Key result
Trypanosoma cruzi infection in rats significantly reduced exercise tolerance and caused marked contractile dysfunction in right atrium and left ventricle myocytes compared to controls.
Why the study?
Does Trypanosoma cruzi infection impair myocardial morphology, single cardiomyocyte contractile function, and exercise tolerance in rats?
RCT (n=28)
randomized
Does Trypanosoma cruzi infection impair myocardial morphology, single cardiomyocyte contractile function, and exercise tolerance in rats?
Trypanosoma cruzi infection in rats induces myocardial morphological changes and single cardiomyocyte contractile dysfunction, which correlates with reduced exercise tolerance, providing mechanistic insights into Chagas cardiomyopathy.
Rat model data are hypothesis-generating for Chagas cardiomyopathy mechanisms; should not yet inform clinical practice.
The aim of this study was to investigate the effects of Trypanosoma cruzi (T. cruzi) infection on myocardial morphology, single cardiomyocyte contractile function and exercise tolerance in rats. Adult Wistar rats were randomized into control (n = 14) and infected (n = 14) groups. Infected animals were inoculated with T. cruzi Y strain (300,000 trypomastigotes/50 g body weight). After 9 weeks, the animals were subjected to a treadmill running protocol. Then, the right atrium (RA) and left ventricle (LV) were removed for morphological and cell contractile evaluation. The infected animals exhibited a significant reduction in distance travelled, total time to fatigue and workload. In addition, these animals had hypertrophy, increased myocardial cellularity, and an increase in the proportion of collagen and blood vessels. RA and LV myocytes from infected animals showed marked contractile dysfunction under basal conditions and a reduced contractile response to β-adrenergic stimulation. The workload of infected animals was correlated closely with the amplitude of cell shortening of RA and LV myocytes. T. cruzi infection influenced the myocardial morphology and the mechanical properties of RA and LV single myocytes negatively and reduced exercise tolerance. Single cardiomyocyte contractile dysfunction could constitute an additional mechanism of cardiac impairment and reduced exercise tolerance in this infection.
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Novaes et al. (2011) conducted an RCT in Trypanosoma cruzi infection (n=28). Trypanosoma cruzi infection vs. Control was evaluated on myocardial morphology, single cardiomyocyte contractile function and exercise tolerance. Trypanosoma cruzi infection in rats significantly reduced exercise tolerance and caused marked contractile dysfunction in right atrium and left ventricle myocytes compared to controls.
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