28 
CARDIAC MODELS 
DISCUSSION 
Chairman Kezdi: Dr. Hardaway, do you 
think that in hemorrhagic shock, extreme vaso- 
constriction, capillary stasis and sludging con- 
tribute to some problems which relate to the 
deterioration of these animals? 
R. M. Hardaway: Yes, unquestionably. In 
fact, shock essentially is a vasoconstriction 
with an accompanying and consequent slowing 
of capillary blood flow. The vasoconstriction 
pinches oif some of the flow in the body's at- 
tempt to maintain adequate blood pressure. It 
is a good first aid mechanism. It keeps the 
blood pressure near-normal, but it is not satis- 
factory as a long-term measure. In other words : 
if the vasoconstriction persists for any length 
of time, it becomes a negative instead of a posi- 
tive value and the first organs to deteriorate 
are those which are most vasoconstricted, 
namely the kidneys and some of the other vital 
organs. 
I therefore believe that vasoconstriction con- 
tinued over a period of time is very definitely a 
detrimental factor and should not be allowed to 
continue. It is usually best prevented by just 
giving volume; this will cause a fall of the 
catacolamine level. We have, in fact, abundant 
data on this: when the catacolamine level is 
high, it returns to normal as fluid is given. A 
physiologic vasodilation occurs simultaneously 
with the above. 
Chairman: That is why vasodilators and 
volume extension work. 
C. G. La Farge, Children's Hospital Medical 
Center, Boston, Mass. : You mentioned pretreat- 
ment with good results when using fibrinolysin 
in animals. Did you use fibrinolysin, urocarnase 
or something of that type ex post facto while 
you had the already developed deteriorated 
state ? 
R. M. Hardaway: I used fibrinolysin preter- 
minally in a few clinical cases. I have usually 
been afraid to give fibrinolysin clinically because 
these patients always have a completely inco- 
agulable blood at that time. 
If one gives even a mild or small dose of fi- 
brinolysin in the presence of a hypercoagulable 
state and in the presence of shock, it will reduce 
the fibrinogen to zero. I have been afraid to 
try this, even though theoretically, it would 
dissolve the clots. Heparin is somewhat similar ; 
it is even worse, however, because it does not 
dissolve already formed clots. Nor does it do 
anything to prevent platelet agglutination, 
which I believe is perhaps the first step in 
coagulation. Thirdly, it is inactivated in any 
pH levels which we have to cope with in the 
capillaries. Heparin, I believe, is currently 
given to prevent DIG, particularly in shock due 
to meningococcal septicemia, apparently with 
clinically good results. But I have been person- 
ally afraid to use it. I think that it is much 
easier and safer and perhaps more effective to 
promote blood flow by means of adequate vol- 
ume and, if necessary, vasodilators, since they 
will prevent DIG. 
