Cyclooxygenase Products of Arachidonic Acid Metabolism in Cat Cerebral Cortex After Experimental Concussive Brain Injury

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Abstract
The purpose of this study was to chemically determine if prostaglandins [PG] are altered following this injury. To facilitate interpretation of neurochemical measurements the cats were ventilated, blood pressure was measured and a cranial window, for microscopic observation of pial arteriolar diameter was inserted. PG levels were determined in quick-frozen cortical tissue removed from control and 3 groups of injured cats at 1.5, 8.0 and 60 min after injury. Analysis of PGE2, PGF2.alpha. and 6-keto-PGF1.alpha. was performed by HPLC [high pressure liquid chromatography] and GC/MS [gas chromatography/mass spectromethy]. The control levels of PGF2, PGF2.alpha. and 6-keto-PGF1.alpha. were 216 .+-. 44, 210 .+-. 48 and 48 .+-. 12 ng/g wet wt, respectively. Following injury, produced by a 22 ms increase in intracranial pressure, the pial arterioles dilated irreversibly and a transient hypertensive response occurred, thereby producing hyperemia. During the maximum hyperemic response, the total PG were 75% of control. At 8 min after injury, when blood pressure returned to control level, the PG were 158% of control and PG fell to 111% of control at 60 min. These experiments supported previous studies implicating increased PG synthesis in the genesis of the physiologic and morphologic sequelae of experimental concussive brain injury.