Acute decrease of cerebrocortical microflow and lack of carbon dioxide reactivity following subarachnoid haemorrhage in the rat.

Experiments were designed to study the extent, duration and severity of the impairment of cerebrocortical microciroflow during acute ischemia following experimental SAH in the rat. Twenty five male, adult anesthetized and mechanically ventilated Wistar rats were used. SAH was induced by perforation of the middle cerebral artery (MCA) using intravascular filament. Cerebrocortical microflow (LDF) was recorded bilaterally in the territory supplied by the MCA at normocapnia before SAH and up to 180 min thereafter. Reactivity of microcirculation to CO2 was also studied. In order to further explain mechanisms of post-SAH microcirculatory changes, L-arginine--a precursor of NO and 17-octadecynoic acid (17-ODYA)--an inhibitor of the enzymes of cytochrome P-450 family were administered. SAH resulted in acute decrease of microflow on both sides although during the first 20 min this effect was much better pronounced on the side ipsilateral to ruptured MCA (p < 0.05). Pretreatment with L-arginine or 17-ODYA didn't improve microflow after SAH. On the contrary, in rats pretreated with 17-ODYA LDF on the side ipsilateral to bleeding significantly deteriorated (p < 0.05 vs. control group at all times beginning 10 min after SAH). Following SAH the impairment of CO2 reactivity was also observed.