Structural and electrical ventricular remodeling in rat acute myocarditis and subsequent heart failure

Wakisaka, Yoshinari; Niwano, Shinichi; Niwano, Hiroe; Saito, Junko; Yoshida, Tohru; Hirasawa, Shoji; Kawada, Hideaki; Izumi, Tohru

doi:10.1016/j.cardiores.2004.04.020

Cited by 43 publications

(52 citation statements)

References 35 publications

(64 reference statements)

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“…In rats, hemodynamic deterioration and myocarditis have been reported after 3 weeks of immunization with cardiac a-myosin or a-myosin peptides [173,305]. This was associated with increased expression and activity of inducible nitric oxide synthase (iNOS) and an inhibitor of that enzyme effectively attenuated the histopathologic changes, thus pointing to a relevant pathophysiologic role of nitric oxide (NO) [103,104].…”

Section: Myocarditis-induced Hfmentioning

confidence: 99%

Rodent models of heart failure: an updated review

et al. 2012

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Heart failure (HF) is one of the major health and economic burdens worldwide, and its prevalence is continuously increasing. The study of HF requires reliable animal models to study the chronic changes and pharmacologic interventions in myocardial structure and function and to follow its progression toward HF. Indeed, during the past 40 years, basic and translational scientists have used small animal models to understand the pathophysiology of HF and find more efficient ways of preventing and managing patients suffering from congestive HF (CHF). Each species and each animal model has advantages and disadvantages, and the choice of one model over another should take them into account for a good experimental design. The aim of this review is to describe and highlight the advantages and drawbacks of some commonly used HF rodents models, including both non-genetically and genetically engineered models, with a specific subchapter concerning diastolic HF models.

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Section: Myocarditis-induced Hfmentioning

confidence: 99%

Rodent models of heart failure: an updated review

et al. 2012

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“…13,14) The sham rats received injections of the same amount of saline (0.25 mL) in the same manner (n = 20). EAM was induced in all 110 rats immunized, however, 7 rats died during the acute phase so 103 of 110 were used in the experiments.…”

Section: Methodsmentioning

confidence: 99%

“…The dosages used were determined based on previous reports, [15][16][17] ie, the lower and higher dosages represented the middle and highest doses of the therapeutic range, respectively. Noninvasive echocardiography: The left ventricular dimension and function in vivo were assessed using transthoracic echocardiography (ProSound SSD-4000, Aloka, Tokyo) as previously described 13) and were performed in randomly selected rats at day 21 or day 60 after the initial immunization as summarized in Table I. The assessment was done noninvasively under light anesthesia with an intraperitoneal injection of 2,2,2-tribromoethanol (80-120 mg/kg).…”

Section: Methodsmentioning

confidence: 99%

“…For the hemodynamic parameters, the left ventricular systolic pressure (LVSP) and left ventricular end-diastolic pressure (LVEDP) were monitored by a needle tip micromanometer (SPR477, Millar, USA) as previously described. 13,14) For the electrophysiological evaluation, a pair of platinum needle electrodes (φ 0.1 mm) was directly inserted into the left ventricular free wall, and used for electrical stimulation and recording. The analogue signals were converted into digital signals at a sampling frequency of 1000 Hz (Power Lab 8sp, Bio Research, Tokyo) and stored on a computer hard disk.…”

Section: Methodsmentioning

confidence: 99%

“…11) This prolongation of the action potential duration may increase transient calcium and may exaggerate intracellular calcium overload, resulting in the deterioration of myocardial dysfunction. 12) We documented that this electrophysiological change can also be observed in acute inflammatory conditions in an experimental autoimmune myocarditis (EAM) model in rats, 13,14) which is a model showing acute myocarditis in the acute phase followed by dilated cardiomyopathy in the chronic phase. In the acute phase of this model, there would be a worsening cycle between the intracellular calcium overload and prolonged action potential duration as a result of the myocardial injury, which may also adversely affect mitochondrial function.…”

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confidence: 95%

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Cardioprotective Effects of Sarcolemmal and Mitochondrial K-ATP Channel Openers in an Experimental Model of Autoimmune Myocarditis

et al. 2012

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SummaryIt has been reported that K-ATP channel openers have a cardioprotective effect in acute ischemia as a pharmacological preconditioning effect. In the present study, the chronic effects of clinical K-ATP channel openers, ie, nicorandil (Nic) and mexiletine (Mex), on cardiac function were evaluated in a rat model of experimental autoimmune myocarditis (EAM). Nicorandil (3 or 10 mg/kg/day) or Mex (10 or 25 mg/kg/day) was administered to the EAM rats, and the effects were compared with those in untreated EAM rats (control EAM) and sham rats without EAM on day 21 (acute phase) or day 60 (chronic phase). In the acute phase, the control EAM rats exhibited a reduced left ventricular ejection fraction (LVEF) and prolonged monophasic action potential duration (MAPD). Neither drug had an affect on the LVEF or degree of myocarditis, but Mex 25 mg suppressed the MAPD prolongation. In the chronic phase, EAM+Nic and EAM+Mex 25 mg exhibited a higher LVEF than the control EAM. Although the control EAM exhibited sustained MAPD prolongation, the other groups showed recovery of the MAPD in the chronic phase. The mitochondorial redox state was lower in the control EAM than in the sham, and EAM+Nic exhibited a similar level of the redox state as the sham in the chronic phase. Nicorandil exhibited a cardioprotective effect through the protection of mitochondrial function. Mexiletine exhibited a cardioprotective effect possibly through a reduction in the calcium overload by shortening the MAPD in the acute phase. (Int Heart J 2012; 53: 139-145)

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Antibodies Against Potassium Channel Interacting Protein 2 Induce Necrosis in Isolated Rat Cardiomyocytes

et al. 2014

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Auto-antibodies against cardiac proteins have been described in patients with dilated cardiomyopathy. Antibodies against the C-terminal part of KChIP2 (anti-KChIP2 [C-12]) enhance cell death of rat cardiomyocytes. The underlying mechanisms are not fully understood. Therefore, we wanted to explore the mechanisms responsible for anti-KChIP2-mediated cell death. Rat cardiomyocytes were treated with anti-KChIP2 (C-12). KChIP2 RNA and protein expressions, nuclear NF-κB, mitochondrial membrane potential Δψm, caspase-3 and -9 activities, necrotic and apoptotic cells, total Ca(2+) and K(+) concentrations, and the effects on L-type Ca(2+) channels were quantified. Anti-KChIP2 (C-12) induced nuclear translocation of NF-κB. Anti-KChIP2 (C-12)-treatment for 2 h significantly reduced KChIP2 mRNA and protein expression. Anti-KChIP2 (C-12) induced nuclear translocation of NF-κB after 1 h. After 6 h, Δψm and caspase-3 and -9 activities were not significantly changed. After 24 h, anti-KChIP2 (C-12)-treated cells were 75 ± 3% necrotic, 2 ± 1% apoptotic, and 13 ± 2% viable. Eighty-six ± 1% of experimental buffer-treated cells were viable. Anti-KChIP2 (C-12) induced significant increases in total Ca(2+) (plus 11 ± 2%) and K(+) (plus 18 ± 2%) concentrations after 5 min. Anti-KChIP2 (C-12) resulted in an increased Ca(2+) influx through L-type Ca(2+) channels. In conclusion, our results suggest that anti-KChIP2 (C-12) enhances cell death of rat cardiomyocytes probably due to necrosis.

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Structural and electrical ventricular remodeling in rat acute myocarditis and subsequent heart failure

Cited by 43 publications

References 35 publications

Rodent models of heart failure: an updated review

Rodent models of heart failure: an updated review

Cardioprotective Effects of Sarcolemmal and Mitochondrial K-ATP Channel Openers in an Experimental Model of Autoimmune Myocarditis

Antibodies Against Potassium Channel Interacting Protein 2 Induce Necrosis in Isolated Rat Cardiomyocytes

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