Effects of Postischemic Halothane Administration on Outcome From Transient Focal Cerebral Ischemia in the Rat
Autor: | Robert D. Pearlstein, Ann D. Brinkhous, Huaxin Sheng, David S. Warner, Shiva Sarraf-Yazdi |
---|---|
Rok vydání: | 1999 |
Předmět: |
Male
Time Factors Ischemia Hemiplegia Neuroprotection Body Temperature Interquartile range Animals Medicine Single-Blind Method Middle cerebral artery occlusion Rats Wistar Wakefulness Cerebral Cortex Neurologic Examination business.industry Brain Cerebral Infarction Infarct size medicine.disease Pathophysiology Rats Neuroprotective Agents Anesthesiology and Pain Medicine Hemiparesis Ischemic Attack Transient Anesthesia Anesthetics Inhalation Reperfusion Surgery Neurology (clinical) Halothane medicine.symptom Anesthesia Inhalation business medicine.drug |
Zdroj: | Journal of Neurosurgical Anesthesiology. 11:31-36 |
ISSN: | 0898-4921 |
DOI: | 10.1097/00008506-199901000-00006 |
Popis: | This study examined the effect of prolonged postischemic halothane administration on outcome from transient focal cerebral ischemia in rats. Conscious normothermic rats were subjected to 75 minutes of filament middle cerebral artery occlusion (MCAO). Animals were then divided into two groups. The Awake group (n = 15) remained awake following ischemia. The Halothane group (n = 15) received 1.3-1.4% halothane for 5 hours after onset of recirculation. In both groups, brain temperature was maintained at 37.5 degrees C during ischemia and the first 22 hours of recovery. Seven days after ischemia, the severity of hemiparesis and cerebral infarct size were examined. Neurologic scores did not differ between groups (Awake = 1+/-2.75; Halothane = 2+/-2; p = 0.772, median +/- interquartile range). Neurologic scores and total infarct volumes were correlated (R = 0.653; p = 0.0004). Cortical (Awake = 76+/-57 mm3; Halothane = 90+/-57 mm3; p = 0.494, mean +/- standard deviation), subcortical (Awake = 71+/-33 mm3; Halothane = 80+/-35 mm3; p = 0.472), and total (Awake = 147+/-88 mm3; Halothane = 171+/-91 mm3; p = 0.477) infarct volumes were not significantly different between groups. The data indicate that postischemic halothane administration offers no benefit in ameliorating damage from focal cerebral ischemia. This suggests that the neuroprotective effect of halothane observed in other studies is consistent with influences on intra-ischemic pathophysiology only. |
Databáze: | OpenAIRE |
Externí odkaz: |
Pro tento záznam nejsou dostupné žádné jednotky.