Value of remote ischaemic preconditioning in rat dorsal skin flaps and clamping time

Masaoka, Kosuke; Asato, Hirotaka; Umekawa, Kohei; Imanishi, Masaya; Suzuki, Ayako

doi:10.3109/2000656x.2015.1106410

Cited by 7 publications

(3 citation statements)

References 19 publications

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“…RIPC induced HO-1 in kidney, heart, and skeletal muscles, but not in the skin. Although RIPC had previously been shown to target the skin [44,45,46,48], both early and late RIPC did not affect cutaneous wound closure. In addition, skin morphology and collagen deposition at day-7 wounds did not change after early or late RIPC.…”

Section: Discussionmentioning

confidence: 99%

“…Data from animal and human studies demonstrated the need for careful interpretation because of translational differences [38,39,40,41,42,43]. RIPC improves microcirculation by an increase in tissue oxygenation and capillary blood flow in the skin [44] and skin flaps [45], and forms a novel target for skin flap transplantation [46] and the healing of diabetic foot ulcers [47,48]. Although RIPC has been shown to protect in several models of tissue injury, its role in cutaneous excisional wound healing is still unclear.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Remote Ischemic Preconditioning on Heme Oxygenase-1 Expression and Cutaneous Wound Repair

Cremers

Wever

Wong

et al. 2017

IJMS

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Skin wounds may lead to scar formation and impaired functionality. Remote ischemic preconditioning (RIPC) can induce the anti-inflammatory enzyme heme oxygenase-1 (HO-1) and protect against tissue injury. We aim to improve cutaneous wound repair by RIPC treatment via induction of HO-1. RIPC was applied to HO-1-luc transgenic mice and HO-1 promoter activity and mRNA expression in skin and several other organs were determined in real-time. In parallel, RIPC was applied directly or 24h prior to excisional wounding in mice to investigate the early and late protective effects of RIPC on cutaneous wound repair, respectively. HO-1 promoter activity was significantly induced on the dorsal side and locally in the kidneys following RIPC treatment. Next, we investigated the origin of this RIPC-induced HO-1 promoter activity and demonstrated increased mRNA in the ligated muscle, heart and kidneys, but not in the skin. RIPC did not change HO-1 mRNA and protein levels in the wound 7 days after cutaneous injury. Both early and late RIPC did not accelerate wound closure nor affect collagen deposition. RIPC induces HO-1 expression in several organs, but not the skin, and did not improve excisional wound repair, suggesting that the skin is insensitive to RIPC-mediated protection.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of Remote Ischemic Preconditioning on Heme Oxygenase-1 Expression and Cutaneous Wound Repair

Cremers

Wever

Wong

et al. 2017

IJMS

View full text Add to dashboard Cite

show abstract

“…We evaluated several different methods of preconditioning to include direct skin flap tissue IP and remote hind limb IP in diabetic rats. Existing studies regarding the effects of IP on skin flaps showed that in normal physiological conditions this approach has therapeutic potential [ 18 – 21 ]. These studies are conducted in healthy rats, in the absence of decreased responsiveness of the endothelium.…”

Section: Discussionmentioning

confidence: 99%

Ischaemic Preconditioning Suppresses Necrosis of Adipocutaneous Flaps in a Diabetic Rat Model Regardless of the Manner of Preischaemia Induction

Ottomann

Küntscher

Hartmann

et al. 2017

Dermatology Research and Practice

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Ischaemic insult in the skin flaps is a major problem in reconstructive surgery particularly in patients with diabetes mellitus. Here, we sought to investigate the effectiveness of ischaemic preconditioning (IP) on diabetic skin flaps in rat animal model. Hundred Wistar rats (90 streptozotocin treated animals and 10 nondiabetic controls) were used. Diabetes mellitus was confirmed by measuring glucose level in blood, HbA1c, and ketonuria. We used blood vessel clamping, hind limb tourniquet, and NO donors (Spermine/NO complex) to induce short-term ischaemia of tissues that will be excised for skin flaps. Animals were followed for 5 days. Flaps were photographed at day 5 and percent of necrosis was determined using planimetry. Significant decrease in percent of necrotic tissue in all groups that received preconditioning was observed. Results show that ischaemic preconditioning suppresses flap necrosis in diabetic rats irrespective of direct or remote tissue IP and irrespective of chemically or physically induced preischaemia. Spermine/NO complex treatment 10 minutes after the flap ischaemia suppressed tissue necrosis. Treatment with NO synthase inhibitor L-NAME reversed effects of IP showing importance of NO for this process. We show that IP is a promising approach for suppression of tissue necrosis in diabetic flaps and potential of NO pathway as therapeutic target in diabetic flaps.

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Impacts of arterial ischemia or venous occlusion on vascularized groin lymph nodes in a rat model

Tinhofer

Yang

Chen

et al. 2019

Journal of Surgical Oncology

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BackgroundReported ischemia time of vascularized lymph nodes was 5 hours. This study investigated the effects of arterial ischemia and venous occlusion on vascularized lymph node function in rats.MethodsBilateral pedicled groin lymph node flaps were raised in 27 Lewis rats. Femoral artery and vein were separated and clamped for 1, 3, 4, or 5 hour(s). Lymph node flap perfusion and drainage were assessed by laser Doppler flowmetry and indocyanine green lymphography. Histologic changes were assessed using hematoxylin and eosin stain, terminal deoxynucleotidyl transferase‐mediated dUTP nick end‐labeling (TUNEL), and glutathione assays.ResultsPerfusion units of 2.84 ± 1.41, 2.46 ± 0.64, 2.42 ± 0.37, and 2.01 ± 0.90 were measured in arterial ischemia groups, and 1.71 ± 0.45, 2.20 ± 0.98, 1.49 ± 0.35, and 0.81 ± 0.20 in venous occlusion groups after 1, 3, 4, and 5 hours of clamping, respectively. Lymphatic drainage showed mean latency periods of 5.33 ± 0.88, 9.00 ± 3.21, 10.00 ± 2.08, and 24.50 ± 11.50 seconds in arterial clamping groups, and 25.00 ± 3.61, 26.00 ± 3.06, 23.33 ± 4.41, and 152.00 ± 0 seconds in venous clamping groups, respectively. Severe medullary and cortical congestion and hemorrhage on histology and cell damage by glutathione levels and TUNEL assay were found after 4 hours of venous clamping.ConclusionsArterial ischemia and venous occlusion impact the function and viability of vascularized lymph node flaps differently. The critical venous occlusion time was 4 hours.

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Value of remote ischaemic preconditioning in rat dorsal skin flaps and clamping time

Abstract: RIPC consisting of 60 min of ischaemic preconditioning may be clinically useful as a method of preventing skin flap necrosis.

Cited by 7 publications

References 19 publications

Effects of Remote Ischemic Preconditioning on Heme Oxygenase-1 Expression and Cutaneous Wound Repair

Effects of Remote Ischemic Preconditioning on Heme Oxygenase-1 Expression and Cutaneous Wound Repair

Ischaemic Preconditioning Suppresses Necrosis of Adipocutaneous Flaps in a Diabetic Rat Model Regardless of the Manner of Preischaemia Induction

Impacts of arterial ischemia or venous occlusion on vascularized groin lymph nodes in a rat model

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