Journal of neurosurgical anesthesiology
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J Neurosurg Anesthesiol · Sep 1990
Transcranial Doppler sonography as a supplement in the detection of cerebral circulatory arrest.
The effects of compromised cerebral hemodynamics on intracranial blood flow velocity patterns (BFV) were studied by noninvasive transcranial Doppler sonography (TCD). Pulsatility index (PI) as an estimation of peripheral cerebral vascular resistance was additionally analyzed. TCD patterns were determined in 19 mechanically ventilated brain dead patients (group A) and 8 resuscitated or severely head injured patients (group B) with intermittent elevated intracranial pressure (ICP). ⋯ In these patients, resistive Doppler signals with normal or reduced systolic peaks and decreased diastolic flow velocities were expressed as increases in PI. Noninvasive transcranial Doppler sonography appears to confirm cerebral circulatory arrest. Additionally, TCD may be of value for the early detection of impaired cerebral hemodynamics due to changes in intracranial compliance.
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J Neurosurg Anesthesiol · Mar 1990
Perioperative monitoring of the electrocardiogram during cerebral aneurysm surgery.
Electrocardiographic (ECG) abnormalities occur frequently following a subarachnoid hemorrhage and may also occur intraoperatively and postoperatively in patients undergoing neurovascular procedures. The aim of this study was to assess the relationship between ECG changes and the neurological status of the patient, the size and the location of the aneurysm, and the influence of these changes on the cardiac and neurological outcome. The preoperative ECG was analyzed in 270 patients. ⋯ Intraoperative and postoperative changes occurred in 35 and 65% of the patients, respectively, and were independent of the studied factors. There were no documented cardiac events. The presence of an abnormal preoperative ECG did not influence the neurological outcome of the patient, but fluctuating postoperative changes were associated with a worse outcome.
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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.