PubMed · 9652014
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N A Forbes. 1998. Avian anesthesia.. https://doi.org/10.1080/01652176.1998.10807418
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Many properties of nitric oxide, NO, (localization, diffusiveness, half-life, vasodilatory affects) have supported its potential role in mediating the link between local cerebral activity and blood flow. However, evidence that both supports and refutes a role for NO in functional hyperemia have been presented. The present study employed multiple nitric oxide synthase inhibitors, two anesthetic regimes and laser-Doppler flowmetry to test the hypothesis that NO is critically involved in mediating the functional hyperemic response within rodent whisker-barrel cortex (WBC). In urethane anesthetized animals, functional hyperemic responses were obtained both before and after 1 mg/kg atropine infusion, 30 mg/kg i.v. L-NAME (N-Nitro-L-arginine methylester) infusion, 30 mg/kg L-NA (N-Nitro-L-arginine) infusion or 25 mg/kg 7-NI (7-nitroindazole). L-NAME was also tested in a group of animals pretreated with halothane before urethane anesthesia. Neither the magnitude of the blood flow response nor its time course was altered by NO blockade or atropine administration when compared to pre-infusion controls in urethane anesthetized rats. In contrast, animals that were pretreated with halothane exhibited a 33% inhibition of functional hyperemia after L-NAME administration. Taken together, these data do not support a primary role for NO in rat WBC functional hyperemia and suggest that previous reports of inhibition may have been secondary to the anesthesia employed.
BASIC STRATEGY: Generalized tonic-clonic status epilepticus is a medical emergency requiring very rapid administration of anti-epilepsy drugs to avoid or prevent neurological damage. First intention treatment is based on rapid-action intravenous benzodiazepine (BZD) associated with another long-action anti-epilepsy drug. General anesthesia with respiratory assistance may be needed if the seizures are refractory. We considered the pharmacodynamic, pharmacokinetic and pharmacoeconomic properties of drugs proposed for the treatment of status epilepticus. TREATMENT EFFICACY: An analysis of the literature and clinical practice show that, used alone, BZDs have a rapid effect and are effective in 54 to 84% of the cases. When hydantoins are combined with BZD, cessation of seizures can be achieved in 94% of the patients compared with 82% when phenobarbital is used alone. However, the administration of hydantoins requires 15 to 30 min whereas phenobarbital is effective in 5 minutes. Irrespective of the type of BZD combined with hydantoins, no difference has been observed concerning clinical efficacy. Midazolam appears to be as effective as barbiturics. Cardiac function must be monitored when hydantoins are used although admission in an intensive care unit may not be required, unlike the situation with phenobarbital that may lead to intubation. IN CLINICAL PRACTICE: Considering non-refractory status epilepticus, a comparison of the efficacy of the proposed drugs, their side effects and their cost demonstrates a good cost/benefit ratio for phenobarbital and good tolerance for fosphenytoin. If cessation of the seizures cannot be achieved, other therapeutic strategies may have be to used: induction of barbituric coma with thiopental, general anesthesia using propofol, or midazolam or lidocaine.
Functional brain mapping based on changes in local cerebral blood flow (lCBF) or glucose utilization (lCMR(glc)) induced by functional activation is generally carried out in animals under anesthesia, usually alpha-chloralose because of its lesser effects on cardiovascular, respiratory, and reflex functions. Results of studies on the role of nitric oxide (NO) in the mechanism of functional activation of lCBF have differed in unanesthetized and anesthetized animals. NO synthase inhibition markedly attenuates or eliminates the lCBF responses in anesthetized animals but not in unanesthetized animals. The present study examines in conscious rats and rats anesthetized with alpha-chloralose the effects of vibrissal stimulation on lCMR(glc) and lCBF in the whisker-to-barrel cortex pathway and on the effects of NO synthase inhibition with N(G)-nitro-L-arginine methyl ester (L-NAME) on the magnitude of the responses. Anesthesia markedly reduced the lCBF and lCMR(glc) responses in the ventral posteromedial thalamic nucleus and barrel cortex but not in the spinal and principal trigeminal nuclei. L-NAME did not alter the lCBF responses in any of the structures of the pathway in the unanesthetized rats and also not in the trigeminal nuclei of the anesthetized rats. In the thalamus and sensory cortex of the anesthetized rats, where the lCBF responses to stimulation had already been drastically diminished by the anesthesia, L-NAME treatment resulted in loss of statistically significant activation of lCBF by vibrissal stimulation. These results indicate that NO does not mediate functional activation of lCBF under physiological conditions.