Razi Journal of Medical Sciences

fa پاسخ بازتوانی ورزشی همراه با تحریک الکتریکی بر سطوح سرمی ICAM و VCAM موش‌های صحرایی مبتلا به انفارکتوس میوکارد تجربی The Response of Exercise Rehabilitation Combined with Electrical Stimulation on the Serum Levels of ICAM and VCAM in rats with Experimental Myocardial Infarction فیزیوتراپی ورزشی Sports Physiotherapy پژوهشي Research <div style="text-align: justify;">زمینه و هدف: کنترل عوامل التهابی بعد از آنفارکتوس، به‌علت فقدان جریان خون کافی میوکارد از عوامل اثر گذار بر بهبود بیماران سکته قلبی می‌باشد. مولکول‌های چسبان سلولی و عروقی از جمله این عوامل التهابی هستند که در اختلالات قلبی-‌عروقی نقش به‌سزایی دارند. به‌همین منظور هدف از این پژوهش بررسی پاسخ اثر ضد التهابی یک دوره حاد تمرین استقامتی به&lrm;همراه تحریک الکتریکی در موش‌های صحرایی مبتلا به انفارکتوس میوکارد تجربی بود. روش کار: در این مطالعه تجربی-آزمایشگاهی 40 سر موش صحرایی نژاد ویستار (8 هفته‌ای با وزن30±220 گرم) پس از وزن کشی به‌طور تصادفی به 4 گروه انفارکته، انفارکته-بازتوانی ورزشی، انفارکته-تحریک الکتریکی و انفارکته-بازتوانی ورزشی-تحریک الکتریکی تقسیم شدند. سپس انفارکتوس میوکارد با استفاده از دو تزریق زیرجلدی ایزوپروترونول (150 میلی‌گرم/کیلوگرم) به فاصله 24 ساعت در گروه‌های انفارکته القاء گردید. گروه‌های مداخله برای یک جلسه تحت بازتوانی ورزشی (تردمیل با سرعت 20 متر/دقیقه برای 1 ساعت) و تحریک الکتریکی (دستگاه فوت شوک برای 5/0 میلی‌آمپر و 20 دقیقه) قرار گرفتند. بلافاصله بعد از مداخله، سطوح سرمی مولکول چسبان سلولی و مولکول چسبان عروقی به روش الایزا بررسی شدند. برای آنالیز داده‌ها از آزمون آنووا یکطرفه و تعقیبی توکی در سطح معنی‌داری 05/0>P استفاده شد. یافته‌ها: نتایج نشان داد تحریک الکتریکی در نمونه‌های انفارکته منجر به افزایش معنی‌دار سطوح سرمی مولکول چسبان سلولی (021/0P=) میشود. اما میزان مولکول چسبان عروقی در گروه تحریکی الکتریکی(040/0P=) و گروه تحریک الکتریکی-بازتوانی ورزشی(038/0P=) کاهش معنی‌داری را نشان داده است. نتیجه‌گیری: به نظر می‌رسد با توجه به نتایج مطالعه حاضر هنوز نمیتوان با قطعیت سمت و سوی اثر بازتوانی حاد ورزشی و تحریک الکتریکی فوت شوک را بر مولکول های چسبان تعیین نمود.</div> <div style="text-align: justify;">Background & Aims: Controlling inflammatory factors after myocardial infarction (MI), due to the lack of sufficient myocardial blood flow, is one of the factors influencing the recovery of infarction patients. Therefore, it is very necessary to know the causes of MI as one of the main causes of death in worldwide. The disease affects nearly three million people global and kills more than one million people in the United States each year (1) and cardiovascular problems caused by MI are the most common cause of MI (2). Research has shown that adhesion molecules play an important role in the pathogenesis of MI. New markers of intercellular adhesion molecule (ICAM) and vascular adhesion molecule (VCAM) have high sensitivity and accuracy in predicting and identifying the risk of heart damage and play an important role in the Prevalence of heart problems (2). It seems that the reduction of inflammatory markers has a positive effect on improving the condition of MI patients (4). Also, finding appropriate training methods and different training intensities has been the focus of researchers in the field of exercise physiology in recent years. There are conflicting studies between endurance training and the expression of ICAM and VCAM genes (5, 6). Also considering that electrical stimulation (ES) is used as a new and effective modality in the treatment of ischemia (8). Therefore, it was used as another intervention in the present study. According to research, it is expected that ES is a rehabilitation method for people who participate in exercise training (10) and also patients with heart failure (HF) (11). However, in other studies, the positive effects of exercise and ES on various aspects of heart health in patients with MI have been noted. For that reason, the researchers of the present study intend to investigate the exercise rehabilitation response with electrical stimulation on serum ICAM and VCAM levels of rats with myocardial infarction. Methods: In this experimental study, 40 Wistar rats (8 weeks old with an average weight of 220 ± 30 g) were randomly divided into 4 infarction groups, infarction-exercise rehabilitation, infarction electrical stimulation and infarction-exercise rehabilitation-electrical stimulation groups were divided. Then, MI was induced using two subcutaneous injections of Isoproterenol (ISO) (150 mg/kg) with an interval of 24 hours in the infarcted groups. This substance is one of the common methods of inducing MI in animal models, especially rats (14). In this study, heart infarction was confirmed based on electrocardiographic changes (ST segment elevation) along with the increase of cardiac enzyme cTnI (344.01 pg/ml). The intervention groups underwent exercise rehabilitation (treadmill at a speed of 20 m/min for 1 hour) and ES (foot shock device for 0.5 mA and 20 minutes) for one session. Groups were anesthetized and killed immediately after the end of the training protocol with a combination of ketamine (75 mg/kg) and xylazine (10 mg/kg). Blood sampling was done directly from the right atrium of the rat. The serum levels of ICAM and VCAM were checked by ELISA method. After confirming the normal distribution of the data using the Shapiro-Wilk test, one-way ANOVA and Tukey's post hoc test were used to analyze the data at a significance level of P<0.05. Results: The results of the analysis of ICAM levels showed a statistically significant difference between MI and MI.ES groups (F=4.4 and P=0.021), MI.EX and MI.ES (F=5.9 and P=0.002). But this difference between MI with MI.EX (F=1.4 and P=0.762), MI with MI.EX.ES (F=1.17, P=0.838), MI.EX with MI.EX. ES (F=2.56, P=0.292) and MI.ES with MI.EX.ES (F=3.26, P=0.124) were not significant. The results of VCAM levels showed a statistically significant difference between MI and MI.ES groups (F=3.9 and P=0.040) and MI and MI.EX.ES groups (F=2.3 and P=0.038). But between the groups, MI with MI.EX (F=1.60 and P=0.659), MI.EX with MI.ES (F=2.4, P=0.343, MI.EX with MI.EX .ES (F=2.4, P=0.331) and MI.ES with MI.EX.ES (F=0.034, P=0.999), this difference was not significant. Conclusion: Deficiency in the function of cell adhesion molecules is one of the main causes of pathological progress in many diseases, including cardiovascular disorders. Therefore, investigating inflammatory pathways and cellular and molecular processes involved in it is very necessary. The cholinergic anti-inflammatory pathway consisting of the Vagus nerve and its transporter acetylcholine play an important role in regulating the inflammatory response. When the body is injured, the excitability of the Vagus nerve increases, which causes the release of acetylcholine from peripheral nerve endings. This process can inhibit the release of pro-inflammatory cytokines such as IL-1, TNF-a, IL-6 and IL-17 and lead to the reduction of heart damage. Also, ES can change the function of inflammatory cells at the molecular level, thereby preventing the spread of inflammation by affecting the number of immune cells as a mediator. In general, it seems that according to the results of the present study, it is still not possible to determine with certainty the direction and direction of the effect of acute sports rehabilitation and foot shock electrical stimulation on adhesive molecules, and it needs more study.  </div> انفارکتوس میوکارد, بازتوانی ورزشی, تحریک الکتریکی, مولکول چسبان سلولی, مولکول چسبان عروقی Myocardial Infarction, Exercise Rehabilitation, Electrical Stimulation, Cell Adhesion Molecule, Vascular Adhesion Molecule 127 138 http://rjms.iums.ac.ir/browse.php?a_code=A-10-7221-1&slc_lang=fa&sid=1 Mohammad MalekiPooya محمد ملکی پویا maleki.p@gmail.com 3900319475328460077140 3900319475328460077140 Yes Assistant Professor Department of Physical Education and Sports Sciences, Islamic Azad University, Arak Branch, Arak, Iran استادیار، گروه فیزیولوژی ورزشی، دانشگاه آزاد اسلامی واحد اراک، اراک، ایران Mojtaba Khansooz مجتبی خان سوز 3900319475328460077141 3900319475328460077141 No Assistant Professor, Department of Physical Education and Sports Sciences, Islamic Azad University, Arak Branch, Arak, Iran استادیار، گروه فیزیولوژی ورزشی، دانشگاه آزاد اسلامی واحد اراک، اراک، ایران