Pulmonary vascular response to angiotensin ii in canine pacing
-induced heart failure.
Roy, Beverly J., Vicki H. Pitts, Mary I. Townsley.
Departments of Physiology and Pediatrics, University of South
Alabama, Mobile, Al 36688
APStracts 2:0536H, 1995.
The effects of angiotensin II (AII) on pulmonary vascular resistance
and microvascular permeability were studied in isolated, blood
perfused, ventilated canine lung lobes from control animals (n=40)
and animals with pacing-induced heart failure (n=15). Conditioned
dogs were paced (245 beats per minute) for 30.6+/-0.9 days (mean+/
-SE) until left ventricular shortening fraction decreased by 56%
(p<0.05). Baseline pulmonary arterial (Ra) (19.1+/-1.6 vs 8.0+/
-1.1) and venous (Rv) (17.1+/-2.3 vs 7.8+/-1.0 cmH2O/l/min/100g)
resistances were greater (p<0.05) in the paced group compared to
controls, respectively. Increments in Ra (_Ra) and Rv (_Rv) were
measured after intra-arterial boluses of AII (1-10 [mu]g). AII
produced a dose-dependent response in _Ra which was enhanced after
pacing (p<0.05). There was no effect on _Rv in either group. At
increased venous pressure (Pv=20 cmH2O), the increments in _Ra were
significantly attenuated in both groups. In control lobes at low Pv,
_Ra and _Rv both tended to decrease with increased lobar blood flow,
suggesting that blood flow affects the pulmo nary vascular response
of AII. The baseline capillary filtration coefficient (Kf,c) was not
different in the paced group compared to control, nor was there any
effect of AII on Kf,c in the paced group. However, Kf,c did increase
after AII in the control groups evaluated at either low or high Pv
(p<0.05). This differ ence in Kf,c was not seen if the
experiment was done at increased venous pressure but without AII
administration. We conclude that the pulmonary vasoconstrictor
activity of AII is modestly enhanced in canine pacing-induced heart
failure. Nonetheless, AII does not likely contribute to increased
pulmonary vascular resistance in vivo in heart failure since this
effect was abolished at increased venous pressure. Finally, the
absence of any effect of AII on pulmonary microvascular permeability
in the paced group is suggestive of some adaptive remodeling of the
capillary endothelial barrier.
Received 18 September 1995; accepted in final form 22 November
1995.
APS Manuscript Number H875-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 December 95