Abstract
To assess fluoxetine effects on mitochondrial structure of the right ventricle in rats exposed to cold stress. The experimental study procedures were performed in 250-300g male EPM-Wistar rats. Rats (n=40) were divided into four groups: 1) Control group (CON); 2) Fluoxetine (FLU); 3) Induced hypothermia (IH) and; 4) Induced hypothermia treated with fluoxetine (IHF). Animals of FLU group were treated by the administration of gavages containing 0.75 mg/kg/day fluoxetine during 40 days. The induced hypothermia was obtained by maintaining the groups 3 and 4 in a freezer at -8 degrees C for 4 hours. The animals were sacrificed and fragments of the right ventricle (RV) were removed and processed prior to performing electron microscopic analysis. The ultrastructural changes in cardiomyocytes were quantified through the number of mitochondrial cristae pattern (cristolysis). The CON (3.85%), FLU (4.47%) and IHF (8.4%) groups showed a normal cellular structure aspect with preserved cardiomyocytes cytoarchitecture and continuous sarcoplasmic membrane integrity. On the other hand, the IH (34.4%) group showed mitochondrial edema and lysis in cristae. The ultrastructural analysis revealed that fluoxetine strongly prevents mitochondrial cristolysis in rat heart, suggesting a protector effect under cold stress condition.
Highlights
Induced cold state by low temperature exposure may be considered as a significant stressing agent [1]
The ultrastructural changes in cardiomyocytes were quantified through the number of mitochondrial cristae pattern
The ultrastructural analysis revealed that fluoxetine strongly prevents mitochondrial cristolysis in rat heart, suggesting a protector effect under cold stress condition
Summary
Induced cold state by low temperature exposure may be considered as a significant stressing agent [1]. Neurogenic lesion relayed on hypertrophic cardiomyopathy or change on myocardial tissue metabolism can be caused by the cardiovascular reactivity to cold stress that is hypothesized to be a marker for subsequent cardiovascular disease as well as a predictor of hypertension [2]. Mitochondrial lesions were defined as a partial or complete cristae lysis and their substitution by lacunar areas [3]. The ultrastructural changes in the cardiomyocytes of rats subjected to cold stress are characterized by myofilament dearrangement, increasing the gap between mitochondrial cristae sometimes causes erasings, and partial or total rupture of cristae originating in lacular areas [4,5,6,7]. We speculate that through its sympathetic activity decrease effect, fluoxetine may reduce the mithocondrial heart damage caused by the cold stress exposure
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