Summary:The circular contractile responses to various stimuli have been measured in segments of cerebral ar teries (both middle cerebral and basilar) taken from dogs either 3 or 7 days following the cisternal injection of au tologous blood under anaesthesia. The maximum con tractile response to 5-hydroxytryptamine was increased significantly 7 days following subarachnoid haemorrhage; the response to noradrenaline also increased but not sig nificantly at 7 days. The contractile response to a raised extracellular potassium concentration (25 and 100 mM) was slightly depressed by 7 days, and the response to a fall in extracellular pH was depressed by 43% both 3 and 7 days following subarachnoid haemorrhage. The ability of these arteries to handle a sodium load was also as sessed. The arteries were sodium loaded for various pe riods of time in mock cerebrospinal fluid with a zero po-The ability of the cerebral circulation to respond to changes either in arterial blood pressure or in arterial blood gases may be impaired in both hu mans and animals following a recent subarachnoid haemorrhage (Heilbrun et aI., 1972; Nornes et aI., 1977; Symon, 1978; Pickard et aI., 1979). The greater the impairment of the cerebrovascular reac tivity, the greater may be the risk of developing late neurological deficits (Pickard et aI., 1980; Farrar et aI., 1981). To study the mechanism of this change in reactivity, we have first sought to establish that this altered reactivity persists in vitro by examining the contractile responses to a variety of stimuli of
599tassium concentration. On transfer to 25 mM potassium solution, the duration but not the magnitude of the initial relaxation phase prior to a final contraction was greater with increasing time spent in the zero potassium solution. Both the magnitude and the duration of this relaxation phase, which reflect in part the ability of the vascular smooth muscle to extrude the sodium load, were in creased in arteries following subarachnoid haemorrhage when compared with control arteries. These results dem onstrate that the altered reactivity of cerebrovascular smooth muscle following subarachnoid haemorrhage per sists in vitro and is more than simply an enhanced re sponse to biogenic amines.