COXSACKIE B3 MYOCARDITIS INDUCES A DECREASE IN ENERGY-CHARGE AND ACCUMULATION OF HYALURONAN IN THE MOUSE HEART

Citation
A. Waldenstrom et al., COXSACKIE B3 MYOCARDITIS INDUCES A DECREASE IN ENERGY-CHARGE AND ACCUMULATION OF HYALURONAN IN THE MOUSE HEART, European journal of clinical investigation, 23(5), 1993, pp. 277-282
Citations number
45
Categorie Soggetti
Medicine, Research & Experimental
ISSN journal
00142972
Volume
23
Issue
5
Year of publication
1993
Pages
277 - 282
Database
ISI
SICI code
0014-2972(1993)23:5<277:CBMIAD>2.0.ZU;2-D
Abstract
Interstitial oedema in chronic inflammation and ischaemia is related t o an accumulation of hyaluronan (hyaluronic acid; HA) in the interstit ium. As interstitial oedema will affect the oxygen transport in the in terstitium we have evaluated whether accumulation of HA is related to signs of myocardial energy depletion in virus induced myocarditis. Myo carditis was induced in Balb/c mice by inoculation of Coxsackie B3 vir us. The extractable HA content of the myocardium increased progressive ly from a baseline value of 153 +/- 26 mug g-1 dry weight to a maximum of 286 +/- 78 mug g-1 dry weight at day 7, whereafter there was a sli ght decline. Affinity histochemistry visualized HA in the endo-perimys ium in healthy myocardium. At day 5 after Coxsackie B3 inoculation the re was a general widening of the endomysium, which exhibited a positiv e staining for HA. In conjunction with focal inflammatory infiltrates the staining for HA was even more pronounced. The energy rich adenylat es were reversibly affected by the Coxsackie B3 infection. There was a slight, but significant decline in EC from 0.74 +/- 0.05 in the contr ol group to a minimum value of 0.64 +/- 0.10 at day 5, whereafter a re stitution was observed at days 7 and 10. The total adenine nucleotide pool was similarly decreased from 27.8 +/- 2.9 mumol g-1 dry weight in controls to 24.6 +/- 2.1 mug g-1 dry weight at day 5, and normalized at days 7 and 10. The data suggest that virus induced myocarditis is a ssociated with a local accumulation of HA in the myocardium. Accumulat ion of HA is reasonably not a major pathophysiological component in th e disturbed energy metabolism seen, but may be of interest for genesis of arrhythmias and possibly sudden death.