@entity205 ameliorates mitochondrial ultrastructural injury in the ileum during acute XXXX .

@entity5694 @entity295 @entity5 @entity26 @entity205 @entity519 @entity520 @entity468 @entity2383
OBJECTIVE: This study was designed to determine the role, if any, of the mitochondrial permeability transition in the pathogenesis of @entity2383 in a representative systemic organ during the acute phase of @entity5694 . DESIGN: A well-established, normotensive feline model was employed to determine whether pretreatment with @entity205 , a potent inhibitor of the mitochondrial permeability transition, reduces the severity of @entity2383 in the ileum during acute @entity5694 . SETTING: The Ohio State University Medical Center research laboratory. SUBJECTS Adult, male conditioned @entity468 . INTERVENTIONS: Volume resuscitation and maintenance of acid/base balance and tissue @entity26 availability were provided, as needed, to minimize the potentially confounding effects of tissue @entity519 and/or @entity520 on the experimental results. Following isotonic saline vehicle (control; n = 6), lipopolysaccharide (3.0 mg/kg, intravenously; n = 10), or @entity205 (6 mg/kg, intravenously; n = 7) followed in 60 mins by lipopolysaccharide (3.0 mg/kg, intravenously) administration, ileal samples were obtained at 4 hrs posttreatment, and mitochondrial ultrastructure was assessed. Objective comparisons of mitochondrial ultrastructural morphology were performed by using digital image analyses. MEASUREMENTS AND MAIN RESULTS: As expected, significant @entity2383 was apparent in the ileal tissues by 4 hrs following LPS treatment, despite maintenance of regional tissue @entity26 availability. Objective evaluation of mitochondrial morphology demonstrated characteristics consistent with high-amplitude swelling. @entity205 pretreatment protected against the development of these LPS-induced @entity2383 , an effect not attributable to the suppression of lipopolysaccharide-induced @entity5 necrosis factor-alpha production. CONCLUSIONS: These investigations are the first to demonstrate a protective effect of @entity205 against @entity2383 in a representative systemic organ during acute @entity5694 . We propose that @entity2383 likely related to induction of the mitochondrial permeability transition may participate in the pathogenesis of systemic organ injury and organ failures during acute @entity295 .
