Inhaled nitric oxide: diameter response patterns in feline small
pulmonary arteries and veins.
Shirai, Mikiyasu, Akito Shimouchi, Akira T. Kawaguchi, Kenji Sunagawa,
and Ishio Ninomiya.
Departments of Cardiac Physiology, Cardiovascular Dynamics, and
Surgical Research, National Cardiovascular Center Research Institute,
Suita, Osaka 565, Japan, Department of Physiology, Institute of
Health Sciences, Hiroshima University, School of Medicine, Kasumi
-cho, Hiroshima 734, Japan
APStracts 2:0396H, 1995.
Using an X-ray television system on the in vivo cat lung, we directly
measured internal diameter (ID) changes in the small pulmonary
arteries and veins (100-1100 [mu]m ID) in response to 5, 15, and 40
ppm nitric oxide (NO) inhalations. We also measured to what extent 40
ppm NO inhalation can attenuate large ID constrictions at the
different serial segments of the small vessels due to unilobar anoxic
(0% O2) exposure._Under normoxic conditions, 5-40 ppm NO inhalations
significantly increased the ID of both arteries and veins < _900
[mu]m dose-dependently, but caused no significant, or only slight, ID
increases in the vessels larger than this, if any at all. The ID
increase in the serially connected arteries was nonuniform (4-18, 8
-28 and 7-35% with 5, 15 and 40 ppm NO inhalations, respectively),
whereas that for the veins was relatively uniform (4-9, 6-17 and 7
-18% with 5, 15 and 40 ppm NO). The maximum ID increase occurred in
the 200-500 and 200-700 [mu]m arteries in response to 5-15 and 40 ppm
NO, respectively. Unilobar anoxic exposure significantly decreased
the ID of the 100-700 [mu]m arteries and veins, but not the ID of the
other-sized vessels. The ID decrease in the serially connected
arteries was nonuniform (13-29%), but relatively uniform in the
veins(8-12%). The maximum ID decrease occurred in the 200-300 [mu]m
arteries. However, adding 40 ppm NO to the lobe completely eradicated
the ID decreases at all segments of the arteries and veins and,
instead, caused significant ID increases, (11-21%) in the arteries
and (10-12%) in the veins. The data indicate that, according to
dosage, 5-40 ppm NO inhalations cause selective dilation of _100-900
[mu]m pulmonary arteries and veins, particularly the 200-700 [mu]m
arteries. During anoxic exposure, the vasodilator effect of NO is
preserved and can completely reverse the marked pulmonary
vasoconstriction.
Received 10 April 1995; accepted in final form 30 August 1995.
APS Manuscript Number H353-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 September 1995.