[Clinical and experimental studies on the role of Ca++ in etiology of cerebral vasospasm].

Total Ca and Ca++ in cerebrospinal fluid were measured from the patient with subarachnoidal hemorrhage due to ruptured cerebral aneurysm. Relationship was studied between the values of total Ca and Ca++ and grades of cerebral vasospasm on cerebral angiograms. Additionally, experimental studies were performed on helical strip of dogs' basilar arteries with constrictable substances such as serotonin (5-HT), prostaglandin F2 alpha (PGF2 alpha), KC1 and oxy-hemoglobin (Oxy-Hb). Findings were as follows: There was a gradual increasing of vasospasm in the patients whose cerebrospinal fluid contained high values of total Ca at one or two days after rupture of aneurysm. In all samples of bloody cerebrospinal fluid, values of Ca++ were almost the same or lower than that of control group. The time course of Ca++ concentrations was remarkably decreased in the groups with increased vasospasm. In the experimental study, continuous constriction of helical strips were induced with high concentration of KC1 and physiological values of Oxy-Hb, but 5-HT and PGF2 alpha constricted only in a short time. The effects of KC1 and Oxy-Hb were remarkably inhibited when Ca++-antagonist was added to the artificial cerebrospinal fluid or Ca++ was freed from the fluid. With these results, it was thought that Oxy-Hb might be the most important substance for cerebral vasospasm and it may affect cerebral vessels with Ca++ in cerebrospinal fluid. It was, however, an unreasonable result that time course of Ca++ decreased on the patients with severe vasospasm when vasospasm increased. Then, high concentration of total Ca at acute stage after subarachnoidal hemorrhage was considered as it may trigger the incidence of cerebral vasospasm.