Effect of Ischemia and Reperfusion on Skeletal Muscle Damage

2010 ◽  
Author(s):  
Sandra Loerakker ◽  
Emmy Manders ◽  
Gustav J. Strijkers ◽  
Frank P. T. Baaijens ◽  
Dan L. Bader ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Soft Tissues ◽  
Ischemia Reperfusion Injury ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Ischemia And Reperfusion ◽  
Skin Damage ◽  
Deep Tissue ◽  
Skeletal Muscle Damage

Sustained mechanical loading of soft tissues covering bony prominences, as experienced by bedridden and wheelchair-bound individuals, may cause skeletal muscle damage. This can result in a condition termed pressure-related deep tissue injury (DTI), a severe kind of pressure ulcer that initiates in deep tissue layers, and progresses towards the skin. Damage pathways leading to DTI can involve ischemia, ischemia/reperfusion injury, impaired lymphatic drainage, and sustained tissue deformation. Recently, we have provided evidence that in a controlled animal model, deformation is the main trigger for damage within a 2h loading period [1,2]. However, ischemia and reperfusion may play a more important role in the damage process during prolonged loading periods.

Effect of Continuous and Intermittent Mechanical Loading on the Development of Skeletal Muscle Damage - A Combined Experimental/Numerical Approach

2009 ◽  
Author(s):  
Sandra Loerakker ◽  
Anke Stekelenburg ◽  
Gustav J. Strijkers ◽  
Klaas Nicolay ◽  
Dan L. Bader ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Mechanical Loading ◽  
Soft Tissues ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Clear Correlation ◽  
Tissue Deformation ◽  
Deep Tissue ◽  
Skeletal Muscle Damage

Prolonged mechanical loading of soft tissues, as present when individuals are bedridden or wheelchair-bound, can lead to degeneration of skeletal muscle tissue. This can result in a condition termed pressure-related deep tissue injury (DTI), a severe kind of pressure ulcer that initiates in deep tissue layers, e.g. skeletal muscle, near bony prominences and progresses towards the skin. Complications associated with DTI include sepsis, renal failure, and myocardial infarction. Damage pathways leading to DTI involve ischemia, ischemia-reperfusion injury, impaired lymphatic drainage, and sustained tissue deformation. Recently, the role of tissue deformation in the onset of skeletal muscle damage was established by combining animal experiments with finite element (FE) modeling [1]. After 2 hours of continuous loading, a clear correlation between maximum shear strain and damage was found.

Modelling the effect of repositioning on the evolution of skeletal muscle damage in deep tissue injury

2012 ◽  
Vol 12 (2) ◽  
pp. 267-279 ◽  
Author(s):  
Jan Demol ◽  
Dorien Van Deun ◽  
Bart Haex ◽  
Hans Van Oosterwyck ◽  
Jos Vander Sloten
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Tissue Injury ◽  
Deep Tissue ◽  
Deep Tissue Injury ◽  
Skeletal Muscle Damage

The Relative Contributions of Muscle Deformation and Ischemia to Pressure Ulcer Development

2012 ◽  
Author(s):  
Sandra Loerakker ◽  
Gustav J. Strijkers ◽  
Klaas Nicolay ◽  
Frank P. T. Baaijens ◽  
Dan L. Bader ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Tissue ◽  
Pressure Ulcer ◽  
Soft Tissues ◽  
Tissue Injury ◽  
Skeletal Muscle Tissue ◽  
Ischemia And Reperfusion ◽  
Deep Tissue ◽  
Deep Tissue Injury ◽  
Damage Process

Sustained mechanical loading of soft tissues covering bony prominences may lead to degeneration of skeletal muscle tissue. This can result in a condition termed deep tissue injury (DTI), a severe kind of pressure ulcer that initiates in deep tissue layers, and progresses towards the skin. Previously, we have provided evidence that in a controlled animal model, deformation is the main trigger for damage within a 2 h loading period [1,2]. Recently, we also showed that ischemia and reperfusion may contribute to the damage process during prolonged loading [3]. In the present study, we investigated the relative effects of deformation, ischemia, and reperfusion on the temporal and spatial damage process of skeletal muscle tissue during a 6 h period using magnetic resonance imaging (MRI) techniques.

Ischemia-reperfusion injury in isolated rat hindquarters

1990 ◽  
Vol 68 (1) ◽  
pp. 387-392 ◽  
Author(s):  
W. L. Sexton ◽  
R. J. Korthuis ◽  
M. H. Laughlin
Keyword(s):  
Skeletal Muscle ◽  
Vascular Resistance ◽  
Plasma Proteins ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ischemia And Reperfusion ◽  
Ischemic Period ◽  
Osmotic Reflection Coefficient ◽  
Period Duration ◽  
Isolated Rat

The purpose of this study was to determine the suitability of the maximally vasodilated (papaverine) isolated rat hindquarters preparation to study the effects of ischemia and reperfusion on the microvasculature of skeletal muscle. The osmotic reflection coefficient for plasma proteins (sigma) and total vascular resistance (RT, mmHg.ml-1.min.100 g-1) were determined before ischemic periods of 30, 60, 120, 180, and 240 min in intact (with skin) and 30, 60, and 120 min in skinned hindquarters and again after 60 min of reperfusion. In both intact and skinned hindquarters, reductions in sigma and increases in RT were observed during reperfusion and were correlated with the ischemic period duration. After 120 min of ischemia in intact and skinned hindquarters, sigma was reduced from preischemia values of 0.92 +/- 0.02 and 0.89 +/- 0.02 to 0.61 +/- 0.03 and 0.57 +/- 0.03, respectively, whereas RT was increased from preischemia levels of 8.9 +/- 0.3 and 8.1 +/- 0.1 to 28.4 +/- 2.9 and 74.2 +/- 16.8, respectively. The increases in RT were associated with proportional increases in skeletal muscle vascular resistance. Thus, in isolated rat hindquarters, increasing the duration of ischemia results in progressive increases in the permeability to plasma proteins (decreased sigma) and RT, which are associated primarily with skeletal muscle.

Serum and Urine Biomarker Elevation Indicating the Onset of Deep Tissue Injury as Examined on a Rat Model

2010 ◽  
Author(s):  
Mohsen Makhsous ◽  
Atek Pandya ◽  
Mauli Modi ◽  
Briana Reprogle ◽  
Christopher C. Chadwick ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Rat Model ◽  
Tissue Injury ◽  
Muscle Layer ◽  
Release Time ◽  
Deep Tissue ◽  
Fatty Acid Binding ◽  
Deep Tissue Injury ◽  
Serum And Urine

Deep tissue injury (DTI) is a serious pressure ulcer (PU) which initiates in deep tissue, mainly muscle, and progresses rapidly to a full-thickness wound [1, 2]. Therefore, an early indication should help in increasing awareness and providing prompt intervention to prevent it from progressing to an open wound, which is susceptible to infection and typically needs prolonged and aggressive care. However, the diagnosis of DTI is currently still vague at best[2] with only subjective tools. This situation calls for tools for objectively sensing the tissue changes while the skin is still intact, to allow development of evidence-based protocols for early diagnosis and treatment. Since DTI initiates from deep muscle layer around a bony prominence, a tool that sensitive to muscle damage may have the potential to objectively sense the onset of a DTI in clinical application. A number of molecular biomarkers have been reported in the literature as suitable for indicating muscle damage. Some of the most promising biomarkers are myoglobin and heart-type fatty acid binding protein (H-FABP). Myoglobin and H-FABP are two relatively small muscle proteins that show a very fast release time after skeletal muscle damage/necrosis when no myocardial infarction or damage is present; therefore, they may be used to identify skeletal muscle injury in DTI formation. The objective of this study was to initially test whether myoglobin and H-FABP in serum and urine respond quickly to pressure induced deep tissue injury on a rat model. It is expected that knowledge gained from this study may lead to a promising new methodology to sense the visually invisible DTI.

scholarly journals Cryotherapy reduces skeletal muscle damage after ischemia/reperfusion in rats

2012 ◽  
Vol 222 (2) ◽  
pp. 223-230 ◽  
Author(s):  
Gustavo O. Puntel ◽  
Nélson R. Carvalho ◽  
Fernando Dobrachinski ◽  
Andréia C. F. Salgueiro ◽  
Robson L. Puntel ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Ischemia Reperfusion ◽  
Skeletal Muscle Damage

No conversion of xanthine dehydrogenase to oxidase in canine cerebral ischemia

1990 ◽  
Vol 259 (6) ◽  
pp. H1655-H1659 ◽  
Author(s):  
R. B. Mink ◽  
A. J. Dutka ◽  
K. K. Kumaroo ◽  
J. M. Hallenbeck
Keyword(s):  
Free Radical ◽  
Cerebral Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Xanthine Dehydrogenase ◽  
Global Cerebral Ischemia ◽  
Ischemia And Reperfusion ◽  
Pentobarbital Sodium Anesthesia ◽  
Layer Chromatography

Xanthine oxidase (XO) has been implicated as a source of free radicals mediating ischemia-reperfusion injury. Conversion of the non-free radical generating xanthine dehydrogenase (XD) to the free radical producing XO during ischemia has been demonstrated in several tissues. We examined the irreversible conversion of XD to XO in the dog brain after ischemia and after ischemia and reperfusion. Under pentobarbital sodium anesthesia and by use of a cerebrospinal fluid compression model of global cerebral ischemia, dogs were subjected to 30 min of ischemia (n = 8) or 30 min of ischemia and 60 min of reperfusion (n = 8). A cerebral perfusion pressure of 60 mmHg was maintained during reperfusion. Eight control dogs were not subjected to ischemia. After the dogs were killed their brains were rapidly removed and frozen in liquid nitrogen. XO and XD + XO activities were measured with a radioassay utilizing 8-[14C]hypoxanthine and separating substrate and products by thin-layer chromatography. Total XD + XO activity was significantly (P less than 0.05) decreased after ischemia and reperfusion (35.6 +/- 8.0 vs. 60.8 +/- 20.8 nmol.min-1.g protein-1 in controls, means +/- SD) but not after ischemia alone (48.2 +/- 20.4). XO/(XD + XO) was approximately 20% in all three groups. Irreversible XD to XO conversion is not an important mechanism leading to early tissue injury in global cerebral ischemia.

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