264 
PULMONARY MODELS 
show extreme congestion and edema and most 
of the alveoli appear airless. This picture re- 
mains much the same during the first hour post 
reinf usion but then may show gradual improve- 
ment during the next several hours. 
RESPONSE TO STEROIDS 
In this group of animals 30 mgs per kilogram 
of methyl prednisolone (solu-medrol) was ad- 
ministered to the animals just prior to rein- 
fusion. All changes prior to this time had been 
exactly as above. Thus, this situation is quite 
analogous to treatment rendered in the emer- 
gency room to a patient entering in shock. 
Following reinfusion, the superior portion of 
the lung shows a very rapid reinstitution of 
blood flow with far less clumping than demon- 
strated previously and with much less develop- 
ment of interstitial edema or perivascular hem- 
orrhage. 
An even more impressive change is noted in 
the inferior portion of the lung where flow 
through the hypostatic areas immediately re- 
turns to a very vigorous level following reinfu- 
sion. Flow continues and steadily improves, and 
there is far less alveolar collapse, interstitial 
edema and perivascular hemorrhage. The stain- 
ing representing the margination of leukocytes, 
platelets and red cells along the margins of the 
arterioles, disappears rapidly in a fashion never 
demonstrated in untreated animals. 
EFFECT OF LOW MOLECULAR WEIGHT DEXTRAN 
In these experiments low molecular weight 
Dextran was administered in doses of 5 cc per 
kilogram at the time of reinfusion of the shed 
blood. In this post shock treatment, the changes 
previously noted in the superior and inferior 
portions of the lung are ameliorated though the 
improvement does not approach that achieved 
with large doses of prednisolone. 
DISCUSSION 
In 1945 Eaton et al.* observed the pulmonary 
changes following acute arterial blood loss and 
reported elevation of the peripheral venous and 
pulmonary arterial pressures. The pulmonary 
artery pressures were initially increased by in- 
travenous infusions. Rounthwaite in 1952^2 
studied variations in blood pressure in both the 
pulmonary artery and pulmonary veins during 
hemorrhagic shock and resuscitation. He con- 
cluded that both the heart and lungs play im- 
portant roles though those animals with the 
higher pulmonary venous pressures exhibited 
greater degrees of congestion. 
Berry, McLaughlin, Clark, and Morrow^ in 
1965, reported that acute hypoxia caused in- 
creases in pulmonary flow, arterial pressure 
and pulmonary arterial wedge pressure with a 
marked rise in the post capillary pulmonary 
vascular resistance. This suggested that this 
constriction had occurred primarily in the pul- 
monary veins. Keller,^ Murakami^ and their 
co-workers, using a model of hemorrhagic hypo- 
tension, found an increased resistance in the 
small pulmonary veins and decreased outflow of 
blood from the lungs leading to acute congestive 
lesions of the lung. Sugg, Webb and Ecker« 
demonstrated prevention of the gross and mi- 
croscopic pulmonary changes by removal and 
reimplantation of the lung but these were not 
prevented by heparinization, atropine, Dibenzy- 
lene or unilateral or bilateral vagotomy. These 
observations suggested a neural mechanism in 
the pathogenesis of the lesion. Cook and Webb,^ 
studying the alterations in pulmonary and sys- 
temic blood flow distribution and pressure like- 
wise suggested that pulmonary venous constric- 
tion is- a major factor in the development of 
acute congestive atelectasis. A most interesting 
related observation is that of Moss et al.^^ who 
showed that cerebral hypoxia with a p02 of 35 
± 5 mm Hg for 2 hours would produce exactly 
the same pulmonary pathologic changes 
(congestion, patchy atelectasis, interstitial and 
intraalveolar edema and hemorrhage) as seen 
following hemorrhagic hypotension of 2 hours 
duration. This supports our previous conclusion 
that the pathophysiologic changes may be me- 
diated by the autonomic nervous system. 
Our microscopic observations suggest that in 
early shock in the uppermost portions of the 
lung, blood flow almost ceases. This might in 
part be due to precapillary constriction, but ap- 
pears to be due more likely to the lower pulmo- 
