CINEMICROSCOPY OF THE PULMONARY 
MICROCIRCULATION IN SHOCK 
Watts R. Webb, Stennis D. Wax, K. Kusajima, Frederick B. Parker, T. M. Kamiyama and T, Murakami' 
Hemorrhagic hypotension to 40 mm Hg for 2 hours 
in the dog produces the full pathologic picture of 
congestive atelectasis with patchy atelectasis, conges- 
tion, interstitial and intraalveolar edema and hemor- 
rhage. Pressure studies show the initial vascular re- 
sponse to be constriction of the small pulmonary veins. 
Motion pictures have been made of the pulmonary 
microcirculation at powers up to 450x by using a met- 
allurgic epi-objective microscope with dark field illumi- 
nation by reflected light. 
The upper portion of the lung shows early loss of 
capillary circulation during shock with restored flow 
following reinfusion, but with rapidly progressing 
edema, etc. However, the dependent, under side of 
the lung, which initially shows a much fuller vascular 
bed, continues with rapid flow during shock, but then 
has almost complete circulatory arrest on reinfusion. 
Stagnation, clumping of the erythrocytes and edema be- 
come more prominent and remain so. 
These changes are almost completely prevented by 
large doses of methylprednisolone and less effectively 
by low molecular weight dextran. 
INTRODUCTION 
The pulmonary changes in irreversible hem- 
orrhagic shock have been studied by many 
investigators.^"* Our previous work^ confirmed 
that two hours of hemorrhagic shock at 40 mm 
of mercury folloM^ed by reinfusion of the shed 
blood usually produces widespread pulmonary 
capillary congestion. This was found to be par- 
ticularly true in anemic or infected animals. It 
was found^ that pulmonary reimplantation is 
one of the few effective methods of preventing 
the congestive atelectasis in the lung secondary 
to hemorrhagic shock, suggesting that this en- 
tity is at least in part neurogenically controlled. 
Subsequent work'^'^ involving multisite pres- 
sure studies on each side of the capillary bed 
suggested that the key response is post-capil- 
lary or small vein constriction. In summary, the 
initial lesion appears to be pulmonary small 
Department of Surgery — SUNY Upstate Medical Center, Syracuse, 
N.Y. 13210. 
vein constriction with the development of a 
gradient between small pulmonary veins and 
the large pulmonary veins and left atrium. Sub- 
sequently during shock and particularly after 
reinfusion, an additional gradient develops 
across the alveolar capillary bed compatible 
with the interstitial edema and capillary 
congestion which are demonstrable microscopi- 
cally. 
Recently, we have been able to refine in vivo 
in situ microscopy viewing and photography of 
the pulmonary microcirculation. Direct micro- 
scopic observation of the pulmonary circulation 
was reported as early as 1925 by Hall using the 
transillumination method. In 1930, using a spe- 
cial Zeiss objective, Olkon^^ described the cap- 
illary circulation of the alveoli in detail, and 
similarly Irwin" published photographs of the 
alveolus at 500 x magnification in 1954 again 
using the transillumination method. 
MATERIALS AND METHODS 
Our apparatus consists of an inverted metal- 
lurgic epi-objective microscope using reflected 
incident light with dark field illumination (see 
Figure 1 and Figure 2). With a quartz-halogen 
or high pressure xenon light source it is possible 
to view and photograph pulmonary circulation to 
a depth of 1.5 mm beneath the pleura. We have 
been able to obtain satisfactory visualization up 
to 900 power and have produced bright color 
motion pictures at powers up to 450 with a 
crisp focus and a high degree of stability. A 
special microscope objective-tissue interface ap- 
paratus stabilizes the lung without any intrinsic 
damage or physiological interferences yet al- 
lowing visualization of the same alveolus 
and/or repeated scanning of many hundreds of 
adjacent alveoli for several hours. In addition, 
the instrumentation has been modified so that 
261 
