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Cerebrospinal Fluid and Plasma Concentrations of Phospholipase A2 in Postoperative Patients with Subarachnoid Hemorrhage
Yoshiaki Terao, M.D., Shuhei Matsumoto, M.D., Masafumi Takada, M.D., Chiaki Inadomi, M.D., Koji Sumikawa, M.D.
Anesthesia, Nagasaki Rosai Hospital, Sasebo, Japan.
Background: The mechanisms leading to vasospasm following subarachnoid hemorrhage (SAH) remains unclear. Several studies have implicated a role for arachidonic acid metabolites in cerebral vasospasm and edema 1). It was demonstrated that free fatty acids including arachidonic acid in cerebrospinal fluid increased in a biphagic manner after SAH 2). Although phospholipase A2 (PLA2) is a key enzyme in the production of arachidonic acid metabolites, the role of PLA2 after SAH remains unclear. The present study was carried out to determine the time course of changes in cerebrospinal fluid and plasma PLA2 and PGE2 after SAH.

Methods: After approval of Institutional Research Committee, informed consent was obtained from each patient's relatives. We studied consecutive 10 patients who underwent aneurysm clipping after aneurysm-induced SAH and required a ventricular catheter for 10 days postoperatively. Ruptured aneurysm was clipped within 24hrs after ictus, and a ventricular catheter was placed. Cerebrospinal fluid was intermittently drained to maintain the intracranial pressure below 20 mmHg. After the operation, conventional hypervolemic hemodilution, and induced hypertension methods were applied for prevention and treatment of SAH-induced cerebral vasospasm. Symptomatic cerebral vasospasm was detected with neurological deficits and transcranial Doppler sonography. Arterial blood and ventricular cerebrospinal fluid were sampled every day from day 1 to day 10 after operation. Plasma and cerebrospinal fluid PLA2 was measured by Dole assay using 14C-phosphatidyl ethanolamine as exogenous substrate. Plasma and cerebrospinal fluid PGE2 was measured by radioimmunoassay. Results were presented as mean±SEM. Comparisons of the concentrations over time were made using the one way analysis of variance for repeated measures and Student's t-test with p< 0.05 regarded as significant.

Results: The mean age of the patients was 61±3 yrs (range, 48 -73). The mean Glasgow Coma Scale score on admission was 12±1 (range, 6 -14). Three patients had a symptomatic vasospasm. There were no significant differences over time in plasma PLA2 (pmol/min/mL) or PGE2 (pg/mL) concentrations after SAH. As shown in table, cerebrospinal fluid PLA2 (pmol/min/mL) on days 1-3 and PGE2 (pg/mL) on days 1-2 in SAH patients were increased significantly compared with those on days 4-10 and 3-10, respectively. The concentrations of PLA2 and PGE2 in plasma and cerebrospinal fluid were similar between the patients with and without symptomatic vasospasm.

Conclusions: The results show that the cerebrospinal PLA2 and PGE2 concentrations increaseswere elevated within 1-3 days after SAH. The increase in cerebrospinal fluid PLA2 after SAH may be involved in the acute brain edema, rather than cerebral vasospasm.

References:1.Prostaglandins. 34: 877-878, 1987, 2. J Neurosurg. 97: 272-279, 2002.

Anesthesiology 2003; 99: A430
cerebrospinal fluid PLA2 and PGE2
POD, postoperative day; #p<0.05, compared with other days