Evidence for active control of perfusion within lung microvessels

Abstract

Watson KE, Dovi WF, Conhaim RL. Evidence for active control of perfusion within lung microvessels. J Appl Physiol 112: 48-53, 2012. First published October 13, 2011 doi:10.1152/japplphysiol.00820.2011Vasoconstrictors cause contraction of pulmonary microvascular endothelial cells in culture. We wondered if this meant that contraction of these cells in situ caused active control of microvascular perfusion. If true, it would mean that pulmonary microvessels were not simply passive tubes and that control of pulmonary microvascular perfusion was not mainly due to the contraction and dilation of arterioles. To test this idea, we vasoconstricted isolated perfused rat lungs with angiotensin II, bradykinin, serotonin, or U46619 (a thromboxane analog) at concentrations that produced equal flows. We also perfused matchedflow controls. We then infused a bolus of 3 m diameter particles into each lung and measured the rate of appearance of the particles in the venous effluent. We also measured microscopic trapping patterns of particles retained within each lung. Thirty seconds after particle infusion, venous particle concentrations were significantly lower (P Յ 0.05) for lungs perfused with angiotensin II or bradykinin than for those perfused with U46619, but not significantly different from serotonin perfused lungs or matched flow controls. Microscopic clustering of particles retained within the lungs was significantly greater (P Յ 0.05) for lungs perfused with angiotensin II, bradykinin, or serotonin, than for lungs perfused with U46619 or for matched flow controls. Our results suggest that these agents did not produce vasoconstriction by a common mechanism and support the idea that pulmonary microvessels possess a level of active control and are not simply passive exchange vessels. pulmonary circulation; microcirculation; vasoconstriction; circulatory control; vasoreactivity ARTERIOLAR VASOCONSTRICTION is generally thought to be responsible for the control of perfusion distribution among microvessels. The latter are considered to function passively and exist solely for the purpose of transvascular exchange. However, there is considerable inferential evidence to suggest that microvessels in the lung may be capable of active control of perfusion through them.This evidence includes that of Morel and colleagues (20) who showed that when pulmonary microvascular endothelial cells (PMVECs) grown in culture were exposed to the vasoconstrictors angiotensin II and bradykinin, they contracted enough to deform the silicone rubber substrate on which they were cultivated. These authors also reported that endothelial cells obtained from pulmonary arteries and retinal microvessels did not contract under these conditions, suggesting that the contractile properties of PMVECs were unique to those cells. They speculated that the contractile properties of PMVECs meant that they might have a role in regulating local perfusion in situ.Additional evidence was provided by Weibel who used electron microscopy to show the presence of pericytes aroun...

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