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Annual Meeting of the German Society for Microcirculation and Vascular Biology

Cardiac contraction causes a rhythmic compression of the intramyocardial blood vessels. As a result, both transvascular pressure and flow are highly pulsatile, notably in sub-endocardial vessels. Such pulsatility affects regulation of both tone and structure of these vessels. We studied the behaviour of single vessels subjected to mechanical regimes mimicking the beating heart. Small arteries of F100–200 Im were isolated from the porcine heart and cannulated. Vascular pressure and flow profiles were controlled independently by manipulating left and right cannula pressures. In acute experiments we found that pulsatile pressure causes endothelium-independent vasodilation. This was not associated with a reduction in intracellular calcium, and may reflect a direct effect on the contractile elements. Vessels became remarkably more sensitive to vasodilators under a pulsatile pressure profile. While steady flow caused flowinduced dilation, oscillating flow did not induce dilation at all. However, such dilation was uncovered in the presence of superoxide dismutase or the NADPH oxidase inhibitor, DPI. These data indicate that the pattern of flow sets the balance between NO and O2 – production in the vessel wall. In cannulated vessels in organoid culture, inward remodeling occurred after sustained deep tone. E.g., inward remodeling was found in the absence but not in the presence of flow. Such remodeling was found to be related to activity of the crosslinking enzyme, tissue type transglutaminase. Supported by the Netherlands Heart Foundation grants to Erik Bakker and Ed VanBavel.