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Coxsackie B3 myocarditis induces a decrease in energy charge and accumulation of hyaluronan in the mouse heart
A Waldenström1, J Fohlman, N G Ilbäck
1Department of Internal Medicine, University Hospital, Uppsala, Sweden.
Insights
Virus-induced myocarditis leads to hyaluronic acid (HA) accumulation in heart tissue, causing interstitial edema. This accumulation correlates with myocardial energy depletion, impacting cardiac function.
Area of Science:
- Cardiology
- Pathology
- Biochemistry
Background:
- Interstitial edema in chronic inflammation and ischemia is linked to hyaluronan (HA) accumulation.
- Interstitial edema can impair oxygen transport within tissues.
Purpose of the Study:
- To investigate the relationship between hyaluronan accumulation and myocardial energy depletion in virus-induced myocarditis.
- To assess changes in myocardial HA content and energy status following Coxsackie B3 virus infection.
Main Methods:
- Myocarditis was induced in Balb/c mice using Coxsackie B3 virus.
- Extractable HA content and adenine nucleotide levels (energy status) were measured in myocardial tissue.
- Affinity histochemistry was used to visualize HA distribution.
Main Results:
- Myocardial HA content significantly increased post-infection, peaking at day 7.
- Hyaluronan accumulated in the endomysium, particularly around inflammatory infiltrates.
- Energy charge (EC) and total adenine nucleotide pool showed a significant decline at day 5, with subsequent recovery.
Conclusions:
- Virus-induced myocarditis is associated with localized hyaluronan accumulation in the myocardium.
- The observed HA accumulation may contribute to interstitial edema and impact myocardial energy metabolism.
- These findings suggest a potential role for HA in the pathogenesis of viral myocarditis.
Abstract:
Interstitial oedema in chronic inflammation and ischaemia is related to an accumulation of hyaluronan (hyaluronic acid; HA) in the interstitium. As interstitial oedema will affect the oxygen transport in the interstitium we have evaluated whether accumulation of HA is related to signs of myocardial energy depletion in virus induced myocarditis. Myocarditis was induced in Balb/c mice by inoculation of Coxsackie B3 virus. The extractable HA content of the myocardium increased progressively from a baseline value of 153 +/- 26 micrograms g-1 dry weight to a maximum of 286 +/- 78 micrograms g-1 dry weight at day 7, whereafter there was a slight decline. Affinity histochemistry visualized HA in the endo-perimysium in healthy myocardium. At day 5 after Coxsackie B3 inoculation there was a general widening of the endomysium, which exhibited a positive staining for HA. In conjunction with focal inflammatory infiltrates the staining for HA was even more pronounced. The energy rich adenylates were reversibly affected by the Coxsackie B3 infection. There was a slight, but significant decline in EC from 0.74 +/- 0.05 in the control group to a minimum value of 0.64 +/- 0.10 at day 5, whereafter a restitution 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 micrograms g-1 dry weight at day 5, and normalized at days 7 and 10. The data suggest that virus induced myocarditis is associated with a local accumulation of HA in the myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)