816 
ANATOMY AND PATHOLOGY 
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DISCUSSION 
Chairman Kusserow: Thank you, Dr. 
Hackel, for your very fine presentation of some 
of the ultramicroscopic aspects of the shocked i 
state. 
Richard E. Clark, Washington University,, 
St. Louis, Mo.: To continue with the subject of I 
anoxia, some years ago Dammond and I pub- 1 
lished a paper covering a spectrum of animals 
including rats, guinea pigs, rabbits, dogs, and 
humans. The earliest sign of subendocardial 
hemorrhage occurred within the bundle of His 
which probably has the richest blood supply per i 
square millimeter of any place in the heart. If 
you kill a rat within two or three minutes by 
totally flooding a closed environment with nitro- 
gen, for example, then immediately autopsy 
him and section the bundle of His area, you'll 
find gross hemorrhage. We found from 30 to 
709'' in every species studied. We entered this 1 
area due to a patient who, when his PO2 was j 
raised, would go into sinus rhythm. Then when > 
we decreased his PO2 on a ventilator, he went 
into an AV block. This was repeated time and j 
time again. I honestly believe that these lesions 
occur very, very rapidly even though these 
animals obviously went into a shocked state in 
a few minutes from the time of initiation of 
anoxia to death. I also believe hypoxia does play 
an important role in subendocardial hemor- 
rhage. 
Dr. Hackel : Yes, I agree absolutely. I think 
it does. And I think that it can be caused by 
several things, such as putting animals in nitro- 
gen. Stellate ganglion stimulation alone will 
also do it, presumably by its hypoxic effect on 
the myocardium. So I'd agree that this is true. 
