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Department of Human Anatomy and Physiology, University College, Dublin 2, Ireland
We examined the
changes in isolated pulmonary artery (PA) wall tension on switching
from control conditions (pH 7.38 ± 0.01, PCO2 32.9 ± 0.4 Torr) to
isohydric hypercapnia (pH change 0.00 ± 0.01, PCO2 change 24.9 ± 1.1 Torr) or
normocapnic acidosis (pH change 
0.28 ± 0.01, PCO2 change 0.3 ± 0.04 Torr) and the role of the endothelium in these responses. In rat PA, submaximally contracted with phenylephrine, isohydric hypercapnia did not cause a significant change in mean (± SE) tension [3.0 ± 1.8% maximal phenylephrine-induced tension
(Po)]. Endothelial removal did not alter this response. In aortic
preparations, isohydric hypercapnia caused significant
(P < 0.01) relaxation (27.4 ± 3.2% Po), which was
largely endothelium dependent. Normocapnic acidosis caused relaxation
of PA (20.2 ± 2.6% Po), which was less
(P < 0.01) than that observed in aortic
preparations (35.7 ± 3.4%
Po). Endothelial removal left
the pulmonary response unchanged while increasing
(P < 0.01) the aortic relaxation
(53.1 ± 4.4% Po).
These data show that isohydric hypercapnia does not alter PA tone.
Reduction of PA tone in normocapnic acidosis is endothelium independent
and substantially less than that of systemic vessels.
acidosis; vascular smooth muscle; nitric oxide; carbon dioxide
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