This paper is only available as a PDF. To read, Please Download here.
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.
To read this article in full you will need to make a payment
Purchase one-time access:Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
One-time access price info
- For academic or personal research use, select 'Academic and Personal'
- For corporate R&D use, select 'Corporate R&D Professionals'
Subscribe:Subscribe to Prostaglandins, Leukotrienes and Essential Fatty Acids
Already a print subscriber? Claim online access
Already an online subscriber? Sign in
Register: Create an account
Institutional Access: Sign in to ScienceDirect
- Leukotrienes and their action in the coronary circulation.in: Piper P.J. Leukatrienes and Other Lipoxygenase Products. Research Studies Press, 1983: 94 (94)
- Studies on the mechanism of leukotriene induced coronary artery constriction.Prostaglandins. 1983; 26: 573
- Generation of a leukotriene-like substance from porcine vascular and other tissues.Prostaglandins. 1983; 25: 591
- Release of slow-reacting substance of anaphylaxis from layers of guinea pig aorta.Prostaglandins. 1983; 25: 823
- Mediators of immediate hypersensitivity.in: Sirois P. Rola-Pleszczynski M Immunopharmacology. Vol 4. Elsevier Biomedical, 1982: 201
- The heart as a target organ in systemic allergic reactions. Comparison of cardiac anaphylaxis in vivo and in vitro.Circul. Res. 1975; 36: 520
- The heart in human anaphylaxis.Annals of Allergy. 1971; 29: 399
- Asthma induced myocardial infarction in a patient with normal coronary arteries: A case report and a pathogenetic hypothesis.J. Med. 1983; 14: 351
- Food antibodies and myocardial infarction.Lancet. 1974; 1: 1012
- Coronary artery spasm and myocardial infarction in the absence of angiographically demonstrable obstructive coronary disease.in: Mayo Clin Proc.56. 1981: 700
- Myocardial infarction following an acute viral illness.Arch. Intern. Med. 1983; 143: 1466
- Viral myopericarditis presenting as acute myocardial infarction.Circulation. 1982; 64: IV-25
- Evaluation of mild acute infectious myocarditis.Br. Heart J. 1982; 47: 381
- Association of acute respiratory symptoms with onset of acute myocardial infarction:Prospective investigation of 150 consecutive patients and matched control patients.Am. J. Cardiol. 1984; 53: 481
- Influenza and ischaemic heart disease - a possible trigger for acute myocardial infarction?.Intl. J. Epidemiology. 1978; 7: 231
- Inflammation and the onset of myocardial infarction.Ann. Int. Mad. 1985; 102: 699
- The development of sensitive and specific radio-immunoassays for leukokotrienes.Prostaglandins, Leukotrienes and medicine. 1984; 13: 21
- Focal myocytolysis of the heart.Amer. J. Pathol. 1955; 31: 443
- Influence of variations in electrolyte intake upon the development of cardiac necrosis produced by vasopressor amines.Lab Invest. 1964; 13: 757
- Reversible acute cardiac injury during cefoxitin-induced anaphylaxis in a patient with normal coronary arteries.Am. J. Med. 1984; 77: 729
- Electrocardiographic changes during human anaphylaxis.J. Am. Med. Assoc. 1970; 211: 627
- Myocardial lesions in anaphylaxis.Arch Pathos. 1973; 95: 185
- Myocardial damage during protracted anaphylactic shock in guinea pigs.Res. exp. Med. 1975; 166: 173
- SRS-A, leukotrienes, and immediate hypersensitivity reactions of the heart.in: Samuelsson B. Paoletti R. Leukotrienes and Other Lipoxygenase Products. Raven Press, New York1982: 215
- Effect of inhibition of synthesis and receptor antagonist of SRS-A in cardiac anaphylaxis.Br. J. Pharmac. 1983; 80: 73
© 1986 Published by Elsevier Inc.