Document Detail


Cerebral aterial spasm. I. Adrenergic mechanism in experimental cerebral vasospasm.
MedLine Citation:
PMID:  148833     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This study demonstrates that an adrenergic mechanism plays an important role in producing the delayed cerebral vasospasm which follows subarachnoid hemorrhage. Results were as follows: 1. Experimental subarachnoid hemorrhage (SAH) was produced by injection of fresh arterial blood into the cisterna magna in cats. The cerebral vasospasm was shown angiographically to be biphasic in nature: immediate constriction lasting 1 h and marked prolonged spasm occurring between the 3rd and 5th day after SAH. The amount of noradrenaline (NA) and dopamine-beta-hydroxylase (DBH) activity decreased over a period of 24 h both within the wall of the basilar artery and in the locus ceruleus and then gradually increased, reaching a maximum on the 3rd day after SAH. 2. Topical application of spasmogenic substances (NA and blood) produced a marked constriction of the hypersensitive basilar artery on the 3rd day after SAH. 3. 6-Hydroxydopamine (6-OHDA) injection into the cisterna magna produced prolonged vasocilatation. The dilated vessel responded with mild transient constriction after the topical application of NA or fresh blood. DBH activity and NA concentration in the vessels, locus ceruleus and medial hypothalamus decreased markedly on the 3rd day after the cisternal injection of 6-OHDA. 4. Various spasmogenic substances (i.e. serotonin, NA, prostaglandins and methemoglobin) were measured in a mixture of equal volume of CSF and blood in cats. ONly the serotonin in the mixed fluid produced vasoconstriction. Spasmogenic substances decreased markedly in the mixed fluid incubated for 3 days at 37 degrees C, and none of these substances apart from methemoglobin was present in a concentration sufficient to produce constriction of vessels. 5. These results suggest that early spasm is induced by serotonin around the arteries of the cranial base, and delayed spasm might be caused by hyperreaction of cerebral vessels to spasmogenic substances such as methemoglobin, during the accumulation of excess NA in the cerebral vessel wall.
Authors:
H Morooka
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Acta medica Okayama     Volume:  32     ISSN:  0386-300X     ISO Abbreviation:  Acta Med. Okayama     Publication Date:  1978 Apr 
Date Detail:
Created Date:  1978-07-24     Completed Date:  1978-07-24     Revised Date:  2003-11-14    
Medline Journal Info:
Nlm Unique ID:  0417611     Medline TA:  Acta Med Okayama     Country:  JAPAN    
Other Details:
Languages:  eng     Pagination:  23-37     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Basilar Artery / drug effects
Blood
Brain Chemistry
Cats
Cerebral Arteries / analysis,  innervation,  physiopathology
Dopamine beta-Hydroxylase / analysis
Ischemic Attack, Transient / etiology,  physiopathology*
Norepinephrine / cerebrospinal fluid,  pharmacology
Prostaglandins / cerebrospinal fluid,  pharmacology
Serotonin / cerebrospinal fluid,  pharmacology
Sympathetic Nervous System / physiopathology*
Chemical
Reg. No./Substance:
0/Prostaglandins; 50-67-9/Serotonin; 51-41-2/Norepinephrine; EC 1.14.17.1/Dopamine beta-Hydroxylase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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