Journal of neurosurgical anesthesiology
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J Neurosurg Anesthesiol · Sep 1989
Flumazenil does not impair autoregulation of CBF in dogs when given with or without prior administration of midazolam.
The effects of flumazenil (a benzodiazepine antagonist) on autoregulation of cerebral blood flow (CBF) were examined in dogs receiving midazolam and in dogs not receiving midazolam. Both groups were anesthetized with halothane (0.3% end-expired) and nitrous oxide (66%) in oxygen. Auto-regulation of CBF was assessed by determining the slope relating CBF to cerebral perfusion pressure (CPP). ⋯ In dogs with normal CSF pressure that were receiving midazolam, both doses of flumazenil altered the electroencephalogram and the highest dose of flumazenil decreased cerebral vascular resistance and increased CBF and CSF pressure. No such changes were seen at the other experimental conditions. It is concluded that flumazenil does not severely disturb autoregulation of CBF, although flumazenil 0.16 mg/kg causes a statistically significant increase of CBF in dogs with normal CSF pressure that are receiving midazolam.
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J Neurosurg Anesthesiol · Jun 1989
Effects of hypoxic hypoxia and reoxygenation on H2O2 production in rat brain in vivo.
The effects of hypoxic hypoxia and subsequent reoxygenation on hydrogen peroxide (H2O2) production was studied in the rat brain in vivo. Brain H2O2 production was measured by H2O2-dependent aminotriazole inactivation of endogenous brain catalase activity. Brain catalase activities of rats breathing air (0.2 ATA O2, control) were 168 +/- 5 (n = 10), 125 +/- 4 (n = 6), and 100 +/- 5 (n = 8) U/g brain (mean +/- SEM) at 0, 30, and 60 min after i.p. aminotriazole injection, respectively. ⋯ Reoxygenated on room air, 100% O2, and hyperbaric 3 ATA O2 for 30 min immediately after each period of hypoxia, brain catalase activity at 60 min after aminotriazole injection in the group of pre-exposure to 6% O2 with N2O was 67 +/- 3, 74 +/- 3, and 67 +/- 6 U/g brain with 0.2 ATA O2 (n = 6), 1.0 ATA O2 (n = 5), and 3.0 ATA O2 (n = 5), respectively. All of these were significantly different from control and other hypoxic pre-exposure groups with N2 (p <0.01) but not from each other. Reoxygenation of the brain after hypoxia with N2O could exacerbate cerebral damage by increasing oxygen free radical production.
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J Neurosurg Anesthesiol · Mar 1989
Hypocapnia prevents the decrease in regional cerebral metabolism during isoflurane-induced hypotension.
In neurologic surgery, induced hypotension is often used while the patient is hypocapnic. We investigated, by tissue biopsy methods and scintillation counting, the regional cerebral glucose utilization (rCMRglc) and blood flow (rCBF) in rats subjected to hypocapnia alone and in combination with hypotension. Anesthesia was maintained with 1.0% isoflurane in nitrous oxide/oxygen. ⋯ During hypocapnia/hypotension, rCBF was unaltered in cortical areas, while increases were seen in all subcortical areas compared to hypocapnia. Regional values of the ratio of rCBF/rCMRglc indicated that during hypocapnia and hypotension induced by isoflurane in nitrous oxide/oxygen, the individual brain areas were perfused according to their metabolic needs. It is suggested that hypocapnia may prevent the decrease in rCMRglc, which is usually observed during deep isoflurane anesthesia.
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J Neurosurg Anesthesiol · Mar 1989
Flumazenil reversal of midazolam in dogs: dose-related changes in cerebral blood flow, metabolism, EEG, and CSF pressure.
Large doses of flumazenil, given rapidly (over 5-10 s), are reported to elevate cerebral blood flow (CBF) and intracranial pressure to supranormal values when given to dogs receiving midazolam. This study examined the cerebral effects of giving smaller, graduated doses of flumazenil (0.0025, 0.01, 0.04, and 0.16 mg/kg), slowly (over 60 s), to dogs receiving midazolam and to dogs not receiving midazolam both when cerebrospinal fluid (CSF) pressure was normal and when CSF pressure was elevated (intracranial balloon) to about 30 mm Hg. In dogs with normal CSF pressure that were receiving midazolam, the effects of flumazenil were as follows: (a) low doses of flumazenil caused reversal of the reduction in cerebral metabolic rate for oxygen (CMRO2) and activity of the electroencephalogram produced by midazolam, (b) moderate doses of flumazenil produced a decrease of cerebral vascular resistance, and an increase of CBF and CSF pressure that did not significantly change cerebral perfusion pressure (CPP), and (c) the highest dose of flumazenil increased CBF to supranormal values. ⋯ The results are consistent with a specific, doserelated benzodiazepineantagonist action of flumazenil. Lack of flumazenil effect at elevated CSF pressure may reflect reversible changes in cerebral structure, metabolism, or benzodiazepine receptors produced by the intracranial balloon and elevation of CSF pressure. The doses of flumazenil used here to reverse the cerebral effects of midazolam appear unlikely to produce adverse effects because increase of CMRO2 was matched by increase of CBF, the mean increase of CSF pressure was modest (+9 +/- 3 mm Hg, mean +/- SEM), and CPP was unchanged.