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Effects of halothane, α-chloralose, and pCO2 on injury volume and CSF β-endorphin levels in focal cerebral ischemia

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Molecular and Chemical Neuropathology

Abstract

Anesthetic agent, arterial pCO2 level, and opioid peptides have all been implicated in the pathophysiology of experimental stroke models. The effects of halothane, α-chloralose, and differing concentrations of arterial pCO2 on injury volume and CSF β-endorphin levels were studied in a feline model of experimental focal cerebral ischemia. The type of anesthetic agent used had no effect on injury volume following 6 h of focal cerebral ischemia. Over a 6-h period, β-endorphin levels significantly increased from 10.1±5.0 fmol/mL at zero time to 14.4±7.2 fmol/mL at 6 h under halothane anesthesia (p<0.05), whereas they did not significantly change (10.1±6.7 to 7.8 ±4.7 fmol/mL) under α-chloralose anesthesia. In contrast, hypercapnia had no effect on β-endorphin levels, but significantly increased injury volume from 30.6±5.7% of the ipsilateral hemisphere under normocapnic conditions to 37.1±5.9% under hypercapnic conditions (p<0.05). These results suggest that hypercapnia increases injury volume in a feline model of focal cerebral ischemia, and pCO2 should be controlled in experimental focal cerebral ischemia models.

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Browning, J.L., Heizer, M.L., Widmayer, M.A. et al. Effects of halothane, α-chloralose, and pCO2 on injury volume and CSF β-endorphin levels in focal cerebral ischemia. Molecular and Chemical Neuropathology 31, 29–42 (1997). https://doi.org/10.1007/BF02815158

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