T. W. SWERCZEK 
241 
cats had mild MHPA, but in all cases it was 
very mild and only a few vessels were affected. 
The thickest vessels had only up to 8 cell layers 
in the tunica media as compared with a common 
finding of up to 45 to 50 cell layers in the exper- 
imental groups. 
DISCUSSION 
Medial hyperplasia of the pulmonary arteries 
can be induced experimentally in up to 100% of 
the cats that have parasites migrating through 
the lungs. The most common cause of the lesion 
in naturally infected cats is probably T. cati 
and A. abstrusus. MHPA was also observed in 
cats that probably were not exposed to pulmo- 
nary parasites, but in these cats the thickness of 
the pulmonary arteries was very mild when 
compared with the lesion seen in the experimen- 
tal cats as well as some cats with the natural le- 
sion. The MHPA induced experimentally with 
A. abstrusus and T. cati was identical to the le- 
sion seen in naturally affected cats. The mecha- 
nism which triggers the medial myocytes to 
proliferate is unknown. Since MHPA becomes 
evident approximately 3 weeks, PI, a local ana- 
phylaxis resulting from an antigen-antibody re- 
action may be involved. The many eosinophil 
leukocytes seen in the tunica intima, adventitia 
and occasionally in the media and the eosinophil 
leukocytes, plasma cells and lymphocytes seen 
in the tunica adventitia during the acute stages 
of the lesion suggest an antigen-antibody re- 
sponse. 
Mediators associated with the antigen-anti- 
body reaction, such as histamine, are powerful 
vasocontrictors and may initiate arterial 
spasms. These spasms may cause the medial 
myocytes to proliferate. Since more than one 
pharmacologic mediator acting in a complex 
fashion is associated with anaphylaxis, it would 
be unlikely that MHPA could be experimentally 
produced by a single mediator such as hista- 
mine. 
The mild lesions seen in the control cats may 
be a normal anatomical difference in cats, or 
possibly other allergins in the environment may 
act as less potent antigenic stimuli to the lung. 
McCusker and Aitken suggested that the lung is 
the shock organ of the cat.^^ In light of the 
foregoing studies, possibly the pulmonary ar- 
teries should be considered the shock organ of 
the cat. Cats with MHPA have a mild pulmo- 
nary hypertension.-*' Since MHPA can be con- 
sistently induced experimentally in cats in- 
fected with T. cati and A. abstrusus, the cat 
should be a useful model for the study of pul- 
monary hemodynamics. 
SUMMARY 
Medial hyperplasia of the pulmonary arteries 
was induced experimentally in cats by Aeluro- 
strongylus abstrusus, Toxocara cati, T. canis and 
Ascaris suum. It appears that MHPA can be in- 
duced by any nematode that migrates through 
the lungs of cats, but in natural cases T. cati 
and A. abstrusus are probably the most impor- 
tant cause. The increased thickness of the pul- 
monary arteries seen in a few of the control 
cats was very mild as compared with that 
achieved in the experimental cats and with the 
marked lesions seen in some natural cases. 
The mechanism that triggers hyperplasia of 
the medial myocytes is unknown. Since the le- 
sion in the acute stages is suggestive of an al- 
lergic response, it is theorized that the lesion is 
the result of an antigen-antibody response. Me- 
diators released during the antigen-antibody re- 
action may initiate arterial spasms and subse- 
quent myocyte hyperplasia. 
Since MHPA can be consistently induced ex- 
perimentally in cats with T. cati, as well as A. 
abstrusus, the cat may be a useful model to 
study pulmonary hemodynamics. 
ACKNOWLEDGMENTS 
The investigation reported in this paper (No. 
72-4-8) is in connection with a project of the 
Kentucky Agricultural Experiment Station and 
is published with approval of the Director. Ex- 
perimental work described in this paper was 
completed while the author was at the Univer- 
sity of Connecticut, Storrs, Conn. 
REFERENCES 
1. Campbell, J. A. Further observations on oxygen 
acclimatization. J. Physiol. 63:325-342, 1927. 
