Journal of Applied Physiology, Vol 58, Issue 5 1577-1584, Copyright © 1985 by American Physiological Society
Pulmonary hemodynamics and lung water content during splanchnic ischemic shock
C. F. Pilati and M. B. Maron
Pulmonary hemodynamics and lung water content were evaluated in open-chest
dogs during splanchnic arterial occlusion (SAO) shock. Mean pulmonary
arterial pressure [Ppa = 13.0 +/- 0.6 (SE) mmHg] and pulmonary venous
pressure (4.1 +/- 0.2 mmHg) were measured by direct cannulation and the
capillary pressure (Ppc = 9.0 +/- 0.6 mmHg) estimated by the
double-occlusion technique. SAO shock did not produce a significant change
in Ppa or Ppc despite a 90% decrease in cardiac output. An 18-fold increase
in pulmonary vascular resistance occurred, and most of this increase (70%)
was on the venous side of the circulation. No differences in lung water
content between shocked and sham-operated dogs were observed. The effect of
SAO shock was further evaluated in the isolated canine left lower lobe
(LLL) perfused at constant flow and outflow pressure. The addition of
venous blood from shock dogs to the LLL perfusion circuit caused a
transient (10-15 min) increase in LLL arterial pressure (51%) that could be
reversed rapidly with papaverine. In this preparation, shock blood produced
either a predominantly arterioconstriction or a predominantly
venoconstriction. These results indicate that both arterial and venous
vasoactive agents are released during SAO shock. The consistently observed
venoconstriction in the intact shocked lung suggests that other factors, in
addition to circulating vasoactive agents, contribute to the pulmonary
hemodynamic response of the open-chest shocked dog.
