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Journal of Korean Neurosurgical Society 1983;12(2): 159-168.
In Vitro Effect of Ca++ Antagonist on Contraction of Carotid Artery in the Rabbit.
C S Kim, J O Lee, K C Lee, J W Chu
Department of Neurosurgery, College of Medicine, Korea University, Seoul, Korea.
ABSTRACT
Cerebral vasospasm in subarachnoid hemorrhage is problem of great clinical importance, because its occurrence in the course of the illness is known to affect the outcome of patient. Many humoral and neural causative mechanisms have been postulated for the blood induced vasospasm. In spite of many studies, not only the prevention but also the true nature of causes and therapies remain unclear. Recent reports indicate that calcium antagonist may functions as a physiological cerebral vasodilatator. This present study was undertaken to clarify the effectiveness of calcium antagonist on the carotid arteries in the rabbit. In vitro, arterial constrictions were induced applying the vasoactive subtances such as serum, prostaglandin F2 alpha, norepinephine and potassium chloride. Inhibitor, Diltiazem was added in 1 x 10-4 M amount and responses of relaxation were recorded on the kymograph. Sustainable contraction of carotid arteries developed shortly after the addition of serum, 4 x 10-4 M norepinephrine, 1 x 10-4 M prostaglandin F2 alpha and 2M KCI, and the maximum contraction of the arterial segment at each molar concentration was recorded at 60 min. after the experiment. The contractile response to serum, norepinephrine and prostglandin F2 alpha was considerable greater than that to KCI. Diltiazem in 1 x 10-4 M or 1 x 10-3 M concentration would relax completely the contracted carotid artery, however inhibitory action of Diltiazem(1 x 10-4 M) is highly sensitive to serum, norepinephrine induced contraction and is less sensitive to prostaglandin and KCI induced contraction. Based on this fact author confirmed that Diltiazem may play a significant role in the treatment of vasospasm following subarachnoid hemorrhage.
Key Words: Cerebral vasospasm; Calcium antagonist
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