Abstract 1184: Role of the Pulsatility in the Microcirculation.
Background: The mechanostransduction of flow (shear-stress) and pressure in the microcirculation has not been yet fully investigated and most of the available data come from large arteries. Moreover, the pulsatility, which is a physiological characteristic of perfusion, is also important to take into consideration in small resistance arteries. Whereas large arteries have an important elastic content allowing an efficient compliance, resistance arteries might be sensitive to the pulsatility which remains effective until the capillary bed.
Hypothesis: We assessed the hypothesis that the pulsatility may change the mechanostransduction and/or pharmacological reactivity of resistance arteries.
Methods: Rat mesenteric resistance arteries (internal diameter from 150 to 250 μm) were isolated and mounted in a video monitored perfusion system. They were then perfused at different rates of flow, pressure, and pulsatility. The mechanotransduction (pressure-induced myogenic tone and flow-mediated dilation) and the pharmacological reactivity to phenylephrine and acethylcholine were measured in theses arteries. Expression of eNOS and Caveolin-1 were evaluated using western blot analysis. Detection of Reactive Oxygen Species (ROS) and inflammatory factors such as iNOS, COX-2, TNFα, MCP-1 was conducted using immunofluorescence by confocal microscopy.
Results: In perfused and pressurized resistance arteries, the pulsatility caused a decrease in myogenic tone and a lefward shift of the flow-mediated dilation curve. There was no change in pharmacological reactivity in pulsed arteries compared to arteries submitted to a steady pressure. Pulsatity induced a dissociation of the Caveolin1-eNOS complex. Lack of pulsatility during 180 min led to an important production of the four inflammatory factors tested but no production of ROS in the arterial wall.
Conclusion: Pulsatility has a key role in the microcirculation by reducing myogenic tone and potentiating flow-mediated dilation through dissociation of the Caveolin1-eNOS complex. In addition, the pulsatility seems to have a protective role in the arterial wall by preventing the expression of inflammatory factors.