Structural remodelling of lungs in chronic heart failure.
In order to determine whether morphological changes could account for a previously reported reduction in pulmonary capillary filtration in heart failure, we studied pulmonary morphology in lungs from a guinea-pig chronic heart failure model. Heart failure was induced by banding the ascending aorta with sham operated animals serving as controls; all animals were studied at 158 +/- 6 days post-operation. Following banding, a reduction in aortic flow, increased peripheral vascular resistance and raised left ventricular end diastolic, left atrial and right ventricular pressures together with increased right ventricle to body weight ratio (all p < 0.05) are indicative of established pulmonary hypertension and heart failure. This was associated with an increase in pulmonary septal volume fraction (38.1 +/- 3.1% vs 24.6 +/- 2.3 %, p < 0.01) and reticulin fibre density. There was also evidence of siderophage infiltration and examination of pulmonary ultra structure revealed a significantly thicker alveolar-capillary barrier in heart failure (1278 +/-76 vs 638 +/- 32 nm, p < 0.001), thickening of both the alveolar (89%, p < 0.01) and capillary (69%, p < 0.05) basal laminae with pericyte and collagen in filtration of the alveolar-capillary barrier. We hypothesise that these pulmonary adaptations provide protection from oedema formation, but whilst initially protective, are also likely to confer major long-term disadvantages in chronic heart failure.
Kingsbury
Martyn P
MP
Academic Cardiology Unit, Imperial College School of Medicine, St. Mary's Campus, 10th floor QEQM Wing, South Wharf Road, LondonW2 1NY, UK. m.kingsbury@imperial.ac.uk
Huang
Wenxin
W
Donnelly
J Leo
JL
Jackson
Emma
E
Needham
Emma
E
Turner
Mark A
MA
Sheridan
Desmond J
DJ
D000818:Animals; D001011:Aorta; D004195:Disease Models, Animal; D006168:Guinea Pigs; D006333:Heart Failure / Q000473:pathology* / Q000503:physiopathology; D006439:Hemodynamics; D006976:Hypertension, Pulmonary / Q000473:pathology* / Q000503:physiopathology; D008026:Ligation; D008168:Lung / Q000098:blood supply* / Q000473:pathology* / Q000648:ultrastructure; D008297:Male; D008854:Microscopy, Electron; D013997:Time Factors