiturate Coma Therapy for the Patients with Severe Intracranial Hypertension : A 10-Year Experience

“…Theoretical benefits of barbiturate in IICP patients derive from vasoconstriction in normal brain areas (shunting blood to ischemic brain tissue), and decreased metabolic oxygen demand with accompanying reduction of cerebral blood flow 12) . Other mechanisms by which barbiturate may exert protective effects include stabilization of lysosomal membrane, reduction of intracellular calcium concentration, modification of amino acid and neurotransmitter release, scavenging of free radicals, alteration of fatty acid metabolism, reduction in cerebrospinal fluid production, membrane stabilization, and suppression of seizure 1,2,5,17,22) . Sedatives and analgesics such as morphine sulfate, midazolam, fentanyl, sufentanyl, propofol were also common management strategies for ICP control although there is no evidence to support their efficacy in this regard and they have not been shown to positively affect outcome 9) .…”

A Fatal Adverse Effect of Barbiturate Coma Therapy: Dyskalemia

“…Barbiturate may reduce the cerebral metabolic rate 37). Barbiturates may exert protective effects include stabilization of lysosomal membranes, modification of amino acid and neurotransmitter release, alteration of fatty acid metabolism, suppression of hyperactivity induced by catecholamine, membrane stabilization suppression of seizures and so on 178)…”

Role of Nitric Oxide‐Mediated Signal Transduction in Hypothermia Induced by Intravenous Anesthetics

“…Riluzole, an anesthetic under development, inhibits both pre‐ and postsynaptic release of glutamate 3 . Barbiturates inhibit glutamate receptor subtype‐mediated events, 4,5 although they are primarily known to enhance the gamma‐aminobutyric acid (GABA)‐coupled chloride channels 4 . Glutamatergic neurotransmission is linked to the release of nitric oxide (NO) and activation of guanylate cyclase and subsequent release of cyclic guanosine monophosphate (cGMP).…”