Effects of morphine on cerebral blood flow autoregulation and CO2-reactivity in experimental subarachnoid hemorrhage

Previous reports show that naloxone improves ischemic deficits and clinical conditions in patients after subarachnoid hemorrhage (SAH). These observat ions have raised concern about the routine use of morphine in the treatment of severe headache after SAH. The present study was carried out to investi gate the effects of morphine on cerebral vasoreactivity after experimental SAH. Cerebral blood flow (CBF) autoregulation was studied in two groups of eight rats each with experimental SAH. A bolus intravenous injection of mor phine, 1 mg/kg, was administered in one group and the other was used as a c ontrol group. During eucapnia, CBF was measured by the intrcarotid (133)Xen on method during decreasing mean arterial blood pressure (MABP). CO2-reacti vity was investigated in two corresponding groups when CBF was measured at decreasing PaCO2 levels during constant MABP. Morphine decreased mean basel ine CBF by 34% and 26% in the study of autoregulation and CO2-reactivity, r espectively. Cerebral blood flow autoregulation was found impaired in both controls and the morphine group. However, the mean slope of the linear regr ession lines of CBF/MABP was 0.49 +/- 0.32 ml/100g/min/mm Hg in the morphin e group, which was significantly lower than 1.24 +/- 0.59 ml/100g/min/mm Hg in the controls (p < 0.05). Also the mean CO2-reactivity was significantly lower, 0.64 +/- 0.53 %/0.1kPa, in the morphine group, compared to 2.36 +/- 0.87 %/0.1kPa in the controls (p < 0.001). The results show that in rats w ith SAH, morphine partially restores CBF autoregulation but attenuates CO2- reactivity.