The role of submucosal oedema in increased peripheral airway resistance by intravenous volume loading in dog

Pulmonary congestion leads to an increase in airway resistance. It is still unknown whether this is due to vascular engorgement or to submucosal oedema. The present study was designed to determine the relative contribution of these two potential mechanisms. We examined the effect of intravenous volume loading on canine peripheral airway resistance (Rp). Bronchoscopes were wedged in contralateral sublobar segments and used to record Rp during rapid infusion of normal saline. Volume loading with normal saline increased pulmonary capillary wedge pressure (PCWP) and Rp. Unlike normal saline, dextran 70 did not increase Rp when infused at a rate that produced similar changes in PCWP. During infusion of normal saline, ΔRp was significantly enhanced in lung segments previously challenged with dry air when compared to contralateral control lungs, unexposed to dry air, and the use of dextran 70 significantly reduced this effect. Vasoconstriction with phenylephrine significantly decreased baseline Rp, but did not completely reverse the effect of fluid infusion. In addition, in lung segments exposed to dry air, ΔRp was significantly greater after volume loading and treatment with phenylephrine when compared to contralateral control lung. Finally, muscarinic receptor blockade was ineffective in preventing Rp from increasing during infusion of normal saline. Our results suggest that volume loading- induced increases in Rp are not caused by either vascular engorgement or the stimulation of muscarinic receptors. Our data are consistent with the hypothesis that submucosal oedema formation is the mechanism responsible for normal saline infusion-induced increases in peripheral airway resistance.