Remodeling of lung interstitium but not resistance vessels in canine pacing-induced heart failure

We previously showed that pacing-induced heart failure in dogs results in a n enhancement of pulmonary vascular reactivity. In the present study we hyp othesized that enhanced matrix deposition and structural remodeling of lung resistance microvessels would underlie these functional changes. Using bio chemical measures, we found no difference in the normalized lung content of hyaluronan, uronic acid, and collagen between control dogs and dogs paced for 1 mo, although lung dry weight and noncollagen protein content increase d significantly in the paced group (P < 0.05). From separate Formalin-fixed lung lobes, 5-mu m frozen sections were prepared and stained with Masson's trichrome, and vascular structure was evaluated using standard morphometri c techniques. When perivascular fluid cuffs were excluded from the measure of wall thickness, collagen and media volume fractions in any size range di d not differ between paced and control groups. Similarly in the paced group , medial thickness in <400-mu m arterial or venular microvessels did not va ry significantly from that in the controls. In contrast, the relationship o f interstitial fluid pressure to lung water was significantly shifted to th e right in the paced group, such that normal tissue pressures were observed , despite the increased water content. We conclude that although I mo of pa cing-induced heart failure results in altered interstitial function, the at tendant pulmonary hypertension and/or hormonal responses are insufficient t o induce medial hypertrophy or other remodeling of the extra-alveolar micro vasculature.