We investigated the level of sympathetic hyperactivity in response to stress exposure in an acute myocardial infarction (AMI) model and the contribution of oxidative and nitrosative damage to this phenomenon. Stress was induced by 20-day administration of different emotional stress factors: daylight/darkness exposure, overcrowding, isolation, new hierarchy, tilting the cage and restriction of water or food. AMI was induced surgically. Heart rate (HR) and heart rate variability (HRV) measurements were done before and after AMI. Oxidant parameters were measured in heart tissue and cortisol levels were measured in plasma specimens. Compared with the nonstressed group, stress-exposed rats showed sympathetic hyperactivity characterized by increased HR together with decreased HRV. In the stressed group serum corticosterone levels were high both before and after AMI. Mean infarct size in the stressed group was significantly larger (44.6+/-3.23% and 53.1+/-4.52%, respectively; P<0.05). Increased tissue malondialdehyde (MDA) levels (0.63+/-0.59 and 1.60+/-0.31 nmol/mg protein, respectively; P<0.05) and decreased superoxide dismutase (SOD) activity and glutathione (GSH) content were seen in stress-exposed rats. Likewise, heart peroxynitrite levels were also high in stress-exposed rats (141.8+/-18 nmol/g tissue vs. 164.2+/-21 nmol/g tissue). Chronic emotional stress is a deteriorating factor for the induction and prognosis of MI. Exaggerated sympathetic activity may be the major contributing factor. Oxidative and nitrosative damage in response to this sympathetic hyperactivity is the key mechanism.
fter myocardial infarction (MI), a series of structural changes (expansion and thinning of the infracted area) occur. 1,2 Although these changes help to maintain the cardiac function at the early phase of MI, when they are not controlled, it might lead to left ventricular (LV) dysfunction. 3 Cellular and molecular mechanisms contributing to the LV dysfunction are not fully understood, apoptosis, both in the infarct and healthy myocardium has been shown as an important role. 4,5 Nebivolol, a selective -blocker, 6 was shown to improve the ventricular function and hemodynamic parameters in patients with LV dysfunction. In addition to -blocker activity, nebivolol regulates the releasing nitric oxide (NO) by the activation of endothelial NO synthase (e-NOS) in endothelial cells. NO is related not only to the maintenance of healthy endothelial function, but also to apoptosis.In the present study our aim is to evaluate the NO mediated effects of nebivolol after MI in rats and the role of antiapoptotic mechanisms in this effect. Methods Animal Groups, Dose Selection and Study DurationAnimals were housed in a temperature-controlled animal facility with a 12-h light/dark cycle, with tap water and rodent chow ad libitum and handled in accordance with the Guide for the Care and the Use of Laboratory Animals published by the US National Institutes of Health. All experimental procedures were approved by the Institutional Animal Ethic Committee of Istanbul University Experimental Medical Research Institute.Twelve-week-old male Sprague Dawley rats, with a mean weight of 250-300 g, were divided in 3 groups of 12 each: sham operated control (sham-control), MI induced (MI-control) and nebivolol treated (MI-nebivolol).Nebivolol was administrated within 10 min of reperfusion at dose of 0.1 mg/kg iv and continued orally at dose of 2.0 mg/kg, by gastric gavage once daily for 28 days. The iv dose of nebivolol was selected as the minimum -blocker dose (absence of significant effect on blood pressure and heart rate (HR)), after a preliminary dose-response study, (using 0.1-0.5-1 mg/kg of nebivolol iv) according to Sacco et al (Fig 1). 7 The oral dose was selected according to Sanchez et al. 8 Hemodynamic effects of these 2 dose regimes were compared with metoprolol, a 1-selective adrenoreceptor antagonist (Tables 1,2).To evaluate the effects of nebivolol on the apoptosis both in acute and sub-acute period of MI, time intervals were selected as 2 days (for acute) and 28 days (for sub-acute) of Background In the present study, nitric oxide (NO) was investigated to see if it mediated effects of nebivolol on apoptosis in the rat myocardial infarction (MI) model. Methods and ResultsRats were divided into 3 groups: sham operated (sham-control), MI-induced (MI-control) and nebivolol treated (MI-nebivolol). The initial dose of nebivolol was administrated intravenously (iv) within 10 min of post-MI reperfusion and continued orally for 28 days. NO mediated effects of nebivolol were assessed either in the early (2 nd day) or sub-acute (28 th day) ...
ÖZETBu çalışmada, 170'i hukuk mezunu, 480'i toplumun çe şitli kesimlerinden olmak üzere toplam 650 kişinin evlilikiçi zorla cinsel ilişki konusundaki görüşlerini belirleyen anket formlarının sonuçları değerlendirilmiştir.Çalışmaya katılanların % 65'inin, hukukçuların % 45'inin ve toplumdan katılanların % 71'inin kocanın karısıyla zorla cinsel ilişkide bulunmasının bir ırza geçme suçu oluşturaca ğına inandıkları görülmektedir.Çalışmaya katılanların yarı dan fazlasının bu görüşte olması evlilikiçi zorla cinsel ilişki nin ırza geçme suçu olarak düzenlenmesi yolundaki tartış malara basamak oluşturmaktadır.A nahtar k elim eler: Evlilik, Irza geçme. SUMMARYThe purpose of this study was to determine the opin ions of the jurists and society about marital rape. The ques tionnaires were completed by 170 jurists and 480 from the society.48 % of the jurists, 71 % of the ones from the society and 65 % in general, agree that the forced sexual intercourse in the marriage is a rape crime. As more than the half of the participants have agreement, marital rape should be seri ously discussed to be reserved in Turkish laws as a rape crime.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.