Journal of Applied Physiology, Vol 64, Issue 5 1823-1828, Copyright © 1988 by American Physiological Society
Modulation by endogenous opioids of pulmonary vasoconstrictor response to acute lung injury
A. T. Scardella, J. A. Neubauer, N. H. Edelman and T. V. Santiago
Department of Medicine, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick 08903-0019.
The effects of endogenously generated opioids on distribution of pulmonary
perfusion (as assessed by radiolabeled microspheres) and overall gas
exchange in acute acid-induced lung injury were studied. In 14 anesthesized
dogs, sufficient acid was given to one lung to double shunt fraction
(Qs/Qt) from 14.2 +/- 0.8 to 32.4 +/- 2.6% (SE). This resulted in a
significant decrease in Po2 from 495 +/- 9 to 136 +/- 21 Torr, cardiac
output from 2.47 +/- 0.27 to 1.46 +/- 0.15 1/min, and blood pressure from
139 +/- 3 to 116 +/- 5 mmHg and a significant rise in pulmonary arterial
pressure from 9.6 +/- 0.8 to 14.9 +/- 0.8 mmHg. After acid instillation,
microsphere distribution to the injured lung segments decreased to 50% of
the base-line value. At the same time, microsphere distribution in the
normal segments increased to 160% of base line. In 7 of the 14 dogs the
effects of naloxone (1 mg/kg) given after lung injury were compared with
the other 7 animals that were given saline. Naloxone administration caused
a significant redistribution of regional pulmonary perfusion such that
microsphere distribution in the injured lung segments increased by a factor
of 2 at 35 min compared with the animals given saline. Consistent with this
finding, Qs/Qt in the naloxone group increased to 34.7 +/- 5.0% at 35 min,
whereas that of the saline group decreased to 28.2 +/- 2.5%. The difference
between the two groups was significant at 35 min. These changes occurred
without further alterations in cardiac output, pulmonary arterial pressure,
or systemic blood pressure in either group.(ABSTRACT TRUNCATED AT 250
WORDS)
