Despite the importance of cerebral angiospasm, we are still limited in our knowledge of the mechanisms involved in this phenomenon. Although it has been reported that denervation supersensitivity may be one of the causes of cerebral angiospasm, actually the cause of this phenomenon is still unconfirmed.
In the present experiments, changes in the reactivity of rabbit basilar artery to noradrenaline, serotonin and potassium ion after bilateral superior cervical sympathectomy were studied. 1. Fluorescent micrograph showed disappearance of noradrenaline from nerve fibers and terminals, seven to fourteen days after sympathectomy.
The noradrenaline content of basilar artery was reduced to 140.5±71.9 ng/g wet tissue (M±SE, n=6) seven days after ganglionectomy, and 137.8±49.8 ng/g wet tissue (M±SE, n=6) fourteen days after operation. Control: 2000.7±183.2 ng/g wet tissue (M±SE, n=11).
2. Seven days after operation, sensitivity of the basilar artery to noradrenaline increased. The threshold concentration was fell to 5×10-8 M as compared with that of control (5×10-7 M), while the maximum tension observed at a concentration of 5×10-4 M of noradrenaline increased to about 1.5 fold of that of control.
In a similar manner, the sensitivity to serotonin also increased, and the threshold concentration fell to 5×10-10 M (control: 5×10-9 M). The maximum tension increased about 1.7 fold of the control The response to 24.3 mM K was increased to about 1.7 fold of the control.
These results showed that after denervation, supersensitivity of rabbit basilar artery occured. The present experiments also indicate the possibility that denervation supersensitivity may be one of the causes of cerebral angiospasm.
