An Experimental Neurovascular Island Skin Flap for the Study of the Delay Phenomenon

Finseth, Frederick; Cutting, Court B.

doi:10.1097/00006534-197803000-00016

Cited by 110 publications

(41 citation statements)

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“…Finseth and Cutting describe this survival as (40.5 cm 2 + 10.4 cm 2 ) of an 81-cm 2 flap-62.8% total survival. 5 If a similar pattern/area of survival can be assumed in the present model, then the effect of preischemically administered aprotinin (with 52.3 ± 5.4% survival, close to 62.8%) simply may be negating the global ischemic episode. Further study is warranted to investigate separately these different sides of the ischemia question, using purer models for each type of ischemia (e.g., nonischemic Finseth and Cutting flap or unilateral 10-hour ischemic flap).…”

mentioning

confidence: 68%

Aprotinin in Ischemia-Reperfusion injury: Flap survival and neutrophil response in a rat skin flap model

Cooley

1998

Microsurgery

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Finding a pharmacologic avenue for preventing ischemia/ reperfusion injury remains a continuing quest. Both old and new agents have been investigated in this search. Dr. Stadelmann et al. have explored the use of a relatively old but important compound, aprotinin, for preventing ischemiarelated flap necrosis. A broad-spectrum serine protease inhibitor, aprotinin has achieved clinical status for its hemostatic effects when given during cardiovascular surgery [1][2][3] and hip replacement surgery. 4 Despite its efficacy in reducing blood loss during these procedures, surgeons and scientists have not ascertained the mechanism of action for aprotinin.Dr. Stadelmann's group has found that preischemic (but not postischemic) treatment with aprotinin leads to greater survival territory in ischemic rat flaps. The flap model, originally described by Finseth and Cutting, 5 is an axialpattern island groin flap with a connecting random-pattern (contralateral groin) flap territory. The present authors modified this flap model by applying a 10-hour ischemic episode through clamping of the pedicle. Thus, the model has overlapping elements of both global and marginal ischemia. Along with this modification, these authors have reduced the flap dimensions of the original design from a 9 × 9 to a 6 × 6-cm flap in the same-sized rats. It would be helpful to know the area of flap survival without the ischemic interval in the smaller-dimensioned flaps. Finseth and Cutting describe this survival as (40.5 cm 2 + 10.4 cm 2 ) of an 81-cm 2 flap-62.8% total survival. 5 If a similar pattern/area of survival can be assumed in the present model, then the effect of preischemically administered aprotinin (with 52.3 ± 5.4% survival, close to 62.8%) simply may be negating the global ischemic episode. Further study is warranted to investigate separately these different sides of the ischemia question, using purer models for each type of ischemia (e.g., nonischemic Finseth and Cutting flap or unilateral 10-hour ischemic flap).Dr. Stadelmann et al. have highlighted neutrophils as the potential targets for the beneficial effects of aprotinin. A rigorous control for the myeloperoxidase assay was not applied in their study, specifically, evaluation of the effect of aprotinin administration on neutrophil myeloperoxidase activity. Without this control, we can only assume that aprotinin did not interfere with the assay and that the assay accurately reflected the proportion of retained neutrophils in the biopsied flap tissue. The biopsy site was also located in an area where the effects of marginal and global ischemia may have been overlapping. This may account for the large scatter in the data among groups and time points, i.e., slight variations in the biopsy sites could lead to major differences in neutrophil levels.Clinical use of aprotinin in coronary bypass surgery has emphasized its role in inhibiting enzymes of the coagulation cascade, fibrinolysis, and/or platelet adhesion/aggregation.1-3 Neutrophil function after aprotinin administration is also pro...

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mentioning

confidence: 68%

Aprotinin in Ischemia-Reperfusion injury: Flap survival and neutrophil response in a rat skin flap model

Cooley

1998

Microsurgery

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“…Siemionow et al attributed the acute increases in arteriolar diameters and red blood cell velocities observed in a cremaster muscle model (island flap) and in a replanted composite-limb-cremaster graft to sympathectomy due to pedicle isolation and to muscle denervation following transection of the genitofemoral nerve (12,150). In skin flaps, too, blood flow increases after denervation because of the decline in vascular resistance (42,61,102). In a new skin island flap in Syrian hamsters, Erni et al (36) showed higher flow values than in the control after sympathectomy by neural blockade.…”

Section: Free Muscle Flapsmentioning

confidence: 99%

“…Several studies have shown that blood flow increases in a denervated muscle (23,88,135,149,187). Sympathectomy relieves arteriolar vasoconstriction (23,42,61,149,187) leading to arteriolar vasodilation with increased capillary perfusion (23,149,187). Vasodilation is also due to loss of muscular tone after denervation.…”

Section: Intraoperative Blood Flow In Free Flapsmentioning

confidence: 99%

“…The main reason for the increased blood flow seems to have been a decline in vascular resistance at the arteriolar level in the free muscle flap. Sympathectomy, due to muscle denervation, could significantly increase blood flow by relieving arteriolar vasoconstriction (23,42,61,149,187). Muscular tone is also lost due to denervation, which facilitates vasodilation.…”

Section: Pre-and Postoperative Blood Flow In Free Flaps and The Recipmentioning

confidence: 99%

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Blood flow in free micro-vascular flaps

Lorenzetti¹,

Salmi²,

Tukiainen³

et al. 1998

Pathophysiology

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“…Accordingly, numerous experimental and clinical studies have evaluated the development of necrosis in both, axial pattern flaps (defined blood supply) and random pattern flaps (undefined blood supply) [1][2][3] . The main findings are commonly based on macroscopic evaluation of the size of the necrotic area.…”

Section: Introductionmentioning

confidence: 99%

Ischemic Tissue Injury in the Dorsal Skinfold Chamber of the Mouse: A Skin Flap Model to Investigate Acute Persistent Ischemia

Harder

Schmauß

Wettstein

et al. 2014

JoVE

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Despite profound expertise and advanced surgical techniques, ischemia-induced complications ranging from wound breakdown to extensive tissue necrosis are still occurring, particularly in reconstructive flap surgery. Multiple experimental flap models have been developed to analyze underlying causes and mechanisms and to investigate treatment strategies to prevent ischemic complications. The limiting factor of most models is the lacking possibility to directly and repetitively visualize microvascular architecture and hemodynamics. The goal of the protocol was to present a well-established mouse model affiliating these before mentioned lacking elements. Harder et al. have developed a model of a musculocutaneous flap with a random perfusion pattern that undergoes acute persistent ischemia and results in ~50% necrosis after 10 days if kept untreated. With the aid of intravital epi-fluorescence microscopy, this chamber model allows repetitive visualization of morphology and hemodynamics in different regions of interest over time. Associated processes such as apoptosis, inflammation, microvascular leakage and angiogenesis can be investigated and correlated to immunohistochemical and molecular protein assays. To date, the model has proven feasibility and reproducibility in several published experimental studies investigating the effect of pre-, peri-and postconditioning of ischemically challenged tissue.

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An Experimental Neurovascular Island Skin Flap for the Study of the Delay Phenomenon

Cited by 110 publications

References 0 publications

Aprotinin in Ischemia-Reperfusion injury: Flap survival and neutrophil response in a rat skin flap model

Aprotinin in Ischemia-Reperfusion injury: Flap survival and neutrophil response in a rat skin flap model

Blood flow in free micro-vascular flaps

Ischemic Tissue Injury in the Dorsal Skinfold Chamber of the Mouse: A Skin Flap Model to Investigate Acute Persistent Ischemia

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