Inhaled nitric oxide does not alter the longitudinal distribution of pulmonary vascular resistance

Journal Article · Sun Jan 01 04:00:00 EST 1995 · Journal of Applied Physiology

OSTI ID:209965

Lindeborg, D M; Kavanagh, B P; Van Meurs, K ^[1]

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1. Stanford Univ. Medical Center, CA (United States); and others

Inhaled nitric oxide does not alter the longitudinal distribution of pulmonary vascular resistance. Because the effects of inhaled nitric oxide (NO) may be localized to its site of delivery, we studied the effects of inhaled NO on the longitudinal distribution of pulmonary vascular resistance during pulmonary hypertension in perfused rabbit lungs. Before NO administration, pulmonary hypertension was produced by infusion of the thromboxane A{sub 2} mimetic U-46619 in all lungs. Pulmonary vascular resistance was divided into arterial, microvascular, and venous components by arterial and venous occlusion techniques. In the buffer-perfused lung, all doses of inhaled NO (5, 20, and 80 ppm) produced small decreases ({approximately}3 mmHg) in pulmonary arterial pressure (Ppa), with equivalent proportional reductions in all segmental vascular resistances. Similar results were obtained after an extended inhaled NO dose range of 20, 80, and 240 ppm. In the buffer-perfused lung, inhibition of endogenous NO synthesis with N{sup G}-nitro-L-arginine methyl ester (L-NAME) potentiated the effects of U-46619. Subsequent inhaled NO administration produced larger decreases ({approximately} 7 mmHg) in Ppa with equivalent proportional reductions in all segmental vascular resistances. In the blood-perfused lung, L-NAME did not alter baseline pulmonary pressures. Administration of inhaled NO during U-46619-induced pulmonary hypertension produced dose-related decreases in Ppa. The highest dose (80 ppm) of inhaled NO decreased Ppa by 3.5 mmHg, with equivalent proportional reductions in all segmental vascular resistances. We conclude that inhaled NO does not selectively alter the longitudinal distribution of pulmonary vascular resistance and that the magnitude of reduction in total pulmonary vascular resistance in the isolated perfused rabbit lung depends on the endogenous NO synthesis and on the use of buffer or blood as the perfusate. 47 refs., 4 figs., 4 tabs.

• OSTI ID: 209965
• Journal Information: Journal of Applied Physiology, Journal Name: Journal of Applied Physiology Journal Issue: 1 Vol. 78; ISSN JAPHEV; ISSN 8750-7587
• Country of Publication: United States
• Language: English

Related Subjects

55 BIOLOGY AND MEDICINE
BASIC STUDIES
56 BIOLOGY AND MEDICINE
APPLIED STUDIES
BIOLOGICAL EFFECTS
BLOOD PRESSURE
HYPERTENSION
INHALATION
NITRIC OXIDE
RABBITS
RESPIRATORY SYSTEM
SYNTHESIS