Iloprost and pentoxifylline attenuate ischemia-reperfusion injury in skeletal muscle in rabbit model (original) (raw)
Related papers
The effects of iloprost on ischemia-reperfusion injury in skeletal muscles in a rodent model
Journal of Surgical Research, 2014
Iloprost Heat shock protein 60 Endothelial nitric oxide Malondialdehyde Superoxide dismutase Rat a b s t r a c t Purpose: The aim of this study was to investigate the effects of iloprost (IL) on ischemiareperfusion injury in a rodent model. Materials and methods: Twenty-four Wistar Albino rats were randomized into four groups (n ¼ 6). Laparotomy was performed in all groups under general anesthesia. Only laparotomy was applied in group S (Sham). Ischemia-reperfusion group (group I/R) underwent ischemia and reperfusion performed by clamping and declamping of the infrarenal abdominal aorta for 120 min. The iloprost group (group IL) received intravenous infusion of IL 0.5 ng/kg/min, without I/R. Group I/R þ IL received intravenous infusion of IL 0.5 ng/kg/ min immediately after 2 h period of ischemia. At the end of the reperfusion period, all rats were killed under anesthesia and skeletal muscle samples of lower extremity were harvested for biochemical and histopathologic analyses.
BioMed Research International, 2015
Objective. The objective of this study was to examine the effects of iloprost and N-acetylcysteine (NAC) on ischemia-reperfusion (IR) injuries to the gastrocnemius muscle, following the occlusion-reperfusion period in the abdominal aorta of rats.Materials and Methods. Forty male Sprague-Dawley rats were randomly divided into four equal groups.Group 1: control group. Group 2 (IR): aorta was occluded. The clamp was removed after 1 hour of ischemia. Blood samples and muscle tissue specimens were collected following a 2-hour reperfusion period.Group 3 (IR + iloprost): during a 1-hour ischemia period, iloprost infusion was initiated from the jugular catheter. During a 2-hour reperfusion period, the iloprost infusion continued.Group 4 (IR + NAC): similar to the iloprost group.Findings. The mean total oxidant status, CK, and LDH levels were highest in Group 2 and lowest in Group 1. The levels of these parameters in Group 3 and Group 4 were lower compared to Group 2 and higher compared to G...
Turkish journal of medical sciences, 2017
The protective effects of prostaglandin (PG) analogs on ischemia-reperfusion (I/R) have been well documented; however, comparative studies are lacking. The aim of the present study was to determine whether iloprost or alprostadil is more effective in preventing muscle I/R injury. Thirty-two rats were divided into four groups (n = 8): sham, control, IL (I/R + iloprost), and AL (I/R + alprostadil). I/R was induced by a tourniquet in the hindlimb for 3 h/3 h. The IL and AL groups received iloprost (0.5 ng kg(-1) min(-1)) and alprostadil (0.05 µg kg(-1) min(-1)) during reperfusion, respectively. After 6 h, blood and muscles were collected for analyses. Serum TNF-α and IL-1β levels were decreased in the IL and AL groups compared with the control group (P < 0.05), whereas IL-6 levels did not change significantly. Tissue malondialdehyde levels were significantly lower in the IL and AL groups (P < 0.05). Tissue catalase levels showed no difference. The histological damage scores and a...
Physiology International
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 c...
Pentoxifylline attenuates reperfusion injury in skeletal muscle after partial ischemia
American Journal of Physiology-heart and Circulatory Physiology, 1998
Leukocytes have been shown to contribute to ischemia-reperfusion injury in skeletal muscle. Pentoxifylline (PTXF), a xanthine-derived phosphodiesterase inhibitor, has received recent attention because of its action on leukocytes. To clarify the effects of PTXF in reperfusion injury, we measured the resting transmembrane potential difference (E m) and evaluated postcapillary venule microcirculation using intravital microscopy in rat skeletal muscle during ischemia and reperfusion. The infrarenal aorta was clamped for 90 min and then reperfused for 60 min. Persistent depolarization of the resting E m was observed in an ischemiareperfusion (IR) group and was significantly repolarized in a PTXF group during the reperfusion period. The tissue water content was significantly reduced in the PTXF group, although no difference was noted in the tissue lactate content. Flowing erythrocyte velocity and wall shear rate in the PTXF group were significantly higher than in the IR group during the reperfusion period but without significant differences in vessel diameter and hemoglobin oxygenation. Blood flow measured by laser-Doppler flowmeter was also significantly improved in the PTXF group. Furthermore, the adherent leukocyte count was significantly reduced in the PTXF group during this same period. These results indicate that PTXF attenuated reperfusion-associated membrane injury and tissue edema and that PTXF suppressed leukocyte adhesion and improved hindlimb blood flow during the reperfusion period.
British Journal of Surgery, 1994
During revascularization of skeletal muscle lipid mediators are released that may have a role in the pathogenesis of reperfusion injury. This study investigated the emcacy of the lipid mediator antagonists U74500A (a lipid peroxidation inhibitor), GR32191 (a thromboxane A, receptor antagonist) and SC41930 (a leukotriene B, (LTB,) receptor antagonist) in altering muscle viability and oedema, in a rat hindlimb model of 6-h ischaemia and 4-h reperfusion. Study groups comprised normal, ischaemic (6-h ischaemia) and control rats, and animals receiving the lipid mediator antagonists. Ischaemia itself did not result in muscle oedema or necrosis but both occurred following reperfusion (P<O.Ol). Muscle viability was preserved by all lipid mediator antagonists (P€O.Ol versus controls, P not significant versus normal and ischaemia), with the LTB, receptor antagonist ameliorating limb oedema (P<O61 versus controls). Theae results demonstrate a role for lipid mediators in r e p e h i o n injury and suggest that their antagonists might aid the management of acute limb ischaemia.
Turkish Journal of Trauma and Emergency Surgery, 2018
BACKGROUND: Intestinal ischemia-reperfusion (I/R) injury can lead to multiple organ failure and death. The aim of this study was to investigate the effects of pentoxifylline and iloprost administered before reperfusion in intestinal ischemia. METHODS: In total, 25 male Wistar Albino rats weighing 250-300 g were divided into five groups each comprising five subjects: control group (n=5), sham group (n=5, no I/R), I/R group (n=5, 45 min ischemia, and 120 min reperfusion), I/R + pentoxifylline group (n=5, 45 min ischemia following intraperitoneal 50 mg/kg pentoxifylline and 120 min reperfusion), and I/R + iloprast group (n=5, 45 min ischemia followed by intraperitoneal 2 mcg /kg iloprost and 120 min reperfusion). At the end of the experiment, ileum specimens were stained using hematoxylin-eosin and histopathologically evaluated using the Chiu score. Isometric contraction-relaxation responses were recorded using organ baths for contraction-relaxation responses. RESULTS: Pentoxifylline provided a significant improvement in response to histopathological and contraction-relaxation responses. Although iloprost provided recovery in reperfusion injury, it was not statistically significant. CONCLUSION: Our findings demonstrate that pentoxifylline may be promising in preventing small bowel ischemia-reperfusion injury. We concluded that further clinical and experimental studies for iloprost are needed.
Pharmacologic intervention in ischemia-induced reperfusion injury in the skeletal muscle
Microsurgery, 1993
muscle. Special emphasis is placed on the recent observation of the acute ischemic preconditioning phenomenon for prevention of I/R injury in skeletal muscle. Finally, the mechanism of ischemic preconditioning and its clinical applications for augmentation of skeletal muscle tolerance to prolonged ischemic insult are discussed. o im wiiey-~iss, inc.
Bmc Musculoskeletal Disorders, 2013
Background: Studies have shown that ischemia-reperfusion (I/R) produces free radicals leading to lipid peroxidation and damage to skeletal muscle. The purposes of this study were 1) to assess the histological findings of gastrocnemius muscle (GC) and tibialis anterior muscle (TA) in I/R injury model mice, 2) to histologically analyze whether a single pretreatment of edaravone inhibits I/R injury to skeletal muscle in murine models and 3) to evaluate the effect of oxidative stress on these muscles. Methods: C57BL6 mice were divided in two groups, with one group receiving 3 mg/kg intraperitoneal injections of edaravone (I/R + Ed group) and the other group receiving an identical amount of saline (I/R group) 30 minutes before ischemia. Edaravone (3-methy-1-pheny1-2-pyrazolin-5-one) is a potent and novel synthetic scavenger of free radicals. This drug inhibits both nonenzymatic lipid peroxidation and the lipoxygenase pathway, in addition to having potent antioxidant effects against ischemia reperfusion. The duration of the ischemia was 1.5 hours, with reperfusion at either 24 or 72 hours (3 days). Specimens of gastrocnemius (GC) and anterior tibialis (TA) were removed for histological evaluation and biochemical analysis. Results: This model of I/R injury was highly reproducible in histologic muscle damage. In the histologic damage score, the mean muscle fibers and inflammatory cell infiltration in the I/R + Ed group were significantly less than the corresponding values of observed in the I/R group. Thus, pretreatment with edaravone was observed to have a protective effect on muscle damage after a period of I/R in mice. In addition, the mean muscle injury score in the I/R + Ed group was also significantly less than the I/R group. In the I/R + Ed group, the mean malondialdehyde (MDA) level was lower than in the I/R group and western-blotting revealed that edaravone pretreatment decreased the level of inducible nitric oxide synthase (iNOS) expression. Conclusions: Edaravone was found to have a protective effect against I/R injury by directly inhibiting lipid peroxidation of the myocyte by free radicals in skeletal muscles and may also reduce the secondary edema and inflammatory infiltration incidence of oxidative stress on tissue.