INTRODUCTION: We investigated a novel application of phrenic nerve stimulation (PNS) in diaphragm dysfunction induced by mechanical ventilation (MV). METHODS: Twenty-one Sprague-Dawley rats were assigned randomly to 3 groups: spontaneous breathing, 18-h controlled MV, and 18-h controlled MV with PNS. Upon completion of the experimental protocol, diaphragm contractility, gene expression of insulin-like growth factor-1 (IGF-1) and ubiquitin ligases, and serum IGF-1 levels were analyzed. RESULTS: Compared with the spontaneously breathing rats, impaired diaphragm contractile function, including force-related properties and force-frequency responses, were pronounced with MV. Furthermore, MV suppressed IGF-1 and induced muscle ring finger 1 mRNA expression in the diaphragm. In contrast, PNS counteracted MV-induced gene expression changes in the diaphragm and restored diaphragm function. CONCLUSIONS: PNS exerted a protective effect against MV-induced diaphragm dysfunction by counteracting altered expression of IGF-1 and ubiquitin ligase in the diaphragm.
INTRODUCTION: We investigated a novel application of phrenic nerve stimulation (PNS) in diaphragm dysfunction induced by mechanical ventilation (MV). METHODS: Twenty-one Sprague-Dawley rats were assigned randomly to 3 groups: spontaneous breathing, 18-h controlled MV, and 18-h controlled MV with PNS. Upon completion of the experimental protocol, diaphragm contractility, gene expression of insulin-like growth factor-1 (IGF-1) and ubiquitin ligases, and serum IGF-1 levels were analyzed. RESULTS: Compared with the spontaneously breathing rats, impaired diaphragm contractile function, including force-related properties and force-frequency responses, were pronounced with MV. Furthermore, MV suppressed IGF-1 and induced muscle ring finger 1 mRNA expression in the diaphragm. In contrast, PNS counteracted MV-induced gene expression changes in the diaphragm and restored diaphragm function. CONCLUSIONS:PNS exerted a protective effect against MV-induced diaphragm dysfunction by counteracting altered expression of IGF-1 and ubiquitin ligase in the diaphragm.
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