scholarly journals Structural changes in skeletal muscles of the hind limbs of rats in acute ischemia-reperfusion and its correction by carbacetam, detected by polarization microscopy

2020 ◽  
pp. 30-35
Author(s):  
T. O. Veresiuk ◽  
P. R. Selskyy ◽  
A. T. Televiak
Keyword(s):  
Skeletal Muscle ◽  
Skeletal Muscles ◽  
Structural Changes ◽  
Ischemia Reperfusion ◽  
Acute Ischemia ◽  
Polarization Microscopy ◽  
Early Reperfusion ◽  
Hind Limbs ◽  
Reperfusion Period ◽  
Muscle Remodeling

Arterial tourniquets are used in clinical practice for angioplasty and arthroplasty, and in case of limb injuries, their use often occurs according to vital signs. After removing the tourniquet and blood supply restoration to the limb arises a multifactorial lesion of tissues both ischemic and distant from the site of ischemia. A number of publications have been devoted to the study of morphological disorders in muscle tissue in acute ischemia-reperfusion in the medical literature. However, the researches for effective means for drug correction of these disorders still continues. The aim of the study was to explore peculiarities of skeletal muscle remodeling of the hind limbs of rats, detected by polarization microscopy, in acute ischemia-reperfusion, caused by the application of an arterial tourniquet, and in the correction of reperfusion disorders by carbacetam. Microscopic examination of histological sections of skeletal muscles of the hind limbs of 60 rats below the site of application of the tourniquet under conditions of experimental acute ischemia-reperfusion was performed. Acute ischemia for all animals was caused by application of SWAT rubber bands on the hind limbs of animals, 5–6 mm in width, at the inguinal fold level within 2 hours under thiopental anesthesia. A reperfusion was modeled by removing the tourniquet. Half of the experimental animals in the reperfusion period for the purpose of correction intraperitoneally was administered the nootropic drug 1-oxo-3.3.6-trimethyl-1.2.3.4-tetrahydroindolo[2.3-c]quinoline (carbacetam) at a dose of 5 mg per kilogram of body weight once a day during the entire reperfusion period. The histological specimens of the skeletal muscles were stained with hematoxylin and eosin, and were examined with a light microscope with polarization nozzle. Studies with using the polarization microscopy have shown that in the early reperfusion period morphological criteria for skeletal muscle remodeling expressed by deformation and anisotropy of muscle fibers, disappearance of their transverse striation, cracks and ruptures of fibers, and in the most severe cases there were signs of necrosis of the fibers with their fragmentation into separate lumps. Subject to the correction of reperfusion disorders by carbacetam, there is a decrease in the degree of damage and consistent acceleration of restoration of the skeletal muscles structure, which was the most pronounced in groups of animals with reperfusion terms after 1 and 14 days. Complex of features indicates, that at the tissue level the administration of carbacetam as reduces the ischemic-reperfusion lesion of the muscular fibers, as also accelerates the mechanisms of reparative rhabdomyohistogenesis. Thus, structural changes in the skeletal muscles of the limb after two-hour ischemia and subsequent reperfusion increased in the early reperfusion period and reached its peak after 1 day of reperfusion, and in the late period of reperfusion their reverse development took place. With the correction of disorders by carbacetam, the degree of damage was reduced and the recovery of the skeletal muscle structure of the limb was accelerated.

Role of leukocyte accumulation and oxygen radicals in ischemia-reperfusion-induced injury in skeletal muscle

2001 ◽  
Vol 280 (4) ◽  
pp. H1716-H1721 ◽  
Author(s):  
M. G. Schlag ◽  
K. A. Harris ◽  
R. F. Potter
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Radicals ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Male Rats ◽  
Reactive Oxygen Metabolites ◽  
Early Reperfusion ◽  
Reperfusion Period ◽  
Highly Correlated

The role of leukocytes and nonleukocyte-derived reactive oxygen metabolites (ROMs) in reperfusion-induced skeletal muscle injury was determined. Male rats received 2 h no-flow hindlimb ischemia-reperfusion (I/R, n = 6) or were rendered neutropenic via antineutrophil serum (ANS) before I/R (I/R + ANS, n = 5). Oxygen radicals in the absence of neutrophils were tested by administration of dimethylthiourea (DMTU) (I/R + ANS + DMTU, n = 5). Perfused capillaries (CDper) and rolling (Lr), adherent (La), and extravasated leukocytes (Le) in the extensor digitorum longus muscle were measured every 15 min during 90 min of reperfusion using intravital microscopy. The vital dyes bisbenzimide (BB) and ethidium bromide (EB) provided direct measures of tissue injury (EB/BB). CDper decreased immediately on reperfusion in the I/R and I/R + ANS groups. CDper in the I/R + ANS + DMTU group remained at baseline throughout reperfusion. La increased in the I/R group; however, EB/BB was the same between I/R and I/R + ANS groups. Injury in the I/R + ANS + DMTU group did not differ from other groups ≥60 min, after which EB/BB became significantly lower. Le did not differ between groups and was highly correlated to tissue injury. The results suggest that Le lead to parenchymal injury, and ROMs lead to perfusion deficits during the early reperfusion period after ischemia.

scholarly journals Changes of biochemical indicators of blood serum and the skeletal muscle homogenate of the hind limbs of the rats in acute ischemia-reperfusion and in the condition of using of the carbacetam

2020 ◽  
Vol 24 (3) ◽  
pp. 373-380
Author(s):  
T. O. Veresiuk ◽  
P. R. Selskyy ◽  
A. T. Televiak
Keyword(s):  
Antioxidant Activity ◽  
Blood Serum ◽  
Biochemical Parameters ◽  
Skeletal Muscles ◽  
Total Bilirubin ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Hind Limbs ◽  
Reperfusion Period ◽  
Muscle Homogenate

Annotation. Simulation of ischemia-reperfusion causes the biochemical disorders and changes in the prooxidant-antioxidant system, both in the serum and skeletal muscles of the affected limb. The severity of local and systemic postischemic imbalance decreases in with correction with medicine from the group of nootropics – carabacetam. The aim of the study was determining the degree of metabolic disorders based on the analysis of changes in serum biochemical parameters and muscle homogenate in ischemic-reperfusion disorders caused by the imposition of an arterial tourniquet and under conditions of correction with carbacetam. Materials and methods. A biochemical study of blood serum and muscle homogenate of 60 rats was performed. Ischemia was simulated by applying SWAT rubber tourniquets on the hind limbs of the rats, on the inguinal fold, for 2 hours, and reperfusion was modeled by removing the tourniquet and restoring of blood circulation through 2 hours after its application. Observations of the animals were carried out during for 14 days. 30 rats in the reperfusion period were intraperitoneally administered the carbacetam at a dose of 5 mg per kilogram of body weight 1 time a day for 14 days of the reperfusion period. The Blood serum was separated and the soft tissue samples were taken below the turniquet site for the biochemical studies. Statistical processing of the material was performed using the package of programs “Microsoft Excel”. The largest deviations in serum were observed after 1 day of the reperfusion: an increase in creatinine by 28.16 % (p<0.005), total bilirubin by 20.75 % (p<0,005), ALT by 96.14 % (p<0,005), AST by 147.27 % (p<0.005) and alkaline phosphatase by 70.84 % (p<0.005), as well as an increase in prooxidant activity of CD by 77.27 % (p<0.005), CT 147.47 % (p<0,005) and TBC-AL by 82.52 % (p<0,005) against the background of a decrease in SOD activity by 9.77 % (p<0.005) and an increase in catalase levels by 15.37 % (p<0.005) relative to the value of the control group. The development of ischemia and reperfusion was accompanied by the largest increase in the level of prooxidants (CD – by 27.55 % (p<0.005), CT – by 47.34 % (p<0.05), TBC-AL – by 62.09 %) (p<0.005)) in the homogenate of the skeletal muscles after 2 hours after restoration of the blood supply. Antioxidant activity, on the other hand, decreased by 15.06 % (p<0.005) SOD and by 8.96 % (p<0.005) catalase after 1 day. After 14 days, a gradual increase and return of most of the studied values to the level of the control group. Under the influence of the carbacetam, the biochemical parameters of blood serum most significantly decreased in relative to the value of the groups without correction after 7 days of the experiment. The level of total bilirubin was lower by 29.65 % (p˂0.05), ALT by 14.95 % (p˂0.05), AST by 19.84 % (p˂0.05), alkaline phosphatase by 25.53 % (p˂0.05), and the difference in the content of diene, triene conjugates and TBC-LP was the largest after 1 day – by 17.09 % (p<0.005), 20,41 % (p<0.05) and 11.24 % (p<0.05), respectively. Under the conditions of correction, the indicators of SOD and catalase activity increased, being significantly higher than in the groups of the animals without correction, especially after 7 days of reperfusion – by 29.41 % (p<0.005) and by 15.71 % (p<0.05) in accordance. The content of the diene, triene conjugates and TBC-LP muscle homogenate was statistically significantly lower in the groups with the introduction of the carbacetam than in the groups of the animals without correction. The largest difference between the groups was found after 1 day with a difference of 9.16 % (p<0.05), 7.35 % (p<0.005) and 16.05 % (p<0.05), respectively. Antioxidant activity of SOD and catalase after 1 day was higher by 27.41 % (p<0.005) and by 25.13 % (p<0.005), compared with the group of the animals without introduction of the carbacetam. Thus, simulated ischemia-reperfusion is accompanied by the greatest biochemical disorders in the serum – after 1 day, and in the muscle homogenate – after 2 hours of the reperfusion. After 14 days of the experiment, most indicators still do not return to the level of the control group. The application of the correction helps to reduce the severity of biochemical disorders at the systemic and local levels, especially during periods of their greatest deviations.

Effects ofS-nitroso-N-acetylcysteine on contractile function of reperfused skeletal muscle

1998 ◽  
Vol 274 (3) ◽  
pp. R822-R829 ◽  
Author(s):  
Long-En Chen ◽  
Anthony V. Seaber ◽  
Rima M. Nasser ◽  
Jonathan S. Stamler ◽  
James R. Urbaniak
Keyword(s):  
Skeletal Muscle ◽  
Reperfusion Injury ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Protective Role ◽  
Control Group ◽  
Group Vi ◽  
No Donor ◽  
Early Reperfusion ◽  
Reconstructive Operations

The ultimate goal of replantation and microsurgical reconstructive operations is to regain or improve impaired function of the tissue. However, the data related to the influence of NO on tissue function are limited. This study evaluated the effects of the NO donor S-nitroso- N-acetylcysteine (SNAC) on contractile function of skeletal muscle during reperfusion. Forty-nine rats were divided into six groups. The extensor digitorum longus (EDL) muscles in groups I and II were not subjected to ischemia-reperfusion but were treated with a low (100 nmol/min) or high (1 μmol/min) dose of SNAC. In groups III- V, the EDL underwent 3 h of ischemia and 3 h of reperfusion and was also treated with low (100 nmol/min) or high doses (1 or 5 μmol/min) of SNAC. Group VI was a phosphate-buffered saline (PBS)-treated control group. Twenty additional animals were used to document systemic effects of SNAC and PBS only. SNAC or PBS was infused for 6.5 h, beginning 30 min before ischemia and continuing throughout the duration of reperfusion. Contractile testing compared the maximal twitch force, isometric tetanic contractile forces, fatigue, and fatigue half time of the experimental EDL and the contralateral nontreated EDL. The findings indicate that 1) SNAC does not influence contractile function of EDL muscle not subjected to ischemia-reperfusion, 2) SNAC significantly protects the contractile function of ischemic skeletal muscle against reperfusion injury in the early reperfusion period, and 3) the protective role of SNAC is critically dosage dependent; protection is lost at higher doses. The conclusion from this study is that supplementation with exogenous NO exerts a protective effect on the tissue against reperfusion injury.

scholarly journals Local Cooling Provides Muscle Flaps Protection from Ischemia-Reperfusion Injury in the Event of Venous Occlusion during the Early Reperfusion Period

Hand ◽  
2008 ◽  
Vol 4 (1) ◽  
pp. 19-23 ◽  
Author(s):  
Ryan S. Diederich ◽  
Arian Mowlavi ◽  
Garth Meldrum ◽  
Brad Medling ◽  
Reuben A. Bueno ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Venous Occlusion ◽  
Local Cooling ◽  
Muscle Flaps ◽  
Early Reperfusion ◽  
Reperfusion Period

Ischemic tolerance in skeletal muscle: role of nitric oxide

1998 ◽  
Vol 275 (1) ◽  
pp. H94-H99 ◽  
Author(s):  
S. Pudupakkam ◽  
K. A. Harris ◽  
W. G. Jamieson ◽  
G. DeRose ◽  
J. A. Scott ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Methyl Ester ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Ischemic Event ◽  
Reperfusion Period ◽  
Male Wistar Rats ◽  
Edl Muscle

We tested the hypothesis that ischemic preconditioning (PC) of skeletal muscle provided tolerance to a subsequent ischemic event 24 h later, and that such protection was due to nitric oxide (NO). Male Wistar rats, anesthetized with halothane, were randomly assigned to groups: ischemic (no PC; n = 11), PC ( n = 11), PC + N-nitro-l-arginine methyl ester (l-NAME; 100 μmol/l; n = 5), PC + N-nitro-d-arginine methyl ester (100 μmol/l; n= 4), PC + aminoguanidine (AMG; 100 μmol/l; n = 4), ischemic +l-NAME ( n= 4), or ischemic + AMG ( n = 4). PC consisted of 5× 10 min of ischemia and reperfusion, and, 24 h later, 2 h of ischemia were induced by a tourniquet applied to the limb. With the use of intravital microscopy, the number of perfused capillaries ( N pc) in the extensor digitorum longus (EDL) muscle was measured over a 90-min reperfusion period. The ratio of ethidium bromide- to bisbenzimide-labeled nuclei was used to estimate tissue injury. PC preserved N pc(23.6 ± 2.5) following 2 h of ischemia compared with sham muscles (11.5 ± 5.1), significantly elevating inducible NO synthase (iNOS) activity (81% increase), but did not afford protection to the parenchyma.l-NAME and AMG prevented ischemia-reperfusion-induced reduction in N pc in muscles without PC. However, after 90 min of reperfusion,l-NAME ( N pc = 15.0 ± 1.7), but not AMG ( N pc = 22.8 ± 3.1), significantly reduced the microvascular protection afforded by PC. We conclude that PC of the EDL muscle resulted, 24 h later, in protection to microvascular perfusion only, and that such protection was due to NO from sources other than iNOS.

scholarly journals Exercise Training Attenuates Obesity-Induced Skeletal Muscle Remodeling and Mitochondria-Mediated Apoptosis in the Skeletal Muscle

2018 ◽  
Vol 15 (10) ◽  
pp. 2301 ◽  
Author(s):  
Jun-Won Heo ◽  
Su-Zi Yoo ◽  
Mi-Hyun No ◽  
Dong-Ho Park ◽  
Ju-Hee Kang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
High Fat Diet ◽  
Skeletal Muscles ◽  
Treadmill Exercise ◽  
Sectional Area ◽  
High Fat ◽  
Cross Sectional ◽  
Muscle Remodeling ◽  
Protective Intervention

Obesity is characterized by the induction of skeletal muscle remodeling and mitochondria-mediated apoptosis. Exercise has been reported as a positive regulator of skeletal muscle remodeling and apoptosis. However, the effects of exercise on skeletal muscle remodeling and mitochondria-mediated apoptosis in obese skeletal muscles have not been clearly elucidated. Four-week-old C57BL/6 mice were randomly assigned into four groups: control (CON), control plus exercise (CON + EX), high-fat diet (HFD), and HFD plus exercise groups (HFD + EX). After obesity was induced by 20 weeks of 60% HFD feeding, treadmill exercise was performed for 12 weeks. Exercise ameliorated the obesity-induced increase in extramyocyte space and a decrease in the cross-sectional area of the skeletal muscle. In addition, it protected against increases in mitochondria-mediated apoptosis in obese skeletal muscles. These results suggest that exercise as a protective intervention plays an important role in regulating skeletal muscle structure and apoptosis in obese skeletal muscles.

scholarly journals Aged Skeletal Muscle Retains the Ability to Remodel Extracellular Matrix for Degradation of Collagen Deposition after Muscle Injury

2021 ◽  
Vol 22 (4) ◽  
pp. 2123
Author(s):  
Wan-Jing Chen ◽  
I-Hsuan Lin ◽  
Chien-Wei Lee ◽  
Yi-Fan Chen
Keyword(s):  
Skeletal Muscle ◽  
Extracellular Matrix ◽  
Skeletal Muscles ◽  
Muscle Injury ◽  
Structural Changes ◽  
Transforming Growth Factor ◽  
Tissue Inhibitors Of Metalloproteinases ◽  
Collagen Deposition ◽  
Skeletal Muscle Function ◽  
Ecm Remodeling

Aging causes a decline in skeletal muscle function, resulting in a progressive loss of muscle mass, quality, and strength. A weak regenerative capacity is one of the critical causes of dysfunctional skeletal muscle in elderly individuals. The extracellular matrix (ECM) maintains the tissue framework structure in skeletal muscle. As shown by previous reports and our data, the gene expression of ECM components decreases with age, but the accumulation of collagen substantially increases in skeletal muscle. We examined the structural changes in ECM in aged skeletal muscle and found restricted ECM degradation. In aged skeletal muscles, several genes that maintain ECM structure, such as transforming growth factor β (TGF-β), tissue inhibitors of metalloproteinases (TIMPs), matrix metalloproteinases (MMPs), and cathepsins, were downregulated. Muscle injury can induce muscle repair and regeneration in young and adult skeletal muscles. Surprisingly, muscle injury could not only efficiently induce regeneration in aged skeletal muscle, but it could also activate ECM remodeling and the clearance of ECM deposition. These results will help elucidate the mechanisms of muscle fibrosis with age and develop innovative antifibrotic therapies to decrease excessive collagen deposition in aged muscle.

scholarly journals TLR4/NF-κB-Responsive MicroRNAs and Their Potential Target Genes: A Mouse Model of Skeletal Muscle Ischemia-Reperfusion Injury

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Johnson Chia-Shen Yang ◽  
Shao-Chun Wu ◽  
Cheng-Shyuan Rau ◽  
Yi-Chun Chen ◽  
Tsu-Hsiang Lu ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Reperfusion Injury ◽  
Skeletal Muscles ◽  
Target Genes ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Whole Genome ◽  
Potential Target ◽  
Whole Genome Microarray ◽  
Innate Immunity Pathway

Background. The aim of this study was to profile TLR4/NF-κB-responsive microRNAs (miRNAs) and their potential target genes in the skeletal muscles of mice following ischemia-reperfusion injury.Methods. Thigh skeletal muscles of C57BL/6,Tlr4−/−, andNF-κB−/−mice isolated based on femoral artery perfusion were subjected to ischemia for 2 h and reperfusion for 0 h, 4 h, 1 d, and 7 d. The muscle specimens were analyzed with miRNA arrays. Immunoprecipitation with an argonaute 2- (Ago2-) specific monoclonal antibody followed by whole genome microarray was performed to identify mRNA associated with the RNA-silencing machinery. The potential targets of each upregulated miRNA were identified by combined analysis involving the bioinformatics algorithm miRanda and whole genome expression.Results. Three TLR4/NF-κB-responsive miRNAs (miR-15a, miR-744, and miR-1196) were significantly upregulated in the muscles following ischemia-reperfusion injury. The combined in silico and whole genome microarray approaches identified 5, 4, and 20 potential target genes for miR-15a, miR-744, and miR-1196, respectively. Among the 3 genes (Zbed4, Lrsam1,andDdx21) regulated by at least 2 of the 3 upregulated miRNAs,Lrsam1andDdx21are known to be associated with the innate immunity pathway.Conclusions. This study profiled TLR4/NF-κB-responsive miRNAs and their potential target genes in mouse skeletal muscle subjected to ischemia-reperfusion injury.

scholarly journals Histological changes of the arterial bed of the hind limbs of the rats under condition of the acute ischemia-reperfusion and correction with the carbacetam

2020 ◽  
Vol 26 (2) ◽  
pp. 5-11
Author(s):  
T.O. Veresiuk ◽  
P.R. Selskyy ◽  
A.T. Televiak
Keyword(s):  
Histological Examination ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Acute Ischemia ◽  
Histological Changes ◽  
Arterial Blood ◽  
Vascular Bed ◽  
Hind Limbs ◽  
Group I ◽  
Ischemic Period

The ischemic-reperfusion lesion is a complex multifactorial damage of the primary ischemic tissues as a result of restoration of the arterial blood circulation in them, which is accompanied by local morpho-functional reorganization of the vascular bed of the hind limbs of the rats. One of the promising means in the treatment and prevention of the reperfusion disorders is a carbacetam, which smooths the phenomena of hypo- and hyperperfusion in the post-ischemic period. The aim of the study was to established the manifestations of the morpho-functional remodeling of the vascular bed of the hind limbs of the rats in ischemia-reperfusion and under conditions of correction with carbacetam. Histological examination of the vascular bed of the hind limbs of 30 rats under conditions of ischemia-reperfusion (group I) and 30 rats in the simulation of ischemia-reperfusion, which in the post-ischemic period administered carbacetam once a day (5 mg/kg) for 14 days (group II) were done. There were 6 intact animals in the control group. Simulation of ischemia was performed by applying SWAT rubber tourniquets on the hind limbs for 2 hours, and reperfusion – by removing of the tourniquet. The animals of the experimental groups were divided into 5 subgroups with reperfusion terms after 1, 2 hours and 1 day, as well as after 7 and 14 days. Histological examination was performed according to generally accepted methods. The vascular bed in the middle third of the thigh and the shin below the tourniquet was examined using a Bresser Trino Researcher 40x–1000x microscope. Analyzing of the obtained results, was established that after 1 hour of the reperfusion the histological changes became a systemic, and after 1 day it were more significant. It should be noted that the thickness of the vessel walls increased, and the elastic membranes were partially eligned, thinned and torned. The stepwise clarity of the arterials walls structure was lost. The edema acquired a total nature. The histological examination of the vessels after 7 days revealed that the swelling of the walls decreased and the condition of the elastic frame was improved. There was a proliferation of collagen fibers in the adventitia, which was a response to ischemic effects. It is noted that after 14 days in all wall membranes the proliferative activity of fiboblasts was remained. Under the conditions of the correction with the carbacetam after 2 hours, the structural positive dynamics became more pronounced and increased to a maximum level after 7 days of the experiment. The number of the modified and exfoliated endothelial cells decreased, and the condition of smooth myocytes increased. Histologically, the gradual restoration of endothelial coverage of the intima was established. As follows, ischemia and reperfusion cause vascular remodeling after 1 hour with a peak of the manifestations after 1 day of the reperfusion, which includes edematous syndrome, dystrophic-degenerative changes with an inflammatory response to the damage, and in the late reperfusion period increased a fibroblasts activity. Gradual return of morphological changes occurs after 14 days of the experiment. Under the conditions of correction, the acceleration of the remodeling with stabilization of the process and the most possible structural restoration after 7 days of the study was noted.

scholarly journals Effect of iloprost on contractile impairment and mitochondrial degeneration in ischemia-reperfusion of skeletal muscle

2018 ◽  
Vol 105 (1) ◽  
pp. 61-75 ◽  
Author(s):  
Z Bagis ◽  
M Ozeren ◽  
B Buyukakilli ◽  
E Balli ◽  
S Yaman ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Lower Extremity ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Albino Rats ◽  
Force Frequency ◽  
Muscle Contractility ◽  
Reperfusion Period ◽  
Lower Extremity Ischemia ◽  
Extremity Ischemia

Purpose Acute lower extremity ischemia is still a main cause of mortality and morbidity in orthopedic traumatology and reconstructive surgery. In acute lower extremity ischemia, the skeletal muscles are the tissues that are the most vulnerable to ischemia. The aim of this study was to evaluate the effects of iloprost (IL) therapy on skeletal muscle contractile impairment and mitochondrial degeneration in an acute lower extremity ischemia-reperfusion rat model. Main Methods Forty Wistar albino rats were randomly divided into a control group and four experimental groups. Experimental groups were either subjected to 2 h of lower extremity ischemia followed by a 4-h reperfusion period or to 4 h of ischemia followed by an 8-h reperfusion period. Except for the animals in the control group, all animals received IL (1 ng/kg/min) or saline (1 ml/kg) by intraperitoneal infusion for 10 min immediately before reperfusion. At the end of the recording of skeletal muscle electrical activity and contractility, all rats were sacrificed by decapitation and muscle samples of lower extremity were immediately harvested for histopathologic analyses. Results After ischemia-reperfusion, a breakdown in the force–frequency curves of extensor digitorum longus muscle was observed, showing the diminished muscle contractility. However, IL significantly improved muscle contractility following injury induced by 2 h of ischemia followed by a 4-h reperfusion period. In addition, IL partially ameliorated mitochondrial degeneration in the muscle cells of ischemia groups. Conclusion This study indicates that immediate IL therapy repairs muscle damage especially after 2 h of ischemia and 4 h of reperfusion and therefore that IL improves contractile function.

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