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

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.