Evaluation of Cerebrospinal Fluid Levels of Thromboxane B2 and 6-ketoprostaglandin F1alpha in Patients with Aneurysmal Subarachnoid Hemorrhage.
- Author:
Sang Yeoul KIM
1
;
Man Bin YIM
;
Eun Ik SON
;
In Hong KIM
;
In Kyu LEE
Author Information
1. Department of Neurosurgery, School of Medicine, Keimyung University, Taegu, Korea.
- Publication Type:Original Article
- Keywords:
Cerebral vasospasm;
Arachidonic acid;
Prostacycline;
Thromboxane A2;
Subarachnoid hemorrhage;
Cerebrospinal fluid
- MeSH:
Aneurysm*;
Arachidonic Acid;
Blood Platelets;
Cerebrospinal Fluid*;
Epoprostenol;
Hemorrhage;
Humans;
Metabolism;
Prostaglandins I;
Radioimmunoassay;
Rupture;
Subarachnoid Hemorrhage*;
Thromboxane A2;
Thromboxane B2*;
Vasospasm, Intracranial
- From:Journal of Korean Neurosurgical Society
1989;18(5):671-679
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
In order to find out the relationship between arachidonic acid(AA) metabolites and the development of vasospasm following a subarachnoid hemorrhage(SAH), we evaluated the cerebrospinal fluid(CSF) levels of the two main AA metabolites, prostacyclin(PGI2) and thromboxane A2(TXAZ) by measuring their stable degredation products 6-keto-prostaglandin F1alpha(PGF1) and thromboxane B2(TXB2) using radioimmunoassay methods in 32 patients after an aneurysmal rupture and in 11 patients without an aneurysmal rupture as a control group. We compared the data between aneurysmal ruptured patients and control group patients. We also divided the data of the aneurysmal ruptured patients into 3 groups checking them between 1-4, 5-11, and 12-28 days after the SAH, and compared the data among the groups, then the data was also compared between non-vasospasm and clinical or severe angiographic vasospasm groups of patients. The results showed that the AA metabolism was enhanced after the SAH, The TXB2 increased the greatest amount in 1-4 days after the SAH and significantly decreased statistically 12 days after the SAH(p<0.002). This study also showed that the TXB2 level was significantly higher statistically in 1 to 4 days in the clinical or angiogrophically severe vasospasm group than in the non-vasospasm group of patients(p<0.032). PGF1 did not show any statistically significant changes according to the number of SAH days or a difference between the vasospasm and non-vasospasm groups. This result suggests if the AA metabolites are involved in the pathogenesis of cerebral vasospasm, and the lumbar CSF levels of AA metabolites in aneurysmal patients reflect the arterial synthesis of PGI2 and platelet origin of TXA2, the elevation of TXA2 or other vasoconstrictor prostaglandins is more likely to play a major role in the pathogenesis of vasospasm than PGI2 deficiency. The measurements of the CSF TXB2 in 1 to 4 days after a SAH may have an expectant value in the development of clinical or severe angiographic vasospasm(exclude the accompanying intraventricular hemorrhage patients).
