engleski

Mechanisms of vascular responses to changes in flow in cerebral resistance arteries of healthy Sprague-Dawley rats

Aim: We previously observed that flow induced dilatation (FID) in middle cerebral arteries (MCA) of healthy rats is mediated mainly by NO. However, the metabolites of COX1, 2 and EETs could not be excluded in FID. The aim of this study was to assess potential contribution of other vasodilators in FID. Methods: 12-weeks old healthy male Sprague-Dawley rats were anesthetized with ketamin-chloride (75 mg/kg) and midazolam (2.5 mg/kg) prior to decapitation.MCA were isolated and cannulated for vascular reactivity measurements in response to stepwise increase in pressure (Δ10- Δ100) in the presence of different combination of inhibitors INDO, L-NAME and MS-PPOH (N=4-6 per combination).Two-way ANOVA was used for data analysis ; p<0.05 considered significant. Results: FID was reduced at each pressure gradient in the presence of all 3 inhibitors together compared to baseline. Combination of any 2 inhibitors significantly reduced FID compared to basal values but not compared to any individual inhibitor. All 3 inhibitors reduced FID compared to any individual inhibitor but at different pressure gradient(INDO vs 3 nhibitors Δ40 and Δ100 ; INDO vs 3 inhibitors at Δ20, Δ40 and Δ60 ; MS- PPOH vs 3 inhihitors at Δ20 and Δ40). Conclusions: The results confirmed redundancy of mechanisms mediating FID. Beside NO, metabolites of COX1, 2 and EETs also contribute to FID in MCA of healthy rats.

flow induced dilation; cerebral resistance arteries; rats

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