The effect of tumor necrosis factor-α inhibitor soon after hypoxia-ischemia on heart in neonatal rats

Büyükakıllı, Belgin; Atıcı, Aytuğ; Özkan, Aziz; Ballı, Ebru; Güneş, Sevgi; Turhan, Ali Haydar; Hallioglu, Olgu; Kanık, Arzu

doi:10.1016/j.lfs.2012.03.036

Cited by 6 publications

(14 citation statements)

References 26 publications

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“…This is an important step prior to identifying the cumulative effects of inflammatory factors that occur during the complex process of myocardial inflammation. Furthermore, TNFα inhibition has also developed as a therapy for diseases associated with inflammation (Moe et al, 2004; Buyukakilli et al, 2012), which also increases the significance of understanding how TNFα and its inhibitors may affect cardiac functioning.…”

Section: Limitationsmentioning

confidence: 99%

TNFα Modulates Cardiac Conduction by Altering Electrical Coupling between Myocytes

et al. 2017

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Background: Tumor Necrosis Factor α (TNFα) upregulation during acute inflammatory response has been associated with numerous cardiac effects including modulating Connexin43 and vascular permeability. This may in turn alter cardiac gap junctional (GJ) coupling and extracellular volume (ephaptic coupling) respectively. We hypothesized that acute exposure to pathophysiological TNFα levels can modulate conduction velocity (CV) in the heart by altering electrical coupling: GJ and ephaptic.Methods and Results: Hearts were optically mapped to determine CV from control, TNFα and TNFα + high calcium (2.5 vs. 1.25 mM) treated guinea pig hearts over 90 mins. Transmission electron microscopy was performed to measure changes in intercellular separation in the gap junction-adjacent extracellular nanodomain—perinexus (WP). Cx43 expression and phosphorylation were determined by Western blotting and Cx43 distribution by confocal immunofluorescence. At 90 mins, longitudinal and transverse CV (CVL and CVT, respectively) increased with control Tyrode perfusion but TNFα slowed CVT alone relative to control and anisotropy of conduction increased, but not significantly. TNFα increased WP relative to control at 90 mins, without significantly changing GJ coupling. Increasing extracellular calcium after 30 mins of just TNFα exposure increased CVT within 15 mins. TNFα + high calcium also restored CVT at 90 mins and reduced WP to control values. Interestingly, TNFα + high calcium also improved GJ coupling at 90 mins, which along with reduced WP may have contributed to increasing CV.Conclusions: Elevating extracellular calcium during acute TNFα exposure reduces perinexal expansion, increases ephaptic, and GJ coupling, improves CV and may be a novel method for preventing inflammation induced CV slowing.

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Section: Limitationsmentioning

confidence: 99%

TNFα Modulates Cardiac Conduction by Altering Electrical Coupling between Myocytes

et al. 2017

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“…In these groups, hypoxia-ischemia was induced according to the Levine-Rice model [22]. This model was used in our previous study [2]. A median incision was made in the neck.…”

Section: The Preparation Of the Animals And Surgical Proceduresmentioning

confidence: 99%

“…A median incision was made in the neck. Under microscopic magnification, the right common carotid artery was dissected and ligated with a 6-zero silk suture [2]. After the wound was sutured, the animals were allowed to have a 1 h recovery and feeding period.…”

Section: The Preparation Of the Animals And Surgical Proceduresmentioning

confidence: 99%

“…10 mg/kg etanercept (Enbrel 25 mg flakon, Wyeth) which was dissolved in saline (0.5 mL), the saline group had only saline (0.5 mL i.p.). After the hypoxic period, the rats were survived in the room conditions till the 17 th week [2].…”

Section: The Preparation Of the Animals And Surgical Proceduresmentioning

confidence: 99%

“…Perinatal and neonatal hypoxic-ischemic (HI) insult has acute and long term deleterious effects not only on the brain but on many other tissues, including peripheral nerves [1,2]. Many researchers have also reported that hypoxia/ischemia injury plays an important role in the development of peripheral neuropathy [3,4].…”

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Effects of a Tumor Necrosis Factor-Alpha Inhibitor (Etanercept) on the Sciatic Nerve in a Hypoxic Ischemia-Induced Neonatal Rat Model

Büyükakıllı¹,

Atıcı²,

Ballı³

et al. 2014

Adv Clin Exp Med

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Background. Neonatal hypoxic-ischemic (HI) injury has been considered to have acute and long term deleterious effects on many tissues, including the peripheral nerve. Objectives. In this study, the effects of a tumor necrosis factor-alpha (TNF-α) inhibitor (etanercept) on peripheral nerve damage and the ultrastructure of the sciatic nerve and gastrocnemius muscle in rats exposed to HI during the neonatal period were examined. Material and Methods. In this study, 45 seven-day-old rats were used and they were divided into three groups. The right carotid arteries of the rats in the saline and etanercept groups were ligated and put in a hypoxia chamber containing 8% oxygen for two hours. Just after hypoxia, the etanercept group was given 10 mg/kg etanercept, but the saline group had only saline intraperitoneally. The sham group rats' carotid arteries were not ligated or put in hypoxia. The amplitude, area and latency of sciatic nerve compound motor action potential (CMAP), which mainly reflects axonopathy and myelinopathy, were measured using standard techniques in the seventeenth week following the HI. Sciatic nerve and gastrocnemius muscle were evaluated with a transmission electron microscope, and grading for myelin sheath damage was done to all groups. Results. Neuropathy was seen in rats after HI. While treatment with etanercept showed a protective effect for the axons of sciatic nerve, demyelination could not be recovered with etanercept. Conclusions. This study is the first in literature to show a partial interruption of the signal through the peripheral nerve fibers caused by axonal and myelin dysfunction continuation in rats exposed to HI after birth, in the 17

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

et al. 2018

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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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The effect of tumor necrosis factor-α inhibitor soon after hypoxia-ischemia on heart in neonatal rats

Cited by 6 publications

References 26 publications

TNFα Modulates Cardiac Conduction by Altering Electrical Coupling between Myocytes

TNFα Modulates Cardiac Conduction by Altering Electrical Coupling between Myocytes

Effects of a Tumor Necrosis Factor-Alpha Inhibitor (Etanercept) on the Sciatic Nerve in a Hypoxic Ischemia-Induced Neonatal Rat Model

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

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