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Abstract
Cardiac myolysis was observed in guinea pigs sensitized with vesicular stomatitis
virus (VSV), following challenge with this antigen. The phenomenon developed within
1 h of challenge, appearing as islands in the myocardium. The speed and focal nature
of the damage point to obstruction of blood flow as a cause of the myolysis. The myolysis
was not a toxic effect of the virus itself, but probably a consequence of cardiac
anaphylaxis. It occurred only after challenge, and was abolished in 71% of the animals
by pretreatment with a mixture of the lipoxygenase-cyclooxygenase inhibitor, BW755C
and H1 histamine receptor antagonist, diphenhydramine. Treatment with BW755C alone
before challenge prevented myolysis fran developing in 46% of the animals. Challenge
with VSV to the perfused, spontaneously beating, sensitized isolated guinea pig heart
increased sulfidopeptide-leukotrieze (LTC4, LTD4, LTE4) production from undetectable levels (<0.5 ng LTD4-equivalent/heart/15' to 13 ng
LTD4-equivalent/ heart/15'. At the same time, there were derangements in cardiac rate,
contractility and coronary outflow typical of cardiac anaphylaxis. The reduction in
coronary outflow rate during cardiac anaphylaxis is due largely to the powerful vasoconstrictor
effect of LT, as well as perhaps platelet activating-factor. Thus it is speculated
that there is a causal relationship between LT release, vasoconstruction, ischemia
and myolysis in the heart, following VSV challenge to sensitized guinea pigs.

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© 1986 Published by Elsevier Inc.