Abstract
The pathophysiological role of BK is increasingly recognized in cerebral ischemia and trauma. We studied whether DXM interferes with the BK-dependent effects on the BBB. Pia-arachnoidea vessels were studied by fluorescens microscopy in cats. BK in rising cc. /4x 10−8- 4×10−3M/ were used as superfusion media. Cats received DXM 1 or 5 mg/kgbw, resp. 5 hrs prior to exposure to BK. Na+-fluorescein /MW:376/ iv served as BBB indicator. DXM did neither influence opening of the BBB by BK nor the dose-effect relationship of this process. However, 1mg blunted the vasodilatory response to BK, whereas 5 mg resulted in a regular dilatory reaction although the arterioles did not reconstrict again at higher BK-cc. After pretreatment with DXM /l or 5 mg/ pial veins were found to significantly dilate to BK. Taken together, DXM does not prevent opening of the BBB to BK but it influences the vasomotor response to the vasoactive peptide.
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Temesvari, P., Schürer, L., Unterberg, A. et al. BLOOD-BRAIN BARRIER/BBB/ PERMEABILITY AND VASCULAR REACTIVITY TO BRADYKININ/BK/ AFTER PRETREATMENT WITH DEXAMETHASONE/DXM/. Pediatr Res 22, 220 (1987). https://doi.org/10.1203/00006450-198708000-00040
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DOI: https://doi.org/10.1203/00006450-198708000-00040