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  • Title: [Different severity of brain ischemia between spontaneously hypertensive rats and Wistar-Kyoto rats induced by internal carotid infusion of arachidonic acid].
    Author: Memezawa H, Katayama Y, Sugimoto S, Shimizu J, Suzuki S, Nagazumi A, Terashi A, Ishiharajima S, Asano G.
    Journal: No To Shinkei; 1987 Aug; 39(8):751-60. PubMed ID: 3426860.
    Abstract:
    Arachidonic acid (AA) is a potent stimulator of platelet aggrgation and is known to induce endothelial cell damage and edema in the brain. An ischemic cerebral infarction model can be produced in rats by an internal carotid infusion of AA. In this study, water content, ATP and lactate in the brain and plasma prostaglandins (thromboxane B2; TXB2 and 6-keto-prostaglandin F1 alpha; 6-keto-PGF1 alpha) were measured and histological observations were made after an internal carotid infusion of AA in two strains of rats; stroke-resistant spontaneously hypertensive rat (SHRSR) and normotensive Wistar-Kyoto (WKY) rats. It is known that the blood pressure of the SHRSR begins to rise at about 8 weeks old. Throughout the study, AA was administered into the internal carotid artery under 2% fluothane anesthesia. In the first study, AA (1.7 mg/kg BW) was administered to 8- and 16-week-old rats and the length of survival was observed. In the second study, water content, ATP and lactate in the brain and plasma TXB2 and 6-keto-PGF1 alpha were measured 3 hours after AA (0.85 mg/kg BW) administration. In the third study, rats were perfusion-fixed 3 hours after the AA (1.7 mg/kg BW) infusion and cerebral arteries were observed by scanning electron microscopy (SEM). During the 6 hour observation period, there was no difference between the two groups in the number of 8-week-old rats which survived. However, the figure became significantly lower in the SHRSR at 16 weeks old. The water content in the bilateral cerebral hemispheres was significantly larger in the SHRSR than in the WKY rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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