THE EFFECT OF HYPOXIA ON THE 
PULMONARY MICROCIRCULATION 
W. W. Wagner, L. P. Latham and D. R. Halsey* 
The pulmonary vasopressor response to airway hy- 
poxia has been well established. There is evidence that 
there is a resistance rise in both pre- and postcapillary 
vessels, but the effect on the pulmonary capillary bed of 
vasomotion at both these vascular levels is not clear. 
We have studied the effects of hypoxia on the pulmo- 
nary microcirculation via a thoracic window implanted 
in dogs. An estimation of the number of perfused capil- 
laries was made using a grid count technique. With the 
spontaneously breathing dog lying on his side, studies 
were made of either the dependent lung (bottom of the 
lung) or the superior lung (top of the lung) ; n = 4 in 
each case. Preliminary analysis indicates a significant 
effect of gravity on the number of perfused capillaries: 
capillary grid counts on the top = 53 ± 7 (SEM) ver- 
sus bottom = 153 ± 11 (p < 0.01). With isocapnic 
hypoxia there was a striking and consistant increase in 
the number of perfused capillaries (capillary recruit- 
ment) at the top of the lung: control = 53 ± 7, hy- 
poxia = 92 ± 9 (p < 0.01). At the bottom of the 
lung where the capillary bed was more nearly filled to 
capacity, hypoxia still produced recruitment: control 
153 ± 11, hypoxia 173 ± 14 (p < 0.01). In 12 cases 
cardiac output increased with hypoxia, but in 5 cases it 
decreased. Capillary recruitment occurred in all cases 
regardless of the direction of change in cardiac output. 
Also recruitment was independent of the magnitude of 
the rise in pulmonary artery pressure. Because recruit- 
ment cannot be explained by the magnitude of the 
increase in pulmonary artery pressure or by cardiac out- 
put changes, capillary recruitment with hypoxia is prob- 
ably caused by constriction of postcapillary vessels. 
This pulmonary microcirculatory response to hypoxia 
serves to increase the surface area of the air-blood inter- 
face and therefore could be advantageous for gas ex- 
change during airway hypoxia. 
INTRODUCTION 
To understand the lung as a gas exchange 
mechanism, it is important to define pulmonary 
function both in terms of gas transport from 
the atmosphere to the exchange surface as well 
as blood transport to the alveolar capillary 
membrane. To operate efficiently the two trans- 
♦ Department of Medicine, University of Colorado Medical Center, 
4200 East Ninth Avenue, Denver, Colorado 80220. 
port systems must interact in a balanced fash- 
ion so that blood and gas reach the same regions 
of the lung in proper proportions for optimal 
gas exchange. 
It appears^ that one of the ways a ventilation- 
perfusion (V/Q) balance is maintained is by 
the pulmonary vasopressor response to airway 
hypoxia. Thus if one lung becomes hypoxic, the 
constricting vessels in that lung shunt the blood 
to the normoxic lung.^-^ If both lungs are made 
hypoxic, the normal hydrostatic perfusion gra- 
dient favoring blood flow in the dependent lung 
is diminished,'* i.e., blood flow is directed to- 
ward the relatively underperfused upper part 
of the lung. Such a mechanism probably oper- 
ates on a local level, so that when a small group 
of alveoli becomes hypoxic, blood is shunted to 
adjacent alveoli to maintain a V/Q balance 
within small areas of lung.^ 
It is not clear what effect general airway hy- 
poxia would have on the pulmonary capillaries 
because the relative contribution to elevated re- 
sistance of the pre- and postcapillary vessels to 
the hypoxic pressor response is uncertain. Post- 
capillary constriction would be expected to 
cause an increase in capillary filling (recruit- 
ment and distension) by causing a retrograde 
pressure rise. Precapillary constriction could 
cause recruitment at the top and "derecruit- 
ment" at the bottom of the lung by shifting 
blood from the bottom to the top of the lung 
thereby overcoming the hydrostatic perfusion 
gradient, or cause general derecruitment if 
there is a drop in cardiac output, or cause no 
change in the number of perfused capillaries. 
One reason for these uncertainties is the diffi- 
culty in studying the pulmonary microcircula- 
tion directly. Although many ingenious, indirect 
techniques have been devised, they sufi'er from 
the inability to resolve the small vessels with 
precision in vivo. 
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