Journal of Applied Physiology, Vol 54, Issue 4 1071-1082, Copyright © 1983 by American Physiological Society
Ventilation-perfusion relationships during hemorrhagic hypotension and reinfusion in the dog
J. B. Fortune, R. W. Mazzone and P. D. Wagner
The inert gas elimination technique was used to estimate pulmonary
ventilation-perfusion (VA/Q) mismatching in heparinized, ventilated,
anesthetized dogs during a 90-min period of hemorrhagic hypotension (mean
arterial pressure 40 Torr) and subsequent reinfusion of the shed blood.
Systemic and pulmonary arterial pressures, as well as cardiac output, were
similar to those in previously reported studies using this protocol. Mean
arterial O2 partial pressure (PO2) fell from 86 to 75 Torr after hemorrhage
and rose to a mean value of 78 Torr after reinfusion. The VA/Q
distributions showed that a mean of 56.7% of the ventilation was associated
with unperfused or poorly perfused (VA/Q greater than 10) regions during
hypotension (control 33.7%). After reinfusion, a mean of 47.8% of the
ventilation was still directed to lung with little or no perfusion. This
could not be explained on a hydrostatic basis, since pulmonary arterial
pressure after reinfusion was greater than the control value. Shunt or
blood flow to low VA/Q regions did not increase at any time during
hemorrhagic hypotension or reinfusion. Microscopic examination of lung
tissue revealed extensive leukocyte aggregation that was not seen in
control animals. The mean diameter of obstructed pulmonary vessels was 35
microns (range 13.8-59.8 microns). Storing the shed blood in
acid-citrate-dextrose instead of heparin had no significant effect on the
extent of leukocyte aggregation. We suggest that leukocyte aggregation and
margination may be related to the high VA/Q regions seen in these animals.
