首页   按字顺浏览 期刊浏览 卷期浏览 Role of Prostaglandins in Delayed Cerebral Ischemia after Subarachnoid Hemorrhage
Role of Prostaglandins in Delayed Cerebral Ischemia after Subarachnoid Hemorrhage

 

作者: Padraic O'Neill,   Steven Walton,   Patrick Foy,   Malcom Shaw,  

 

期刊: Neurosurgery  (OVID Available online 1992)
卷期: Volume 30, issue 1  

页码: 17-22

 

ISSN:0148-396X

 

年代: 1992

 

出版商: OVID

 

关键词: Delayed cerebral ischemia;Prostaglandins;Subarachnoid hemorrhage;Vasospasm

 

数据来源: OVID

 

摘要:

Prostaglandin E2, thromboxane B2, and 6-oxo-prostaglandin F1αwere assayed in blood and cerebrospinal fluid samples from patients after subarachnoid hemorrhage (SAH) and from a control population. The levels found in samples obtained from patients after SAH were compared with those found in controls and were also correlated with a number of clinical and radiological variables, many of which are either significantly associated with or represent evidence of cerebral ischemia. The levels of prostaglandin E2, thromboxane B2, and 6-oxo-prostaglandin F1αin blood samples from patients after SAH and from controls were below the level of sensitivity of the assays. Levels of prostaglandin E2, thromboxane B2, and 6-oxo-prostaglandin F1αin cerebrospinal fluid from patients after SAH were significantly elevated when compared with those found in control samples. There was no significant correlation, however, between the level of each prostaglandin measured and the following variables: clinical grade on admission as assessed by the Glasgow Coma Score and the World Federation of Neurological Surgeons grading system; the amount of subarachnoid blood seen on computed tomographic scan; the occurrence of ischemic deterioration; the occurrence of low density change on computed tomographic scan; the presence of vasospasm on angiography; clinical outcome as assessed by the Glasgow Coma Score 3 months after the ictus; and the incidence of ischemia as a cause of death or disability as assessed 3 months after the ictus. A primary role for prostaglandins in the etiology of delayed cerebral ischemia after SAH is not therefore confirmed.

 



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