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Abnormalities in heart membranes and myofibrils during bacterial infective cardiomyopathy in the rabbit
Abstract:
We studied hearts from sham-operated and uninfected catheterized rabbits as well as from rabbits at early and late stages of cardiomyopathy and failure after 3 and 6 days of infection with Streptococcus viridans. No ultrastructural abnormalities or biochemical changes in membrane and myofibrillar activities were seen in 3-day uninfected hearts. In 6-day uninfected hearts there were decreased sarcolemmal M2+ ATPase, Na+-K+ ATPase, adenylate cyclase and calcium binding, microsomal calcium binding and uptake, and myofibrillar Ca2+-stimulated ATPase as well as increased mitochondrial calcium uptake. Slight ultrastructural changes also were apparent in 6-day uninfected hearts. At both early and late stages of infective cardiomyopathy and failure there were varying degrees of depression in sarcolemmal Mg2+ ATPase, Na+-K+ ATPase, adenylate cyclase and calcium binding, microsomal calcium binding, calcium uptake and basal ATPase, and myofibrillar Ca2+-stimulated ATPase activities. However, sarcolemmal Ca2+ ATPase and myofibrillar Mg2+ ATPase activities were decreased only after 6 days of infection. Mitochondrial calcium binding and uptake were increased in early stages but decreased in late stages of disease. Furthermore in infected hearts there were defects in mitrochondrial respiration and phosphorylation. Generalized severe myocardial cell damage involving myofibrils, mitochondria, and the sarcotubular system was seen only in late stages of infection. The results demonstrate impairment of different membrane and contractile protein functions as well as ultrastructural abnormalities in bacterial cardiomyopathic hearts which were absent or of lesser magnitude in hearts with only hypertrophy. The findings reported here suggest to use that there is an association between heart failure and changes in function of cellular components during bacterial infective cardiomyopathy.
Insights
Bacterial infection causes significant heart muscle damage, impairing cellular functions and leading to heart failure. These changes are more severe in infected hearts than in those with only hypertrophy.
Area of Science:
- Cardiology
- Biochemistry
- Cell Biology
Background:
- Bacterial infections can lead to cardiomyopathy and heart failure.
- Understanding the cellular mechanisms of bacterial-induced heart dysfunction is crucial.
Purpose of the Study:
- To investigate the ultrastructural and biochemical changes in rabbit hearts during Streptococcus viridans infection.
- To compare these changes in infected hearts with those in uninfected and sham-operated controls.
Main Methods:
- Studied hearts from sham-operated, uninfected, and infected rabbits at early (3 days) and late (6 days) stages of infection.
- Assessed membrane and myofibrillar activities, including ATPase, adenylate cyclase, and calcium binding.
- Examined mitochondrial function, respiration, and phosphorylation.
- Evaluated ultrastructural changes in myocardial cells.
Main Results:
- Infected hearts showed progressive depression in sarcolemmal and microsomal enzyme activities and calcium handling.
- Mitochondrial function was impaired, with altered calcium uptake and defects in respiration and phosphorylation.
- Severe myocardial cell damage was observed in late stages of infection, affecting myofibrils, mitochondria, and the sarcotubular system.
- Uninfected hearts with hypertrophy showed some biochemical alterations but lacked severe cellular damage.
Conclusions:
- Bacterial infective cardiomyopathy leads to significant impairment of cellular components and ultrastructural abnormalities.
- These cardiac dysfunctions are associated with the development of heart failure.
- The findings highlight the detrimental impact of bacterial infection on heart muscle at a cellular level.