Journal of neurosurgical anesthesiology
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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.
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J Neurosurg Anesthesiol · Mar 1989
Sufentanil, alfentanil, and fentanyl: impact on cerebrospinal fluid pressure in patients with brain tumors.
In order to evaluate the safety of the new synthetic opioids, alfentanil and sufentanil, in neurosurgical patients, we administered sufentanil 1 microg/kg i.v., alfentanil 50 microg/kg i.v. followed by an infusion of 1 microg/kg/min, or fentanyl 5 microg/kg i.v. to 30 patients with supratentorial tumors anesthetized with nitrous oxide (N2O), 60% in O2. Lumbar cerebrospinal fluid pressure (CSFP) and mean arterial pressure (MAP) responses were recorded for 10 min thereafter, while ventilation was held constant [mean PaCO2 = 36.1 +/- 1.0 mm Hg (SEM)]. There was no change in CSFP after fentanyl. ⋯ It is concluded that because sufentanil increased CSFP in patients who have brain tumors, it also may be contraindicated in other neurosurgical patients at risk for intracranial hypertension. Alfentanil may share this propensity, since CSFP increased despite a profound reduction in MAP. Among the three opioids evaluated, only fentanyl appears to be appropriate for supplementing N2O-2 anesthesia in patients who have compromised intracranial compliance.
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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.