JACOB I. HIRSCH, FRITZ STREULI AND FRED GORSTEIN 
37 
intra-arterial thrombi were always associated 
with arterial wall lesions. It was clear that a 
wall lesion was a necessary prerequisite for 
thrombus formation. All of the thrombi pro- 
duced by this method appeared microscopically 
to be of the classical structure associated with an 
in vivo thrombus, including platelets, fibrin and 
other cellular components, and were clearly dis- 
tinct from a simple clot. Where partially occlud- 
ing thrombi were found, the site of attachment 
to the vessel wall was always at the site of in- 
jury. We found that in the course of 7 days, the 
structure of the intra-arterial thrombus was 
not static, but that initially it was composed 
mainly of densely packed platelet aggregates 
surrounded by strands of fibrin. Later platelets 
disintegrated and more fibrin was visible within 
the thrombus, and finally leukocytes appeared 
on and within the thrombus mass. After 2 to 4 
days, the amount of fibrin was reduced as early 
reparative processes became apparent. These 
observations were in agreement with those of 
J0rgensen et al. made in the carotid artery of 
the pig.* The sites of arterial damage and 
thrombus formation were typically just beyond 
artery bifurcations, as shown in Figure 3. In 
addition to the traumatic effect of electric cur- 
rent, such locations also satisfied the other 
prerequisite condition alluded to previously, 
namely, that significant reduction of blood flow 
occurred at these sites. 
Figure 4 is a section of a 3-day old lesion 
stained with H and E. The arterial wall lesion is 
seen at the pericardial aspect of the vessel. A 
complete loss of smooth muscle structure is 
seen, producing a homogeneous, eosinophilic ap- 
pearance. There was destruction of the internal 
elastic membrane with bleeding into the medial 
layers. Infiltration with leukocytes was appar- 
ent in this area. 
Figure 5 shows a 4-day old lesion seen under 
low power. The thrombus which was present 
only partially occluded the lumen and origi- 
nated from a localized lesion of the vessel wall. 
Figure 6 shows a 8-hour old process, with me- 
talic salt visible within the thrombus mass, a 
finding typical of thrombi produced with the in- 
tra-arterial electrode of anodal polarity. Figure 
7 shows a thrombus only 30 minutes old. Under 
low power it appears to be completely occluding 
the vessel lumen. The pericardial aspect of the 
artery appears to be the site of damage in this 
section. 
DISCUSSION AND CONCLUSIONS 
We have found in these experiments that the 
simultaneous occurrence of two factors was 
necessary for thrombus formation. These were : 
(1) a substantial reduction in blood flow, and 
(2) a lesion of the arterial wall. Based upon 
this, it is difficult to conceive how thrombosis 
could occur naturally in the presence of only 
Figure 3. — Schematic representation of a wire-con- 
taining catheter wedged at point of bifurcation of a 
coronary artery. Cross sectional area at A equals sum 
of cross sectional areas at B and C. Ratio of diame- 
ters at A to B or A to C are 1.4 to 1 if B and C are 
of equal size. Flow through C is unmodified com- 
pared to flow through B. 
