An Experimental Study on the Protective Effect of Nimodipine in the Cerebral Neuronal Injury following Cerebral Ischemia.
10.4097/kjae.1990.23.4.536
- Author:
Sie Jeong RYU
1
;
Sung Soo KIM
;
Hae Kyu KIM
;
Inn Se KIM
;
Kyoo Sub CHUNG
Author Information
1. Department of Anesthesiology, College of Medicine, Pusan National University, Korea.
- Publication Type:Original Article
- Keywords:
Cerebral Autoregulation;
Cerebral Ischemia;
Nimodipine
- MeSH:
Anesthesia, General;
Arterial Pressure;
Brain;
Brain Death;
Brain Ischemia*;
Calcium Channels;
Heart Diseases;
Homeostasis;
Humans;
Hypotension;
Hypoxia, Brain;
Lung;
Models, Animal;
Neurons*;
Nimodipine*;
Perfusion;
Persistent Vegetative State;
Resuscitation;
Seizures;
Shock
- From:Korean Journal of Anesthesiology
1990;23(4):536-542
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Cerebral autoregulation is the mainternance of a constant cerebral blood flow over a wide range of cerebral perfusion pressure. But irreversible hypoxic brain damage may occur as a consequence of such diverse conditions as lung and heart disease, shock, seizure or an episode of severe hypotension, and is potential hazard to any patient undergoing general anesthesia. The ultimate degree of neurological recovery may range from brain death and vegetative state to minor psychiatric disturbance and even normality, and is determined by the severity of the initial stress and wheather or not adequate resuscitation was commenced before irreversible brain damage. We performed an experiment to determine the protective effect of the calcium channel blocker nimodipine on the neuronal injury following cerebral ischemia in a rat model. The result were as follows: 1) Mean arterial pressure decreased more significantly in the nimodipine-treated group than the saline-treated group (p<0.01). 2) With respect to the degree of neuronal damage following cerebral ischemia, it decreased more significantly in the nimodipine-treated group than the saline-treated group (p<0.01).
