Journal of Applied Physiology, Vol 65, Issue 6 2617-2623, Copyright © 1988 by American Physiological Society
Pulmonary vascular reactivity in hyperoxic pulmonary hypertension in the rat
R. G. Gore and R. Jones
Department of Pathology, Children's Hospital, Boston, Massachusetts.
Breathing 87% O2 for 7 days causes pulmonary vascular remodeling and
pulmonary hypertension in the rat. In the isolated perfused lung of the
normal and O2-exposed rat, change in pre- and postcapillary resistance was
determined in response to challenge with angiotensin II (ANG II; 5, 25, and
50 micrograms) or histamine (0.5 and 1.0 microgram). In the hyperoxic lung
both pre- and postcapillary resistance were increased at base line,
although the latter less consistently so. In response to each agent
precapillary resistance increased more than postcapillary resistance in the
hyperoxic lung. In the normal lung pre- and postcapillary reactivity to
histamine were similar but the latter was the greater in response to ANG
II. In the hyperoxic lung only the pre- and postcapillary response to the
first challenge of ANG II (5 micrograms) was greater than normal. The
magnitude of the precapillary response was not related to the level of
base-line resistance, and this response was significantly increased in a
small number of hyperoxic lungs with base-line resistance in the normal
range. Tachyphylaxis occurred after the first dose of ANG II. In the
hyperoxic lung only the precapillary response to 0.5 micrograms histamine
was greater than normal. We conclude that exposure to hyperoxia for 7 days
causes an increase in pulmonary arterial reactivity. Furthermore, the
alteration in reactivity is not caused by vascular restriction. We
hypothesize that it is attributable to peripheral extension of smooth
muscle in alveolar wall arteries.
