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Decreased intracellular [Ca ] coincides with reduced expression of Dhprα1s, RyR1, and diaphragmatic dysfunction in a rat model of sepsis. | LitMetric
Introduction : Sepsis can cause decreased diaphragmatic contractility. Intracellular calcium as a second messenger is central to diaphragmatic contractility. However, changes in intracellular calcium concentration ([Ca ]) and the distribution and co-localization of relevant calcium channels [dihydropyridine receptors, (DHPRα1s) and ryanodine receptors (RyR1)] remain unclear during sepsis. In this study we investigated the effect of changed intracellular [Ca ] and expression and distribution of DHPRα1s and RyR1 on diaphragm function during sepsis.Methods : We measured diaphragm contractility and isolated diaphragm muscle cells in a rat model of sepsis. The distribution and co-localization of DHPRα1s and RyR1 were determined using immunohistochemistry and immunofluorescence, whereas intracellular [Ca ] was measured by confocal microscopy and fluorescence spectrophotometry.Results : Septic rat diaphragm contractility, expression of DHPRα1s and RyR1, and intracellular [Ca ] were significantly decreased in the rat sepsis model compared with controls.Discussion : Decreased intracellular [Ca ] coincides with diaphragmatic contractility and decreased expression of DHPRα1s and RyR1 in sepsis. Muscle Nerve 56: 1128-1136, 2017.
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