Capillary filtration is reduced in lungs adapted to chronic heart failure: morphological and haemodynamic correlates.
OBJECTIVE
To determine pulmonary capillary filtration in experimental chronic heart failure and to investigate some morphological and haemodynamic mechanisms that could account for reduced filtration in lungs adapted to chronic heart failure.


METHODS
We studied pulmonary capillary filtration, vascular resistances and morphology in lungs from guinea-pigs adapted to chronic heart failure. Heart failure was induced by banding of the ascending aorta (n=66) or sham control operation (n=78) in guinea-pigs which were studied at 150+/-8 days post-operation.


RESULTS
Reduced cardiac output, increased systemic vascular resistance and LV end diastolic pressure and increased LV and RV weight:body weight ratio (all P<0.05) indicated chronic heart failure at 5 months following aortic banding in guinea-pigs. Lung weight was increased (61%, P<0.05) in heart failure compared with controls, but lung water content was reduced (5.5%, P<0.05), a reversal of the pattern seen acutely. Studies in isolated perfused lungs demonstrated a reduced capillary filtration coefficient (0. 018+/-0.003 vs. 0.003+/-0.002 ml min(-1)mmHg(-1)g(-1), P<0.001), increased arterial (61%) and venous resistance (50%) in heart failure lungs, P<0.05. Wall thickness:lumen ratio was increased in small (<250 microm) pulmonary arterioles (0.15+/-0.02 vs. 0.08+/-0. 01) and venules (0.06+/-0.005 vs. 0.04+/-0.002) in heart failure, P<0.01. Alveolar septal volume fractions (35.2+/-5.1 vs. 23.1+/-2.7) and septal:air-space volume ratios (60.5+/-13.6 vs. 31.9+/-5.3) were also increased in heart failure, P<0.05.


CONCLUSIONS
Pulmonary adaptation to chronic heart failure is associated with vascular and alveolar remodelling that contributes to increased vascular resistance and reduced capillary filtration. These changes are likely to be important in mediating resistance to pulmonary oedema in chronic heart failure.
Huang
W
W
Academic Cardiology Unit, National Heart and Lung Institute, Imperial College School of Medicine, London, UK.
Kingsbury
M P
MP
Turner
M A
MA
Donnelly
J L
JL
Flores
N A
NA
Sheridan
D J
DJ
D000222:Adaptation, Physiological; D000818:Animals; D001834:Body Water; D002199:Capillary Permeability / Q000502:physiology*; D006168:Guinea Pigs; D006333:Heart Failure / Q000473:pathology / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology; D008168:Lung / Q000098:blood supply* / Q000473:pathology; D008297:Male; D009206:Myocardium / Q000473:pathology; D009929:Organ Size; D011652:Pulmonary Circulation / Q000502:physiology*; D014655:Vascular Resistance / Q000502:physiology