Journal of neurosurgical anesthesiology
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J Neurosurg Anesthesiol · Apr 2003
Randomized Controlled Trial Comparative Study Clinical TrialRandomized, double-blinded comparison of tropisetron and placebo for prevention of postoperative nausea and vomiting after supratentorial craniotomy.
This prospective, randomized, placebo-controlled, double-blinded study was designed to evaluate the efficacy of tropisetron in preventing postoperative nausea and vomiting after elective supratentorial craniotomy in adult patients. We studied 65 ASA physical status I-III patients aged 18 to 76 years who were undergoing elective craniotomy for resection of various supratentorial tumors. Patients were divided into two groups and received either 2 mg of tropisetron (group T) or saline placebo (group P) intravenously at the time of dural closure. ⋯ The incidence of emetic episodes was 26.7% and 56.7% in the two groups (P <.05). Rescue antiemetic medication was needed in 26.7% and 60% of the patients (P <.05). Administration of a single dose of tropisetron (2 mg intravenously) given at the time of dural closure was effective in reducing postoperative nausea and vomiting after elective craniotomy for supratentorial tumor resection in adult patients.
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J Neurosurg Anesthesiol · Apr 2003
Case ReportsAcute neurogenic pulmonary edema: case reports and literature review.
Neurogenic pulmonary edema (NPE) is an underdiagnosed clinical entity. Its pathophysiology is multifactorial but largely unknown. We report two cases of NPE and review the literature on NPE cases reported since 1990. ⋯ Our two cases had clinical and laboratory features in common with most NPE cases. Physicians should remember NPE when neurologic patients suddenly become dyspneic. The mortality rate is high, but surviving patients usually recover very quickly.
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J Neurosurg Anesthesiol · Apr 2003
Comparative StudyCerebral blood flow at 0.5 and 1.0 minimal alveolar concentrations of desflurane or sevoflurane compared with isoflurane in normoventilated pigs.
Whether desflurane and sevoflurane have clinical advantages over isoflurane in neuroanesthesia is much debated. A porcine model was used for comparison of desflurane and sevoflurane with isoflurane with respect to their cerebrovascular effects. The minimal alveolar concentration (MAC) of each of the three agents was first determined in a standardized manner in six domestic juvenile pigs to enhance comparison reliability. ⋯ Statistical comparison of desflurane and sevoflurane with isoflurane with respect to CBF and MAP revealed two statistically significant differences-namely, that CBF at 1.0 MAC desflurane was 17% higher than CBF at 1.0 MAC isoflurane (P =.0025) and that MAP at 1.0 MAC sevoflurane was 16% higher than MAP at 1.0 MAC isoflurane (P =.011). Consequently, in this study at normocapnia, these agents did not seem to differ much in their cerebral vasodilating effects at lower doses. At higher doses, however, desflurane, in contrast to sevoflurane, was found to induce more cerebral vasodilation than isoflurane.
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J Neurosurg Anesthesiol · Apr 2003
Effects of ketamine on isoflurane- and sevoflurane-induced cerebral vasodilation in rabbits.
Although ketamine has been reported to have little effect on the cerebral circulation when used with other anesthetics, its effect on the cerebral vascular response to volatile anesthetics, which increase cerebral blood flow in a concentration-dependent manner, remains obscure. A closed cranial window was prepared in 15 pentobarbital-anesthetized adult rabbits. ⋯ In rabbits inhaling sevoflurane, the degree of cerebral vasodilator response was smaller than that by isoflurane, and the cerebral vasodilation was comparable whether in the presence or absence of ketamine (with or without l-arginine). In conclusion, ketamine reduces isoflurane-induced cerebral vasodilation, apparently independently of nitric oxide formation, while sevoflurane-induced cerebral vasodilation is not significantly affected by ketamine.
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J Neurosurg Anesthesiol · Apr 2003
Effects of magnesium administration on brain edema and blood-brain barrier breakdown after experimental traumatic brain injury in rats.
In this study, we examined the effects of magnesium sulfate administration on brain edema and blood-brain barrier breakdown after experimental traumatic brain injury in rats. Seventy-one adult male Sprague-Dawley rats were anesthetized, and experimental closed head trauma was induced by allowing a 450-g weight to fall from a 2-m height onto a metallic disk fixed to the intact skull. Sixty-eight surviving rats were randomly assigned to receive an intraperitoneal bolus of either 750 micromol/kg magnesium sulfate (group 4; n = 30) or 1 mL of saline (group 2; n = 30) 30 minutes after induction of traumatic brain injury; 39 nontraumatized animals received saline (group 1; n = 21) or magnesium sulfate (group 3; n = 18) with an identical protocol of administration. ⋯ Evans blue dye content in the brain tissue was significantly decreased in the magnesium-treated injured group (left hemisphere: group 2, 0.0204 +/- 0.03; group 4, 0.0013 +/- 0.0002 [P <.05]; right hemisphere: group 2, 0.0064 +/- 0.0009; group 4, 0.0013 +/- 0.0003 [P <.05]) compared with the saline-treated injured group. The findings of the present study support that beneficial effects of magnesium sulfate exist after severe traumatic brain injury in rats. These results also indicate that a blood-brain barrier permeability defect occurs after this model of diffuse traumatic brain injury, and magnesium seems to attenuate this defect.