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  • 1
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 293, No. 5 ( 2007-11), p. H3014-H3019
    Abstract: Previous studies have shown that 1 wk after permanent coronary artery ligation in rats, some cellular mechanisms involving TNF-α occur and contribute to the development of cardiac dysfunction and subsequent heart failure. The aim of the present study was to determine whether similar phenomena also occur after ischemia-reperfusion and whether cytokines other than TNF-α can also be involved. Anesthetized male Wistar rats were subjected to 1 h coronary occlusion followed by reperfusion. Cardiac geometry and function were assessed by echocardiography at days 5, 7, 8, and 10 postligation. Before death, heart function was assessed in vivo under basal conditions, as well as after volume overload. Finally, hearts were frozen for histoenzymologic assessment of infarct size and remodeling. The profile of cardiac cytokines was determined by ELISA and ChemiArray on heart tissue extracts. As expected, ischemia-reperfusion induced a progressive remodeling of the heart, characterized by left ventricular free-wall thinning and cavity dilation. Heart function was also decreased in ischemic rats during the first week after surgery. Interestingly, a transient and marked increase in TNF-α, IL-1β, IL-6, cytokine-induced neutrophil chemoattractant (CINC) 2, CINC3, and macrophage inflammatory protein-3α was also observed in the myocardium of myocardial ischemia (MI) animals at day 8, whereas the expression of anti-inflammatory interleukins IL-4 and IL-10 remained unchanged. These results suggest that overexpression of proinflammatory cytokines occurring during the first week after ischemia-reperfusion may play a role in the adaptative process in the myocardium and contribute to early dysfunction and remodeling.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2007
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 2
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 118, No. suppl_18 ( 2008-10-28)
    Abstract: Background: A major complication of diabetes is the development of cardiac dysfunction in absence of vascular disease. Metabolic disorders such as insulin resistance (IR) and dyslipidemia (DL) might contribute to the induction of diabetic cardiomyopathy (DCM). However, few relevant animal models are currently available for studying the time-course of DCM and evaluating experimental therapeutics. We developed a rodent model of dietary-induced IR combined or not with DL in order to investigate the impact of chronic IR and DL on in vivo myocardial function. Methods & Results: Male Sprague-Dawley rats were fed a western-type diet (65% fat; 15% fructose; WD: n=12). DL was induced by combining the western diet with i.p . injections of a nonionic surface-active agent (P-407; 0.2 mg/kg, 3 times/wk; WD-P407 n=9). A chow diet was used as control (Chow: n=9). At 6, 11 and 14 wks, cardiac function was assessed by echocardiography. After 6 wks, plasma insulin was significantly increased in both WD and WD-P407 groups ( P 〈 0.05 vs. Chow). Fasting blood glucose increased in WD group while plasma lipids markedly accumulated in WD-P407-treated rats ( P 〈 0.05 and P 〈 0.01 vs. Chow, respectively). Pulse-wave Doppler indicated impaired diastolic function at 14 wks (E/A wave ratio: WD-P407: 1.42±0.06 vs. Chow: 1.65±0.11). M-mode imaging showed no significant differences in cardiac function and geometry under basal conditions. However, fractional shortening (FS) was significantly depressed under dobutamine stress in WD group at 14 wks (FS in % of baseline: 151±9% vs 196±7%; P 〈 0.05) whereas systolic dysfunction appeared as early as 11 wks and worsened at 14 wks in WD-P407 animals ( P 〈 0.05 and P 〈 0.01 vs. Chow, respectively). Finally, compared to Chow, myocardial lipid tissue content and pro-inflammatory cytokine TNF-α were significantly higher in WD and WD-P407 groups, the cardiac lipid accumulation being more pronounced in the later. Conclusions: DL exacerbated cardiac lipotoxicity and functional complications associated with IR. This experimental model of combined IR and DL closely mimics the main clinical manifestations of DCM and might therefore constitute a useful tool for the evaluation of pharmacological treatments.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
    detail.hit.zdb_id: 1466401-X
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  • 3
    In: Cardiovascular Drugs and Therapy, Springer Science and Business Media LLC, Vol. 22, No. 6 ( 2008-12), p. 437-442
    Type of Medium: Online Resource
    ISSN: 0920-3206 , 1573-7241
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2008
    detail.hit.zdb_id: 2003553-6
    SSG: 15,3
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  • 4
    In: Molecular Nutrition & Food Research, Wiley, Vol. 55, No. 4 ( 2011-04), p. 522-529
    Abstract: Scope : Post‐infarct left ventricular dysfunction and cardiac remodeling are the primary causes of chronic heart failure in industrialized countries. In the present study, we examined the influence of dietary selenium intake on cardiac remodeling after reperfused myocardial infarction and explored one of the possible mechanisms. Methods and results : Rats were fed a diet containing either 0.05 mg/kg (Low‐Se, group of rats receiving the low‐selenium diet) or 1.50 mg/kg (group of rats receiving the high‐selenium diet) selenium. At the end of the 5th week of the diet, rats were subjected to transient (1 h) coronary ligation followed by 8 days of reperfusion. Infarct size and cardiac passive compliance were increased in the Low‐Se group compared with group of rats receiving the high‐selenium diet. Similarly, indices of cardiac remodeling (thinning index and expansion index) were more altered in Low‐Se hearts. These adverse effects of the Low‐Se diet on cardiac remodeling were accompanied by an increase in cardiac TNF‐α content, a decreased activity of antioxidant seleno‐enzymes and an increase in connexin‐43 dephosphorylation. Conclusion : Dietary selenium intake influences post‐infarct cardiac remodeling even when provided within the range of physiological values. Our data suggest that the cardioprotective effect of selenium might be mediated by a reduced oxidative stress, a lower connexin‐43 dephosphorylation, and a decreased TNF‐α expression.
    Type of Medium: Online Resource
    ISSN: 1613-4125 , 1613-4133
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2011
    detail.hit.zdb_id: 2160372-8
    SSG: 12
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