Effective of Naloxone on Cerebral Blood Flow in the Acute Stage of Experimentally Induced Subarachnoid Hemorrhage in Cat.
- Author:
Min Woo BAIK
1
;
Joon Ki KANG
;
Chun Kun PARK
;
Young KIM
;
Tae Hoon JO
;
Jung Chul KU
;
Suck Hoon YOON
;
Dal Soo KIM
;
Jin Un SONG
Author Information
1. Department of Neurosurgery, Catholic University Medical College, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Subarachnoid hemorrhage;
Naloxone;
Cerebral blood flow;
Endogenous opiate
- MeSH:
Adult;
Animals;
Brain Ischemia;
Cardiovascular System;
Cats*;
Humans;
Hydrogen;
Intracranial Pressure;
Naloxone*;
Opioid Peptides;
Pentobarbital;
Prognosis;
Subarachnoid Hemorrhage*;
Vasoconstriction
- From:Journal of Korean Neurosurgical Society
1987;16(1):175-188
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The immediate fall in cerebral blood flow(CBF) and the early clinical picture following subarachnoid hemorrhage(SAH) correlate well with the prognosis of most of the patients. But the cause of this fall in CBF is not fully understood. Recently attention has been focused on the role of endogenous opiates in the pathogenesis of cerebral ischemia. This research was planned to observe the acute change of regional cerebral blood flow(CBF) in experimentally induced SAH, to investigate whether endogenous opiate plays a role in the mechanism of the acute reduction in CBF following SAH, and to document the therapeutic value of naloxone. We have studied the effects of naloxone, an opiate antagonist, on CBF, cardiovascular system, intracranial pressure (ICP) and electroencephalography(EEG) in pentobarbital anesthetized cats. Twenty - five adult cats were divided into four groups as follows : control group (group I; 5 caes), naloxone-treated control group (group II; 5 cats), SAH group (group III; 7 cats) and naloxone-treated SAH group (group IV; 8cats). The measurement of CBF was done by hydrogen clearance methods, and carried out every 20 minutes from the beginning to 140 minutes following SAH. Naloxone(10 mg/kg) was intravenously administered to cats, three times : 40, 80 and 120 minutes following SAH. The results were as follows : 1) We have induced SAH in 18 cats, in which 15 cats showed the immediate reduction in CBF following SAH(incidence rate : 83%). 2) Significant elevations in the mean arterial blood pressure(MABP : 141+/-10.7 to 146+/-12.3 mmHg) and ICP(19+/-3.5 to 21+/-3.9mmHg) were observed immediately after SAH, followed by reduction respectively to the levels of baseline value within 40 minutes after SAH. Naloxone had no significant influence on the changes in MABP and ICP. 3) Baseline values of CBF in group I and II were 44.5+/-6.9 to 50.1+/-5.4 ml/100g/min, and were not changed by naloxone. 4) Induction of SAH resulted in a significant reduction of blood flow to 34.8+/-5.9 to 38.4+/-5.6ml/100g/min(p<0.05), and the reduced value was not significantly changed through the experiment. Reduction in CBF was usually greater on the side of the lesion. 5) In group IV, the initial administration of naloxone made the reduced CBF increase to about 46 ml/100g/min(p<0.05), and the increased CBF value was maintained by the additional injections of naloxone. 6) Cats subjected to SAH exhibited progressive loss of amplitude and decreased frequency in EFG, which were improved by the administration of naloxone. These data suggest that endogenous opiate, which may cause decrease of cerebral metabolic rate and vasoconstriction, can play an important role in the mechanism of the acute reduction in CBF following SAH. Naloxone may induce increase in CBF by reversing the effects of endogenous opiate and its direct cerebral vasodilator properties.
