AJP - Heart and Circulatory Physiology, Vol 249, Issue 6 1106-H1113, Copyright © 1985 by American Physiological Society
Distribution of lung vascular resistance after chronic systemic-to-pulmonary shunts
R. P. Michel, T. S. Hakim, R. E. Hanson, A. R. Dobell, F. Keith and D. Drinkwater
Congenital cardiac shunts produce pathological lesions on the arterial side
of the lung vasculature. We examined the effects of chronic shunts (14.2
+/- 1.2 mo) in 10 young dogs, between the left subclavian and the left
lower lobe (LLL) artery, on pulmonary vascular pressure and flow (P-Q)
relationships, segmental resistance with arterial and venous occlusion
(AVO), and sensitivity to drugs. At final thoracotomy, mean LLL pulmonary
arterial pressure (Ppa) was 23.2 +/- 4.3 mmHg compared with 11.9 +/- 0.9 in
the right lung (P less than 0.05); two animals had LLL Ppa of 41 and 48
mmHg. The LLL artery and vein were cannulated, and pressure-flow (P-Q) and
AVO measurements were made and compared with previous control LLL (n = 11)
and contralateral right lower lobe (RLL, n = 5). Responses to serotonin,
histamine, and vasodilators (diltiazem and isoproterenol) were evaluated.
Comparisons of morphometric measurements were made between LLL and RLL. We
found a significant increase in arterial resistance as measured with AVO
and a hypersensitivity to serotonin in the shunt LLL, without changes in
total pulmonary vascular resistance or P-Q measurements; vasodilators had a
small effect only in the hypertensive lobes. Our data suggest that chronic
shunts to the pulmonary circulation increase arterial resistance and
sensitivity to serotonin, even in the absence of discernible morphometric
changes, and that vasoconstriction may be an important precursor to the
development of morphological lesions.
