Mp. Kingsbury et al., Investigation of distal aortic compliance and vasodilator responsiveness in heart failure due to proximal aortic stenosis in the guinea pig, CLIN SCI, 96(3), 1999, pp. 241-251
Hypotension and syncope are recognized features of chronic aortic stenosis.
This study examined vasomotor responses and dynamic compliance in isolated
abdominal aortae after chronic constriction of the ascending aorta. Guinea
pigs underwent constriction of the ascending aorta or sham operation. Sect
ions of descending aorta were removed for studies of contractile performanc
e and compliance. Dynamic compliance was measured using a feedback-controll
ed pulsatile pressure system at frequencies of 0.5, 1.5 and 2.5 Hz and mean
pressures from 40 to 100 mmHg. Chronic (149 +/- 6 days) aortic constrictio
n resulted in significant increases in organ weight/body weight ratios for
left ventricle (58%), right ventricle (100%) and lung (61%). The presence o
f heart failure was indicated by increased lung weights, left ventricular e
nd-diastolic pressure and systemic vascular resistance, reduced cardiac out
put and increased levels of plasma atrial natriuretic peptide (166%), adren
aline (x 20), noradrenaline (106%) and dopamine (x 3). Aortic rings showed
similar constrictor responses to phenylephrine and angiotensin II, but maxi
mal vasodilator responses to acetylcholine and isoprenaline were significan
tly increased (144% and 48% respectively). Dilator responses to sodium nitr
oprusside, forskolin and cromokalim were unchanged. Compliance of all vesse
ls decreased with increasing pulsatile frequency and to a lesser extent wit
h increased mean pressure, but were similar in aortic-constricted and contr
ol groups. Chronic constriction of the ascending aorta resulted in heart fa
ilure and increased vasodilator responses to acetylcholine and isoprenaline
in the distal aorta while dynamic compliance was unchanged. We hypothesize
that increased endothelium-mediated vasodilatation may contribute to hypot
ension and syncope in patients with left ventricular outflow obstruction.