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• W2740647515 abstract "Background: Critical perfusion conditions may impair the function of surgical flaps resulting in partial or even total necrosis. Statins have shown to exert protection in myocardial ischemia through antioxidative, antiapoptotic, anti-inflammatory and angiogenic effects. Herein we studied, whether simvastatin, an inhibitor of the HMG-CoA-reductase, may be effective to confine necrosis in critically perfused myocutaneous flaps by reducing microvascular dysfunction and ischemia-induced inflammation. Methods: Ar andomly perfused musculocutaneous flap was elevated and fixed into a dorsal skinfold chamber of C57BL/6 mice. Microcirculation in arterioles and capillaries, ischemiainduced inflammatory response, i.e. leukocyte-endothelial cell interaction and apoptotic cell death, neovascularization and tissue necrosis were determined over a 10-day period by intravital fluorescence microscopy. Animals were pretreated with simvastatin (5 mg/kg body weight per injection) 24 h and 30 min before flap elevation (n = 7; simvastatin). Additional simvastatin was administered daily for 3c onsecutive days after flap elevation. Saline-treated animals served as controls (n =7 ; control). Results: Persistent ischemia in controls induced a considerable inflammatory response characterized by leukocyte-endothelial cell interaction whereas simvastatin was able to significantly reduce this response (control: day 1: 408 ± 47 vs simvastatin: 175 ± 64 adherent leukocytes/mm 2 endothelial surface; p < 0.05 vs control). Also, simvastatin resulted in a marked decrease of apoptotic cell death (control: day 3: 218 ± 22 vs simvastatin: 92 ± 12 cells/mm 2 ; p < 0.05). Despite a comparable dilatory response observed in all animals, we noted significant decrease of capillary perfusion within the critically perfused flap tissue only in untreated mice (control: day 1: 84 ± 27 cm/cm2; day 10: 48 ± 20 cm/cm2; simvastatin: day 1: 220 ± 12 cm/cm2; day 10: 244 ± 12 cm/cm2 ;p<0 .001). The new formation of microvascular structures was observed only in simvastatin pretreated animals. Taken together, these effects resulted in a significant reduction of tissue necrosis (control; day 10: 50 ± 4 % vs simvastatin; 23 ±5 % of common flap surface; p<0 .05). Conclusions: These findings indicate, that pretreatment with simvastatin of critically perfused flap tissue is able to reduce ischemia-induced inflammatory response and apoptotic cell death, which is associated with the maintenance of nutritive capillary perfusion and an angiogenic response. Taken together, this interplay of simvastatin-mediated cellular and microvascular protection significantly reduces ischemia-induced tissue necrosis and may thus represent an alternative to pharmacologically manipulate the survival of ischemically challenged flaps." @default.
• W2740647515 created "2017-08-08" @default.
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• W2740647515 date "2009-01-01" @default.
• W2740647515 modified "2023-09-24" @default.
• W2740647515 title "Simvastatin vermindert die ischämiebedingte Entzündung und stimuliert die Neovaskularisierung in kritisch durchbluteten Lappen Simvastatin reduces ischemia-induced inflammation and stimulates neovascularisation of critically perfused flaps" @default.
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