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Am J Physiol Heart Circ Physiol (July 15, 2005). doi:10.1152/ajpheart.00205.2005
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Submitted on March 2, 2005
Accepted on July 12, 2005

Flow inhibits inward remodeling in cannulated porcine small coronary arteries

Adrian Pistea1, Erik N Bakker1, Jos A Spaan1, and Ed VanBavel1*

1 Medical Physics, Academic Medical Center Amsterdam, Amsterdam, Noord-Holland, The Netherlands

* To whom correspondence should be addressed. E-mail: e.vanbavel{at}amc.uva.nl.

The mechanisms of flow-induced vascular remodeling are poorly understood, especially in the coronary microcirculation. We hypothesized that applying flow in small coronary arteries kept in organoid culture would cause a nitric oxide (NO) mediated dilation and inhibit inward remodeling. We developed an organoid culture setup able to drive a flow through cannulated arterioles at constant luminal pressure, using a pressure gradient between the pipettes. Subepicardial porcine coronary arterioles, having a diameter at full dilation and 60 mmHg (D0) of 168 µm (SEM 10), were cannulated. Vessels (without or with L-NNA to block NO production) were pressurized at 60 mmHg for 3 days, with or without flow. Endothelium-dependent dilation to bradykinin 10-7 M was preserved in all groups. Vessels under flow had significantly less tone in the last half of culture period. Vessels regulated their diameter to yield shear stresses of 10.3 dynes/cm2 (SEM 2.1) (without L-NNA) and 14.0 dynes/cm2 (SEM 2.4) (with L-NNA). These values were not significantly different. Without L-NNA, passive pressure-diameter curves at the end of culture revealed inward remodeling in the control group (to 92.3% of D0 (SEM 1.3)) and no remodeling in the flow group (100.2% of D0 (SEM 1.3)); with L-NNA, the flow group showed inward remodeling (92.1% of D0 (SEM 2.5)). Conclusion: pressurized coronary resistance arteries could be maintained in culture for several days with flow. Vessels remained more dilated in the presence of flow, also when NO synthesis was blocked. Inward remodeling occurred in vessels without flow and was inhibited by flow-dependent NO synthesis.




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