Preventive effect of botulinum toxin A in microanastomotic thrombosis: A rabbit model

Fathi, Mehdi; Fathi, Hamidreza; Mazloumi, Mehdi; Khalilzadeh, Omid; Amanpour, Saeid; Meysamie, Alipasha; Mashali, Leila; Kardar, Mohammad H.

doi:10.1016/j.bjps.2010.05.030

Cited by 28 publications

(26 citation statements)

References 12 publications

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“…Several previous studies have reported that treatment of the microvasculature with BTX-A causes an increase in the arteriolar diameter and a subsequent increase in blood flow20212223. In addition, pre-treatment with BTX-A was associated with a lower rate of arterial and venous thrombosis in an animal model microanastomosis31. The damage of the vascular endothelium, including capillary narrowing, vascular infarction and spasm, is associated with the pathogenesis of I/R injury.…”

Section: Discussionmentioning

confidence: 94%

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Protective effect of botulinum toxin A after cutaneous ischemia-reperfusion injury

Uchiyama

Yamada

Perera

et al. 2015

Sci Rep

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Botulinum toxin A (BTX-A) blocks the release of acetylcholine vesicles into the synaptic space, and has been clinically used for aesthetic indications, neuromuscular disorders and hyperhidrosis. Several studies have demonstrated that BTX-A enhanced the blood flow and improved ischemia in animal models. Our objective was to assess the effects of BTX-A on cutaneous ischemia-reperfusion (I/R) injuries, mimicking decubitus ulcers. The administration of BTX-A in I/R areas significantly inhibited the formation of decubitus-like ulcer in cutaneous I/R injury mouse model. The number of CD31+ vessels and αSMA+ pericytes or myofibroblasts in wounds were significantly increased in the I/R mice treated with BTX-A. The hypoxic area and the number of oxidative stress-associated DNA-damaged cells and apoptotic cells in the I/R sites were reduced by BTX-A administration. In an in vitro assay, BTX-A significantly prevented the oxidant-induced intracellular accumulation of reactive oxygen species (ROS) in vascular endothelial cells. Furthermore, the administration of BTX-A completely suppressed the ulcer formation in an intermittent short-time cutaneous I/R injury model. These results suggest that BTX-A might have protective effects against ulcer formation after cutaneous I/R injury by enhancing angiogenesis and inhibiting hypoxia-induced cellular damage. Exogenous application of BTX-A might have therapeutic potential for cutaneous I/R injuries.

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Section: Discussionmentioning

confidence: 94%

“…ROS induced by I/R injury causes apoptosis and subsequent secondary necrosis, and these responses induce inflammation in the I/R area3132. At first, we examined whether hypoxia and/or oxidative stress are related to the apoptosis in I/R area at 1 day after reperfusion.…”

Section: Resultsmentioning

confidence: 99%

Protective effect of botulinum toxin A after cutaneous ischemia-reperfusion injury

Uchiyama

Yamada

Perera

et al. 2015

Sci Rep

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“…Vasospasm can be minimized by local application of papaverine hydrochloride. Fathi et al [11] showed in rabbit ear vessels that botulinum toxin enhances vessel diameter and consequently venous and arterial anastomosis patency.…”

Section: Pathophysiology Of Anastomotic Thrombosismentioning

confidence: 99%

A Review of Thrombosis and Antithrombotic Therapy in Microvascular Surgery

Froemel¹,

Fitzsimons²,

Frank

et al. 2013

Eur Surg Res

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Despite a remarkable expansion of microsurgery, there is still no international consensus about routinely used prophylactic antithrombotic agents. Most treatment regimens still use aspirin, heparin (low-molecular-weight and unfractionated heparin) or colloids (hydroxyphenylacetate 6%/dextran); however, clear evidence for the clinical benefit of an ideal administration regimen or one agent over the other has not yet been established. Instead of searching for the one regime that fits all, an increasing number of reviews from different disciplines describe multistep approaches that optimize what has been shown to be most promising. This includes the use of antithrombotic agents, proper risk assessment, secondary prevention and professional training to optimize microsurgical skills. In this review, we describe factors included in traditional approaches and also emphasize the value of good surgical technique, which while recognized by all to be one of the most important factors for success, receives less emphasis in reviews describing thrombosis prophylaxis in microvascular surgery.

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“…The ROS induced by I/R injury cause apoptosis and subsequent secondary necrosis, and these responses induce inflammation in the I/R area . We previously demonstrated that hypoxia‐induced apoptosis and/or oxidative stress‐induced apoptosis were observed in the cutaneous I/R area .…”

Section: Resultsmentioning

confidence: 99%

Topical betamethasone butyrate propionate exacerbates pressure ulcers after cutaneous ischemia–reperfusion injury

Uchiyama

Yamada

Perera

et al. 2016

Experimental Dermatology

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Ischaemia-reperfusion (I/R) is involved in the development of various organ diseases. There has been increasing evidence that cutaneous I/R injury is associated with the pathogenesis of pressure ulcers (PUs), especially at the early stage presenting as non-blanchable erythema. However, there is no evidence-based treatment for early-stage PUs. Our objective was to assess the effects of topical steroid on the development of PUs after cutaneous I/R injury in mice. Cutaneous I/R was performed by trapping the dorsal skin between two magnetic plates for 12 h, followed by plate removal. Topical application of betamethasone butyrate propionate (BBP) in I/R areas significantly increased the size of PUs after I/R. The number of thromboses was increased, and CD31(+) vessels were decreased in the I/R area treated with topical BBP. The number of oxidative stress-associated DNA-damaged cells and apoptotic cells in the I/R area was increased by topical BBP treatment. In addition, the mRNA level of NADPH oxidase 4 (Nox4), the essential enzyme that produces reactive oxygen species, was significantly increased and that of NF-E2-related factor 2 (Nrf2), a transcription factor that regulates the expression of antioxidant proteins, was inhibited in the I/R area treated by BBP. The number of CD68(+) macrophages and the level of transforming growth factor-beta in lesional skin were also decreased by BBP. These results suggest that a topical steroid might accelerate the formation of PUs induced by cutaneous I/R injury by aggravating oxidative stress-induced tissue damage. Topical steroids might not be recommended for the treatment of acute-phase decubitus ulcers.

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Preventive effect of botulinum toxin A in microanastomotic thrombosis: A rabbit model

Cited by 28 publications

References 12 publications

Protective effect of botulinum toxin A after cutaneous ischemia-reperfusion injury

Protective effect of botulinum toxin A after cutaneous ischemia-reperfusion injury

A Review of Thrombosis and Antithrombotic Therapy in Microvascular Surgery

Topical betamethasone butyrate propionate exacerbates pressure ulcers after cutaneous ischemia–reperfusion injury

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