WEBB, WAX, KUSAJIMA, PARKER, KAMIYAMA AND MURAKAMI 
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minutes as subtotal recruitment of the alveolar 
bed is demonstrated. 
Venules. The capillaries coalesce into venules 
which similarly empty into wider channels. 
Flow through these is non-pulsatile but is quite 
rapid in normal circumstances. Several venules 
converge and the larger vein disappears into 
the deeper pulmonary tissues toward the pul- 
monary hilus. 
Alveoli. The alveoli appear as large bubbles 
or darker structures with traversing variable 
capillary beds. They are roughly spherical in 
shape but are variable in size. The alveoli con- 
tract and expand slightly (18-20% increase in 
volume) with respiration. With normal respira- 
tion, flow through the capillary bed and venules 
around the alveoli shows little alteration, except 
in the alveoli most distant from the arteriolar 
supply, where there is some definite decrease in 
flow with inspiration. 
Early Shock 
Total volume flow appears sluggish and in- 
stead of unidirectional flow the arterial pattern 
shows to and fro pulsation which is accentuated 
by respiration. The number of plugged capillar- 
ies and venules progressively increases and only 
large main channels of wide venules and veins 
remain functional. 
Late Shock 
Most capillary beds are completely closed and 
though the capillary walls are visable, few con- 
tain any blood cells. Blood flow through the ar- 
terioles is now almost totally arrested and 
marked clumping of the red cells appears. Many 
alveoli become partially collapsed and cloudy 
losing their fine transparency. Hyperlucent 
highly refractile areas are seen in the intersti- 
tial areas suggesting interstitial edema. The 
venules may become dilated and very congested 
with packed red blood cells. 
After Reinfusion 
Initially there is streaming of the flow but 
gradually more and more of the capillaries, ven- 
ules and arterioles open and progressively in- 
crease their flow. The capillary beds show 
extreme congestion, perivascular edema and 
hemorrhage. The epithelial walls are noted to be- 
come quite edematous and the venous network 
increases enormously in size. Many of the al- 
veoli show increased irregularity in shape and 
size and many do not respond to ventilation. As 
the animal's general condition improves, some 
parts of the alveoli improve but complete recov- 
ery has not been observed in our acute experi- 
mental model even after periods up to four 
hours. 
DEPENDENT VIEW 
Normal 
The capillaries, venules and arterioles are 
much more prominent and much wider than in 
the superior portion of the lung and the alveoli 
are less distinct. Blood flow is much faster re- 
flecting the effect of the increased volume and 
flow of blood. 
The entire field shows a much more vascular 
pattern reflecting the effects of gravity. 
Early Shock 
The total volume of flow does not appear to 
decrease as in the upper portion of the lung and 
circulation remains open in the arteries, veins 
and capillary beds. 
Late Shock 
The capillary beds still remain open and 
blood flow through the arterioles remains al- 
most as active as during the pre-shock period. 
The major changes to be noted at this time are 
that some of the alveoli are partially collapsed 
and hyperlucent refractile areas are seen in the 
interstitial areas reflecting the development of 
intersitital edema. Some clumping of erythro- 
cytes is seen but nothing to compare with the 
marked clumping of the superior portion of the 
lung. 
After Reinfusion 
Immediately upon reinfusion a very startling 
and dramatic change occurs in that circulation 
almost completely stops. Marked stagnation and 
clumping of the red cells in the arterioles and in 
the capillary bed develop. The capillary beds 
