Abstract 100: Delta Opioid Receptor Blockade Abolishes Exercise-Induced Cardioprotection Against Ischemia-Reperfusion Injury In Vivo

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Juliana P Borges ◽  
Marina Tristao ◽  
Eduardo V Tibiriçá ◽  
Marcos A Lessa
Keyword(s):  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Acute Exercise ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Receptor Subtype ◽  
Kappa Receptor ◽  
Exercise Induced ◽  
Delta Receptor ◽  
And Control

Introduction: Recent studies showed that exercise enhances myocardial tolerance to ischemia-reperfusion (I-R) injury via an opioid receptor-dependent mechanism. However, the specific subtype of opioid receptor involved in this response remains to be determined. Methods: Male Wistar rats were first divided into 2 groups: exercised and control. The exercised group underwent 4 consecutive days of treadmill training (60 min at 70% of maximal oxygen consumption). The exercised group was then divided into 4 subgroups: exercised (Exe; n = 10); exercised + kappa receptor antagonist (Exe + K; n=4); exercised + delta receptor antagonist (Exe + D; n=4); exercised + mu receptor antagonist (Exe + M; n=4). Control group was also divided into 2 groups: control (Ctr; n = 10) and control sham (Sham; n = 10). To induce I-R injury, anesthetized animals were submitted to a left thoracotomy and a 30 min interventricular coronary occlusion followed by 60 min of reperfusion. The hemodynamic parameters were recorded and infarct size was post-mortem determined by double staining using TTC/Evans blue and expressed as a percentage of the area at risk. Results: As shown in the figure, Sham group showed no infarct, Exe group showed a significant reduction in the infarcted area (27.6%) when compared to Ctr group (42.0%). The pretreatment with mu and kappa receptor antagonist did not alter the cardioprotective effect of exercise. However, the pretreatment with delta receptor antagonist prevented the exercise-induced cardioprotection. Conclusions: Endogenous opioid system is involved in cardioprotection conferred by acute exercise, and delta receptor subtype seems to play an important role in this response.

Abstract P500: Naltrindole And Naltrindole Derivatives Exhibit Potent Cardioprotection In Myocardial Ischemia Reperfusion Injury

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Sunit Singh ◽  
Alexis Verwoert ◽  
Michael Bamimore ◽  
Arjun Nair ◽  
Tameka Dean ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Infarct Size ◽  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Kappa Opioid Receptor ◽  
Opioid Antagonist ◽  
Inotropic Effects ◽  
Kappa Receptor

Previously, naltrindole (NTI; selective delta opioid receptor antagonist) was shown to improve post-reperfused cardiac function and reduced infarct size when given prior to ischemia (I)/ reperfusion (R) in ex-vivo rat hearts. Conversely, naloxone (NX, broad-spectrum opioid antagonist) and nor-binaltrophine (BNI, selective kappa receptor antagonist) were similar to control hearts. In this study, the effects of NTI derivatives naltriben (NTB, delta receptor antagonist) and guanidonaltrindole (GNTI, kappa receptor antagonist) were compared to NTI, BNI, and NX. Isolated hearts from male SD rats (300g) were subjected to global I(30min)/R(45min). Treatments were given 5 min before I (preconditioning) and during the first 5 min of R. Left ventricular (LV) cardiac function was measured using a pressure transducer. At the end of reperfusion, infarcted heart tissue was compared to total tissue weight. Data were evaluated using ANOVA. As shown in Table 1, NTI, NTB, and GNTI significantly improved post-reperfused cardiac function and reduced infarct size compared to control hearts. NTI and NTB elicited direct effects on cardiac function when given during preconditioning in contrast to all other study groups and were the most robust at reducing infarct size and restoring post reperfusion cardiac function. The negative inotropic effects of NTI and NTB were correlated with a decrease in the rise of ischemic pressure. GNTI also elicited significant improvement in post-reperfused cardiac function and reduction of infarct size compared to BNI which suggests a separate cardioprotective mechanism that this NTI derivative may exert in contrast to kappa opioid receptor inhibition. Results suggest that NTI and derivatives, GNTI and NTB, are cardioprotective against I/R injury resulting in reduced ischemic peak pressure (NTI/NTB) and infarct size. In future studies, we will examine the mechanism of the protective effects of NTI and derivatives in hearts subjected to I/R injury.

scholarly journals PO-055 Changes of trace elements in skeletal muscle and serum of rats after exercise-induced injury

2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Jingyun Liu ◽  
Qun Zuo
Keyword(s):  
Skeletal Muscle ◽  
Trace Elements ◽  
Nitric Acid ◽  
Vena Cava ◽  
The Body ◽  
Emission Spectrometry ◽  
Control Group ◽  
Exercise Induced ◽  
And Control ◽  
Cu And Zn

Objective This study is to investigate the changes of trace elements (Cu, Fe, Zn, Se, Mg) in serum and skeletal muscle of rats after skeletal muscle injury induced by downhill running, and to find out the change regularity of trace elements in the body after exercise injury. To provide experimental basis for how to use trace elements supplements reasonably. Methods Fifty-four healthy male Sprague-Dawley rats aged 8 weeks were randomly divided into two groups: control group (C, N=6) and exercise group (E, N=48, include: 0 h group, 6 h group, 12 h group, 24 h group, 48 h group, 72 h group, 1- week group and 2- week group). The rats in exercise groups run down a 16°incline at 16m/min for 90 minutes. At the end of the exercise, the rats were killed at 0 h, 6 h, 12 h, 24 h, 48 h, 72 h, 1 week and 2 weeks, respectively. The serum was got from the inferior vena cava blood and diluted by 1% nitric acid. The muscle was got from the right side of the rat's sural which were digested by concentrated nitric acid and 30% hydrogen peroxide in 75℃water bath for 20mins. The content of trace elements in muscle and serum were measured by inductively coupled plasma atomic emission spectrometry (ICP-MS). All the data are analyzed and processed by SPSS22.0 statistical software. Results (1) The contents of trace elements in serum showed: Cu, Zn, Mg, Se decreased immediately after exercise, but the Cu still increased to reach a peak at 24h after decreasing, and after 2 weeks the content of Cu was slightly lower than pre-exercise level. However, the content of Zn did not elevate again, it continued declined to the lowest at 24h which was significantly lower than control group (P < 0.05). And after 2 weeks, Zn did not return to the pre-exercise level. The changes of Mg, Se in serum was not statistically significant. There is no difference between 0h and control groups in content of Fe, after that Fe decreased continually and appeared the least value at 24h, the differences between immediate group and control group were statistically significant (P < 0.05). Fe returned to the pre-exercise level after 2 weeks. (2) The contents of trace elements in muscle showed: Most of trace elements increased to the maximum level at 6 h, after that Mg, Fe, Cu decreased to the lowest value at 72 h which were significant lower than 0h group or 6h group (P < 0. 05). ALL the trace elements were lower than pre-exercise level. There was no statistical difference in the content of Se in muscle. Conclusions (1) The different changes of trace elements in skeletal muscle and serum after exercise injury may be due to the redistribution of trace elements caused by the body adaptability. (2) The most obviously changes of trace element in serum and muscle are Cu and Zn. Both of them did not return to the pre-exercise level after 2 weeks, it suggests that the supplement include Cu and Zn may play an important role in recovering after exercise-induced injury.

scholarly journals Moderate exercise prevents impaired Ca2+ handling in heart of CO-exposed rat: implication for sensitivity to ischemia-reperfusion

2010 ◽  
Vol 299 (6) ◽  
pp. H2076-H2081 ◽  
Author(s):  
C. Farah ◽  
G. Meyer ◽  
L. André ◽  
J. Boissière ◽  
S. Gayrard ◽  
...  
Keyword(s):  
Exercise Training ◽  
Antioxidant Status ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Moderate Exercise ◽  
Plasmic Reticulum ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Exercise Induced ◽  
Moderate Exercise Training

Sustained urban carbon monoxide (CO) exposure exacerbates heart vulnerability to ischemia-reperfusion via deleterious effects on the antioxidant status and Ca2+ homeostasis of cardiomyocytes. The aim of this work was to evaluate whether moderate exercise training prevents these effects. Wistar rats were randomly assigned to a control group and to CO groups, living during 4 wk in simulated urban CO pollution (30–100 parts/million, 12 h/day) with (CO-Ex) or sedentary without exercise (CO-Sed). The exercise procedure began 4 wk before CO exposure and was maintained twice a week in standard filtered air during CO exposure. On one set of rats, myocardial ischemia (30 min) and reperfusion (120 min) were performed on isolated perfused rat hearts. On another set of rats, myocardial antioxidant status and Ca2+ handling were evaluated following environmental exposure. As a result, exercise training prevented CO-induced myocardial phenotypical changes. Indeed, exercise induced myocardial antioxidant status recovery in CO-exposed rats, which is accompanied by a normalization of sarco(endo)plasmic reticulum Ca2+-ATPase 2a expression and then of Ca2+ handling. Importantly, in CO-exposed rats, the normalization of cardiomyocyte phenotype with moderate exercise was associated with a restored sensitivity of the myocardium to ischemia-reperfusion. Indeed, CO-Ex rats presented a lower infarct size and a significant decrease of reperfusion arrhythmias compared with their sedentary counterparts. To conclude, moderate exercise, by preventing CO-induced Ca2+ handling and myocardial antioxidant status alterations, reduces heart vulnerability to ischemia-reperfusion.

Ischemic preconditioning and morphine attenuate myocardial apoptosis and infarction after ischemia-reperfusion in rabbits: role of δ-opioid receptor

2004 ◽  
Vol 287 (4) ◽  
pp. H1786-H1791 ◽  
Author(s):  
Shinji Okubo ◽  
Yujirou Tanabe ◽  
Kenji Takeda ◽  
Michihiko Kitayama ◽  
Seiyu Kanemitsu ◽  
...  
Keyword(s):  
Infarct Size ◽  
Opioid Receptor ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Control Group ◽  
Apoptotic Cells ◽  
Protective Effects ◽  
Δ Opioid Receptor

We examined whether ischemic preconditioning (IPC) attenuates ischemia-reperfusion injury, in part, by decreasing apoptosis and whether the δ-opioid receptor (DOR) plays a pivotal role in the regulation of apoptosis. Rabbits were subjected to 30-min coronary artery occlusion (CAO) and 180 min of reperfusion. IPC was elicited with four cycles of 5-min ischemia and 10-min reperfusion before CAO. Morphine (0.3 mg/kg iv) was given 15 min before CAO. Naloxone (Nal; 10 mg/kg iv) and naltrindole (Nti; 10 mg/kg iv), the respective nonselective and selective DOR antagonists were given 10 min before either morphine or IPC. Infarct size (%risk area) was reduced from 46 ± 3.8 in control to 11.6 ± 1.0 in IPC and 19.5 ± 3.8 in the morphine group (means ± SE; P < 0.001 vs. control). Nal blocked the protective effects of IPC and morphine, as shown by the increase in infarct size to 38.6 ± 7.2 and 44.5 ± 1.8, respectively. Similarly, Nti blocked IPC and morphine-induced protection. The percentage of apoptotic cells (revealed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay) decreased in IPC (3.6 ± 1.9) and morphine groups (5.2 ± 1.2) compared with control group (12.4 ± 1.6; P < 0.001). Nti pretreatment increased apoptotic cells 11.2 ± 2.2% in IPC and 12.1 ± 0.8% in morphine groups. Nal failed to block inhibition of apoptosis in the IPC group (% of cells: 5.7 ± 1.3 vs. 3.6 ± 1.9 in IPC alone; P > 0.05). These results were also confirmed by nucleosomal DNA laddering pattern. We conclude that IPC reduces lethal injury, in part, by decreasing apoptosis after ischemia-reperfusion and activation of the DOR may play a crucial role in IPC or morphine-induced myocardial protection.

Exercise enhances myocardial ischemic tolerance via an opioid receptor-dependent mechanism

2008 ◽  
Vol 294 (1) ◽  
pp. H402-H408 ◽  
Author(s):  
Eric W. Dickson ◽  
Christopher P. Hogrefe ◽  
Paula S. Ludwig ◽  
Laynez W. Ackermann ◽  
Lynn L. Stoll ◽  
...  
Keyword(s):  
Infarct Size ◽  
Opioid Receptor ◽  
Cardiovascular Health ◽  
Ischemic Tolerance ◽  
Control Group ◽  
Mrna Levels ◽  
Standard Protocol ◽  
Vigorous Exercise ◽  
Cardioprotective Effects ◽  
Exercise Induced

Exercise increases serum opioid levels and improves cardiovascular health. Here we tested the hypothesis that opioids contribute to the acute cardioprotective effects of exercise using a rat model of exercise-induced cardioprotection. For the standard protocol, rats were randomized to 4 days of treadmill training and 1 day of vigorous exercise ( day 5), or to a sham exercise control group. On day 6, animals were killed, and global myocardial ischemic tolerance was assessed on a modified Langendorff apparatus. Twenty minutes of ischemia followed by 3 h of reperfusion resulted in a mean infarct size of 42 ± 4% in hearts from sham exercise controls and 21 ± 3% ( P < 0.001) in the exercised group. The cardioprotective effects of exercise were gone by 5 days after the final exercise period. To determine the role of opioid receptors in exercise-induced cardioprotection, rats were exercised according to the standard protocol; however, just before exercise on days 4 and 5, rats were injected subcutaneously with 10 mg/kg of the opioid receptor antagonist naltrexone. Similar injections were performed in the sham exercise control group. Naltrexone had no significant effect on baseline myocardial ischemic tolerance in controls (infarct size 43 ± 4%). In contrast, naltrexone treatment completely blocked the cardioprotective effect of exercise (infarct size 40 ± 5%). Exercise was also associated with an early increase in myocardial mRNA levels for several opioid system genes and with sustained changes in a number of genes that regulate inflammation and apoptosis. These findings demonstrate that the acute cardioprotective effects of exercise are mediated, at least in part, through opioid receptor-dependent mechanisms that may include changes in gene expression.

The μ-opioid receptor subtype is required for the anorectic effect of an opioid receptor antagonist

2006 ◽  
Vol 545 (2-3) ◽  
pp. 147-152 ◽  
Author(s):  
Jiaping Zhang ◽  
Andrea Frassetto ◽  
Ruey-Ruey C. Huang ◽  
Julie Z. Lao ◽  
Alexander Pasternak ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Receptor Subtype ◽  
Opioid Receptor Antagonist ◽  
Anorectic Effect ◽  
Μ Opioid Receptor

Chronic resistance training in women potentiates growth hormone in vivo bioactivity: characterization of molecular mass variants

2006 ◽  
Vol 291 (6) ◽  
pp. E1177-E1187 ◽  
Author(s):  
William J. Kraemer ◽  
Bradley C. Nindl ◽  
James O. Marx ◽  
Lincoln A. Gotshalk ◽  
Jill A. Bush ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Resistance Training ◽  
Resistance Exercise ◽  
Molecular Mass ◽  
Acute Exercise ◽  
Control Group ◽  
Detection Systems ◽  
Molecular Variants ◽  
Exercise Induced

This investigation determined the influence of acute and chronic resistance exercise on responses of growth hormone (GH) molecular variants in women. Seventy-four healthy young women (23 ± 3 yr, 167 ± 7 cm, 63.8 ± 9.3 kg, 26.3 ± 4.0% body fat) performed an acute bout of resistance exercise (6 sets of 10 repetition maximum squat). Blood samples were obtained pre- and postexercise. Resulting plasma was fractionated by molecular mass ( fraction A, >60 kDa; fraction B, 30–60 kDa; and fraction C, <30 kDa) using chromatography. Fractionated and unfractionated (UF) plasma was then assayed for GH using three different detection systems (monoclonal immunoassay, polyclonal immunoassay, and rat tibial line in vivo bioassay). Subjects were then matched and randomly placed into one of four resistance exercise training groups or a control group for 24 wk. All experimental procedures were repeated on completion of the 24-wk resistance training programs. After acute exercise, immunoassays showed consistent increases in UF GH samples and fractions B and C; increases in fraction A using immunoassay were seen only in the monoclonal assay. No consistent changes in bioactive GH were found following acute exercise. Conversely, chronic exercise induced no consistent changes in immunoassayable GH of various molecular masses, whereas, in general, bioassayable GH increased. In summary, although acute exercise increased only immunoactive GH, chronic physical training increased the biological activity of circulating GH molecular variants. Increased bioactive GH was observed across all fractions and training regimens, suggesting that chronic resistance exercise increased a spectrum of GH molecules that may be necessary for the multitude of somatogenic and metabolic actions of GH.

scholarly journals Assessing the Therapeutic Effect of 630 nm Light-Emitting Diodes Irradiation on the Recovery of Exercise-Induced Hand Muscle Fatigue with Surface Electromyogram

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Dandan Yang ◽  
Xiaoying Wu ◽  
Wensheng Hou ◽  
Xiaolin Zheng ◽  
Jun Zheng ◽  
...  
Keyword(s):  
Muscle Fatigue ◽  
Light Emitting Diode ◽  
Voluntary Contraction ◽  
Control Group ◽  
Flexor Digitorum Superficialis ◽  
Light Emitting ◽  
Hand Muscle ◽  
Exercise Induced ◽  
Flexor Digitorum ◽  
And Control

This paper aims to investigate the effect of light emitting diode therapy (LEDT) on exercise-induced hand muscle fatigue by measuring the surface electromyography (sEMG) of flexor digitorum superficialis. Ten healthy volunteers were randomly placed in the equal sized LEDT group and control group. All subjects performed a sustained fatiguing isometric contraction with the combination of four fingertips except thumb at 30% of maximal voluntary contraction (MVC) until exhaustion. The active LEDT or an identical passive rest therapy was then applied to flexor digitorum superficialis. Each subject was required to perform a re-fatigue task immediately after therapy which was the same as the pre-fatigue task. Average rectified value (ARV) and fractal dimension (FD) of sEMG were calculated. ARV and FD were significantly different between active LEDT and passive rest groups at 20%–50%, 70%–80%, and 100% of normalized contraction time (P<0.05). Compared to passive rest, active LEDT induced significantly smaller increase in ARV values and decrease in FD values, which shows that LEDT is effective on the recovery of muscle fatigue. Our preliminary results also suggest that ARV and FD are potential replacements of biochemical markers to assess the effects of LEDT on muscle fatigue.

scholarly journals Serum Periostin Level in Asthmatic Children with Exercise Induced Bronchospasm

2020 ◽  
pp. 53-67
Author(s):  
Reem M. Soliman ◽  
Mohamed B. Hamza ◽  
Rasha M. El-Shafiey ◽  
Hesham A. Elserogy ◽  
Nabil M El-Esawy
Keyword(s):  
Test Group ◽  
Mean Value ◽  
Control Group ◽  
Asthmatic Children ◽  
Group A ◽  
The Mean ◽  
Exercise Induced ◽  
Group B ◽  
And Control ◽  
Serum Periostin

Background: There are few biomarkers that can be easily accessed in clinical settings and may reflect refractory Th2-eosinophlic inflammation and remodeling of the asthmatic airways. Serum periostin may be one such biomarker to aid our understanding of the patho-bio-physiology of asthma and exercise induced asthma. The aim of the study is to explore the relationship between serum periostin level and exercise induced bronchoconstriction in asthmatic children. Materials and Methods: This cross-sectional study was carried out on (90) children both sexes aged from 6 to 15 years including, (60) children with bronchial asthma and (30) children were enrolled as control group in the period from January 2018 to January 2019. Patients were randomly classified into two groups: I) Patient group: divided into 2 groups according to standardized treadmill exercise challenge test: Group A: (30) asthmatic children with positive test. Group B: (30) asthmatic children with negative test. II-Control group: (30) children apparently healthy with no personal or family history of asthma. All children were subjected to the following Investigations: Chest x-ray, pulmonary functions tests (FEV1 & PEFR) except controls, Laboratory investigations as CBC and Serum periostin level. Results: The mean values of both the percentage of PEFR and FEV1 after exercise in group A were significantly lower than those in group B and the percentage of PEFR and FEV1 after exercise in each group were significantly lower than the percentage before exercise in the same group. The mean value of eosinophilic count in group A was significantly higher than (group B and control group) and the mean value of eosinophilic count in group B was significantly higher than control group. The mean value of serum level of periostin in group A was significantly higher than (group B and control group), however, there was no significant difference between group B and control group as regard to serum level of periostin. Chest tightness, cough and wheezes after exercise and eosinophilic count in patients with high serum periostin level were significantly higher than patients with low serum periostin level, and both PEFR and FEV1 after exercise in patients with high serum periostin level were significantly lower than patients with low serum periostin level. Also the normal serum periostin levels vary among different age groups. Conclusion: Serum periostin level can be considered as a useful biomarker for diagnosis of Exercise induced bronchospasm (EIB) in asthmatic children especially when lung function test cannot be done However, cautious is required in evaluating serum periostin levels in children because it varies with age.

scholarly journals Alterations in Exercise-Induced Plasma Adenosine Triphosphate Concentration in Highly Trained Athletes in a One-Year Training Cycle

Metabolites ◽  
2019 ◽  
Vol 9 (10) ◽  
pp. 230 ◽  
Author(s):  
Ewa Anna Zarębska ◽  
Krzysztof Kusy ◽  
Ewa Maria Słomińska ◽  
Łukasz Kruszyna ◽  
Jacek Zieliński
Keyword(s):  
Adenosine Triphosphate ◽  
Endurance Athletes ◽  
Moderate Intensity ◽  
Control Group ◽  
Training Cycle ◽  
Exercise Induced ◽  
One Year ◽  
Age Range ◽  
And Control ◽  
Plasma Adenosine

This study aimed to assess the effect of training loads on plasma adenosine triphosphate responsiveness in highly trained athletes in a 1 y cycle. Highly trained futsal players (11 men, age range 20–31 y), endurance athletes (11 men, age range 18–31 y), sprinters (11 men, age range 21–30 y), and control group (11 men, age range 22–34 y) were examined across four characteristic training phases in response to an incremental treadmill test until exhaustion. A considerably higher exercise and post-exercise plasma adenosine triphosphate concentrations were observed in consecutive training phases in highly trained athletes, with the highest values reached after the competitive period. No differences in plasma adenosine triphosphate concentrations were found in the control group during the 1 y cycle. Sprinters showed a higher absolute and net increase in plasma adenosine triphosphate concentration by 60–114% during exercise in consecutive training phases than futsal players (63–101%) and endurance athletes (64–95%). In this study, we demonstrated that exercise-induced adenosine triphosphate concentration significantly changes in highly trained athletes over an annual training cycle. The obtained results showed that high-intensity but not low- to moderate-intensity training leads to an increased adenosine triphosphate response to exercise, suggesting an important role of ATP for vascular plasticity.

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