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• W2017035808 abstract "S240 INTRODUCTION: Following subarachnoid hemorrhage (SAH), endothelium-dependent relaxation has been shown to be impaired in large cerebral arteries [1]. Using a rat model of SAH, we investigated whether endothelial dysfunction is also observed in small resistance cerebral arteries. METHODS: In accordance with institutional animal care committee standards, Wistar rats, [similar] 300 g, were anesthetized with ketamine 40 mg/kg and xylazine 5 mg/kg intraperitoneally and a percutaneous catheter was inserted into the cisterna magna (CM) [2]. Two days later, 0.2 cc of autologous blood was injected into CM with the head down and 20 min later, the animal was sacrificed for tissue harvest. Sham operated animals were similarly processed, but without injection of blood. Control animals were not manipulated before tissue harvest. Microvessels, [similar] 100 [micro sign]m in diameter, were dissected from the parietal lobe area. Each vessel was monitored for diameter changes in vitro by videomicroscopy [3]. Vasomotion to endothelin-1 (ET) 10-13 - 10-8 M, the thromboxane analogue U46619(U4) 10-9 - 10 (-6) M, isoproterenol(IS) 10-9 - 10-4 M, nitroprusside(NP) 10-9 - 10-4 M, and adenosine diphosphate(ADP) 10-9 - 10-4 M was examined. Data are mean +/- SD of 6-8 vessels. *: P < 0.05 vs. control by 2-way ANOVA with a repeated measures factor. #: P < 0.05 vs. sham-operated. RESULTS: Dilation to the endothelium-dependent dilator ADP was attenuated after either surgical manipulation, but to a greater extent after SAII (Table 1). Constriction to the endothelium-derived constrictor ET was accentuated after either surgical manipulation, but to a greater extent after SAH. On the other hand, dilation to the endothelium-independent dilator NP and the beta-adrenergic agonist IS and constriction to U4 were not altered by SAH.Table 1: % dilation or constriction after SAH (+: dilation, -: constriction)DISCUSSION: In our rat model of SAH, SAH is associated with selective attenuation of endothelium-dependent dilation. Constriction to ET is known to be modulated by ET-induced release of endothelium-derived relaxing factor [4] and accentuated response to ET after SAH may be based on reduced modulation of its constrictive action. Our findings may have implications on the mechanism of vasospasm following SAH." @default.
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• W2017035808 date "1999-02-01" @default.
• W2017035808 modified "2023-09-27" @default.
• W2017035808 title "CEREBRAL MICROVASCULAR ENDOTHELIAL DYSFUNCTION IN A RAT MODEL OF SUBARACHNOID HEMORRHAGE" @default.
• W2017035808 doi "https://doi.org/10.1097/00000539-199902001-00239" @default.
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