Preventive Effect of Dexmedetomidine in Ischemia-Reperfusion Injury

Uysal, Hale Yarkan; Cuzdan, Suat Sedat; Kayran, Oğuz; Başar, Hülya; Fidanc, Vildan; Afyoncu, Ebru; Üstün, Hüseyin; Gülbahçe, Rukiye

doi:10.1097/scs.0b013e3182519f24

Cited by 14 publications

(15 citation statements)

References 12 publications

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“…A decrease in kidney tissue MDA level in the sepsis + dex group suggests that dexmedetomidine attenuates lipid peroxidation. Dexmedetomidine reduced the brain and testis MDA levels in ischemia-perfusion models in previous studies [52–55]. However, we did not find any study that investigates the effects of dexmedetomidine on lipid peroxidation in sepsis.…”

Section: Discussionmentioning

confidence: 56%

The Effects of Dexmedetomidine on Secondary Acute Lung and Kidney Injuries in the Rat Model of Intra‐Abdominal Sepsis

Koca

Olguner

Ergür

et al. 2013

The Scientific World Journal

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In the present study, the effects of dexmedetomidine on secondary lung and kidney injuries were studied in the rat model of intra-abdominal sepsis by immunohistological and biochemical examinations. We measured serum creatinine, kidney tissue malondialdehide and plasma neutrophil gelatinase-associated lipocalin levels. In order to evaluate tissue injury we determined kidney tissue mononuclear cell infiltration score, alveolar macrophage count, histological kidney and lung injury scores and kidney and lung tissue immunoreactivity scores. We demonstrated that dexmedetomidine attenuates sepsis-induced lung and kidney injuries and apoptosis in the rat model of sepsis. There is still need for comparative studies in order to determine the effects of dexmedetomidine on organ functions in early human sepsis.

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Section: Discussionmentioning

confidence: 56%

The Effects of Dexmedetomidine on Secondary Acute Lung and Kidney Injuries in the Rat Model of Intra‐Abdominal Sepsis

Koca

Olguner

Ergür

et al. 2013

The Scientific World Journal

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“…In agreement with these results, an investigation conducted by the authors also demonstrated that, prior to and following the ischemic insult, DEX administration, at doses of 10 and 30 µg/kg, reduced tissue MPO activity levels. This reduction was observed at the end of a 12-h and at the end of a seven-day reperfusion (59). However, DEX, at clinically relevant doses, did not significantly affect the expression of inflammatory molecules in activated macrophages.…”

Section: Inflammatory Responsementioning

confidence: 82%

Molecular targets and mechanism of action of dexmedetomidine in treatment of ischemia/reperfusion injury (Review)

Cai

Jia

et al. 2014

Molecular Medicine Reports

113

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Abstract. Dexmedetomidine (DEX), a highly specific α 2 -adrenergic agonist, which exhibits anaesthetic-sparing, analgesia and sympatholytic properties. DEX modulates gene expression, channel activation, transmitter release, inflammatory processes and apoptotic and necrotic cell death. It has also been demonstrated to have protective effects in a variety of animal models of ischemia/reperfusion (I/R) injury, including the intestine, myocardial, renal, lung, cerebral and liver. The broad spectrum of biological activities associated with DEX continues to expand, and its diverse effects suggest that it may offer a novel therapeutic approach for the treatment of human diseases with I/R involvement.

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“…An epigastric island skin flap 3 × 6 cm in size was made in the left lower quadrant of the abdomen, leaving the superficial epigastric artery and vein as the only connections, as described by Manson et al The femoral artery and vein were isolated proximally and distally. Ischemia was induced by applying a single microvascular clamp across the pedicle vessels (Figure ), as described by Uysal et al After 6 hours of ischemia, the clamp was removed and the pedicles were examined under an operating microscope to document flap reperfusion, and the flap was sutured to its donor site with a 5‐0 silk continuous suture. Flaps that did not reperfuse were not included.…”

Section: Methodsmentioning

confidence: 99%

Role of the p38 mitogen‐activated protein kinase signaling pathway in estrogen‐mediated protection following flap ischemia‐reperfusion injury

Hou

2016

Cell Biochemistry & Function

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Ischemia-reperfusion (I/R) injury often occurs during skin flap transplantation and results in tissue damage. Although estrogen treatment significantly alleviates this I/R injury-induced damage, the detailed molecular mechanism is not clear. In this study, a superficial epigastric artery flap I/R injury model was created in adult Wistar rats. Severe necrosis was observed in skin tissue after I/R injury. Histological examination of skin tissue revealed that I/R injury damages skin structure and results in neutrophil infiltration. Inflammation-related parameters, including neutrophil count, tumor necrosis factor-α, and interleukin-10 levels, were increased due to I/R injury. These pathological phenomena were reduced by estradiol treatment. Further investigation found that I/R injury triggers the p38 mitogen-activated protein kinase (p38-MAPK) pathway. The expression levels of p38-MAPK and phosphorylated p38-MAPK were increased after I/R injury. Estradiol increased the expression level of MAPK phosphatase-2, a putative phosphatase of p38, and reduced the levels of p38-MAPK and phosphorylated p38-MAPK. These results suggest that estradiol can improve skin flap survival, possibly by inhibiting neutrophil infiltration and the expression of p38-MAPK. This study provides an explanation for how estrogen alleviates I/R injury-induced damage that occurs during skin flap transplantation. In a rat pathological model, I/R injury leads to skin necrosis, skin structure damage, neutrophil infiltration, and inflammatory cytokine secretion, which are probably downstream effects of activation of the p38-MAPK pathway. On the other hand, estradiol treatment triggers the expression of MAPK phosphatase-2, a putative phosphatase of p38-MAPK, and reduced all examined pathological phenomena. Therefore, estrogen may reduce the deleterious effect of I/R injury on skin flap transplantation through modulating the p38-MAPK pathway.

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Preventive Effect of Dexmedetomidine in Ischemia-Reperfusion Injury

Abstract: We conclude that administering dexmedetomidine before I/R periods can reduce ischemia-reperfusion injury of flaps, and it has a beneficial effect on flap survival.

Cited by 14 publications

References 12 publications

The Effects of Dexmedetomidine on Secondary Acute Lung and Kidney Injuries in the Rat Model of Intra‐Abdominal Sepsis

The Effects of Dexmedetomidine on Secondary Acute Lung and Kidney Injuries in the Rat Model of Intra‐Abdominal Sepsis

Molecular targets and mechanism of action of dexmedetomidine in treatment of ischemia/reperfusion injury (Review)

Role of the p38 mitogen‐activated protein kinase signaling pathway in estrogen‐mediated protection following flap ischemia‐reperfusion injury

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