Expression of HIF-1α in Ischemia and Reperfusion in Human Microsurgical Free Muscle Tissue Transfer

Dragu, Adrian; Schnürer, Stefan; Surmann‐Schmitt, Cordula; Unglaub, Frank; Kneser, Ulrich; Horch, Raymund E.

doi:10.1097/prs.0b013e318213a01f

Cited by 17 publications

(11 citation statements)

References 39 publications

(33 reference statements)

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“…The protein also has a protective effect on fibroblasts [30]. Expression of HIF-1 α does not increase in muscle flaps during ischemia [31], attributed to the already high levels of HIF-1 α in muscle tissue. In contrast, the HIF-1 α expression in our study was statistically higher after IR injury in all zones of muscle and skin tissues, indicating that the tissue tolerance against ischemia increased.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Botulinum Toxin A on Ischemia-Reperfusion Injury in a Rat Model

Park

2017

BioMed Research International

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Introduction While studies using various materials to overcome ischemia-reperfusion (IR) injury are becoming increasingly common, studies on the effects of botulinum toxin A (BoTA) on IR injury in musculocutaneous flaps are still limited. The purpose of this study was to examine our hypotheses that BoTA provide protection of musculocutaneous flap from ischemia-reperfusion injury. Method Five days after pretreatment injection (BoTA versus normal saline), a right superior musculocutaneous flap (6 × 1.5 cm in size) was made. Ischemia was created by a tourniquet strictly wrapping the pedicle containing skin and muscle for 8 h. After ischemia, the tourniquet was cut, and the musculocutaneous flap was reperfused. Results The overall survival percentage of flap after 8 h of pedicle clamping followed by reperfusion was 87.32 ± 3.67% in the control group versus 95.64 ± 3.25% in the BoTA group (p < 0.001). The BoTA group had higher expression of CD34, HIF-1α, VEGF, and NF-kB comparing to control group in qRT-PCR analysis. Conclusions In this study, we found that local BoTA preconditioning yielded significant protection against IR injury in a rat musculocutaneous flap model.

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Section: Discussionmentioning

confidence: 99%

The Effect of Botulinum Toxin A on Ischemia-Reperfusion Injury in a Rat Model

Park

2017

BioMed Research International

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“…However, 1 report seems to indicate that the protein content of active HIF-1 in muscle cells remains stable during ischemia and subsequent reperfusion. 7 This is attributed to the fact that, in physiologic situations, muscle cells already have a high content of HIF-1 to maintain metabolic homeostasis in normoxia. 7,39 In chronic conditions such as diabetic ulceration and ischemia, HIF plays a pivotal role in endothelial progenitor cell stimulation.…”

Section: Hypoxia-inducible Factor 1>mentioning

confidence: 99%

“…7 This is attributed to the fact that, in physiologic situations, muscle cells already have a high content of HIF-1 to maintain metabolic homeostasis in normoxia. 7,39 In chronic conditions such as diabetic ulceration and ischemia, HIF plays a pivotal role in endothelial progenitor cell stimulation. It may, however, have less of a role in the more acute situations characterized by most IRIs.…”

Section: Hypoxia-inducible Factor 1>mentioning

confidence: 99%

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Ischemia-Reperfusion Injury

Widgerow

2014

Annals of Plastic Surgery

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Ischemia-reperfusion injury forms the basis of tissue damage and cellular apoptosis in many pathologic and traumatic processes. The tissue damage follows a natural progression of cellular and metabolic events initiated by an ischemic episode. Ischemia causes intracellular/extracellular changes principally resulting in increased intracellular calcium, pH changes, and adenosine triphosphate depletion that end in cell death if the process is not interrupted. This interruption takes the form of reperfusion, characterized by a "flushing" of tissues with toxic metabolites, principally reactive oxygen species. The immediate effect is mitochondrial pore permeability, complement activation, cytochrome release, cytokine activation, inflammation, edema, neutrophil platelet adhesion, capillary plugging, and thrombosis. This sets the stage for the long recognized "no-reflow" phenomenon and progressive tissue death. Current recognition of cellular "cross-talk" and molecular events have introduced new logical strategies to sequentially combat the events occurring in relation to ischemia-reperfusion injury. These include mechanical preconditioning and pharmacological preconditioning and postconditioning strategies. It is likely that success in reversing or limiting tissue damage will be found in a sequential multitargeted approach using a combination of these strategies-clinical trials in this regard are sorely needed.

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“…If any delay during the operation occurs while the flap is already harvested from its donor area, ischemic time is critically prolonged. The mechanisms induced during a period of ischemia and reperfusion are not fully explored, but research is being conducted in this direction [14,15]. So far, little standardized approach is presented that solves the free flaps ischemic time issue.…”

Section: Introductionmentioning

confidence: 99%