Cardiac Sarcoplasmic Reticular Function in Rats with Chronic Heart Failure Following Myocardial Infarction

Yamaguchi, Fuminari; Sanbe, Atsushi; Takeo, Satoshi

doi:10.1006/jmcc.1996.0319

Cited by 22 publications

(16 citation statements)

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“…Previous cardiomyopathic hamster studies have reported abnormalities in SR function; however, the underlying mechanisms are not fully understood (8,42,44). In this study, the decrease in heart function was associated with a reduction in SR Ca 2ϩ uptake of the cardiomyopathic heart.…”

Section: Discussionmentioning

confidence: 52%

“…Irregularities in cardiac performance can be linked to alterations in the SR function because of its critical role in regulating intracellular Ca 2ϩ (29,34,44). Although earlier reports (8,42,43) suggested that SR functions of Ca 2ϩ uptake and release were compromised in cardiomyopathic hamster hearts, the major challenge lies in discovering the mechanisms by which this occurs.…”

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confidence: 99%

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Cardiac contractile dysfunction in J2N-k cardiomyopathic hamsters is associated with impaired SR function and regulation

Babick¹,

Cantor²,

Babick³

et al. 2004

American Journal of Physiology-Cell Physiology

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. Cardiac contractile dysfunction in J2N-k cardiomyopathic hamsters is associated with impaired SR function and regulation. Am J Physiol Cell Physiol 287: C1202-C1208, 2004. First published June 30, 2004 doi:10.1152/ajpcell.00155.2004.-Although dilated cardiomyopathy (DCM) is known to result in cardiac contractile dysfunction, the underlying mechanisms are unclear. The sarcoplasmic reticulum (SR) is the main regulator of intracellular Ca 2ϩ required for cardiac contraction and relaxation. We therefore hypothesized that abnormalities in both SR function and regulation will contribute to cardiac contractile dysfunction of the J2N-k cardiomyopathic hamster, an appropriate model of DCM. Echocardiographic assessment indicated contractile dysfunction, because the ejection fraction, fractional shortening, cardiac output, and heart rate were all significantly reduced in J2N-k hamsters compared with controls. Depressed cardiac function was associated with decreased cardiac SR Ca 2ϩ uptake in the cardiomyopathic hamsters. Reduced SR Ca 2ϩ uptake could be further linked to a decrease in the expression of the SR Ca 2ϩ -ATPase and cAMPdependent protein kinase (PKA)-mediated phospholamban (PLB) phosphorylation at serine-16. Depressed PLB phosphorylation was paralleled with a reduction in the activity of SR-associated PKA, as well as an elevation in protein phosphatase activity in J2N-k hamster. The results of this study suggest that an alteration in SR function and its regulation contribute to cardiac contractile dysfunction in the J2N-k cardiomyopathic hamster. sarcoplasmic reticulum; cardiomyopathy; cAMP-dependent protein kinase; Ca 2ϩ /calmodulin-dependent protein kinase; sarco(endo)plasmic reticulum ATPase; phospholamban CARDIOMYOPATHY is defined as a disease of the heart muscle. It is classified as one of the most critical health disorders that cause death and disability among children and adults (10,39,41). Major health problems that have been documented as a result of cardiomyopathy are thromboembolism, arrhythmia, and sudden cardiac death (7,9,10,14,19,36,39,41). As a result of its various maladies, the heart in its diseased state can show pathophysiological changes at the level of myocardium function, chamber remodeling, neurohormonal activation, and altered loading conditions (7,9,10,14,19,36,39,41). Dilated cardiomyopathy (DCM) is a form of cardiomyopathy that is characterized by chamber dilation and impaired cardiac pump function. Although DCM is known to result in cardiac contractile dysfunction, the underlying mechanisms are unclear. In this study we examined the mechanisms underlying contractile dysfunction in cardiomyopathic hamsters, an excellent model of DCM. The Japanese J2N-k cardiomyopathic hamster was used because it uniquely exhibits a deletion in the ␦-sarcoglycan gene located in striated muscle, thereby affecting both skeletal and cardiac entities (25, 32). These hamsters experience cardiomyopathy, in addition to a form of muscular dystrophy, with eventual progression into heart failure (23). This an...

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Section: Discussionmentioning

confidence: 52%

mentioning

confidence: 99%

Cardiac contractile dysfunction in J2N-k cardiomyopathic hamsters is associated with impaired SR function and regulation

Babick¹,

Cantor²,

Babick³

et al. 2004

American Journal of Physiology-Cell Physiology

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“…Still regarding the abovementioned report, one cannot fail to notice the striking similarities between the baroreflex curves and gain curves presented here (for the SIO and TIO protocols; Figure 3) and those of 1-and 30-day infarcted animals (18). Nevertheless, the effects of iron overload on other factors that modulate calcium homeostasis in cardiomyocytes cannot be ruled out, such as Ca 2+ -ATPase pump involvement, low levels of Ca 2+ in the reticular sarcoplasm, Ca 2+ voltage-dependent channel sensitivity, or ryanodine receptor expression, among others (36,37).…”

Section: Groupmentioning

confidence: 79%

Baroreflex function in conscious rats submitted to iron overload

Cardoso

Pedrosa

Silva

et al. 2005

Braz J Med Biol Res

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Our hypothesis is that iron accumulated in tissue, rather than in serum, may compromise cardiovascular control. Male Fischer 344 rats weighing 180 to 220 g were divided into 2 groups. In the serum iron overload group (SIO, N = 12), 20 mg elemental iron was injected ip daily for 7 days. In the tissue iron overload group (TIO, N = 19), a smaller amount of elemental iron was injected (10 mg, daily) for 5 days followed by a resting period of 7 days. Reflex heart rate responses were elicited by iv injections of either phenylephrine (0.5 to 5.0 µg/kg) or sodium nitroprusside (1.0 to 10.0 µg/kg). Baroreflex curves were determined and fitted to sigmoidal equations and the baroreflex gain coefficient was evaluated. To evaluate the role of other than a direct effect of iron on tissue, acute treatment with the iron chelator deferoxamine (20 mg/kg, iv) was performed on the TIO group and the baroreflex was reevaluated. At the end of the experiments, evaluation of iron levels in serum confirmed a pronounced overload for the SIO group (30-fold), in contrast to the TIO group (2-fold). Tissue levels of iron, however, were higher in the TIO group. The SIO protocol did not produce significant alterations in the baroreflex curve response, while the TIO protocol produced a nearly 2-fold increase in baroreflex gain (-4.34 ± 0.74 and -7.93 ± 1.08 bpm/mmHg, respectively). The TIO protocol animals treated with deferoxamine returned to sham levels of baroreflex gain (-3.7 ± 0.3 sham vs -3.6 ± 0.2 bpm/mmHg) 30 min after the injection. Our results indicate an effect of tissue iron overload on the enhancement of baroreflex sensitivity.

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“…4 hearts of each group were examined to estimate infarct size after heart collections, and the other hearts were used to proteomics analysis. Myocardial infarction was induced by ligating the left anterior descending coronary artery according to the method of Yamaguchi [10]. The sham group and MI group rats were given normal sodium (i.p), while MI + verapamil group rats were given verapamil (1 g/kg).…”

Section: Myocardial Infarction Treatment and Histological Studymentioning

confidence: 99%

Proteome analysis of differential protein expression in infarcted rat heart after verapamil treatment

Liu

Wang

et al. 2009

Front. Chem. China

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To explore the protein-level mechanism of action verapamil in acute myocardial infarcted rats, the myocardial proteome was analyzed by two-dimensional electrophoresis (2-DE). Compared with the sham-operated group and the infarcted group, the result shows that 8 protein expressions in the verapamil treated group were up-regulated, and 7 protein expressions in this group were down-regulated significantly. Using MALDI-TOF-MS, 15 proteins with significant changes were identified through a database search. These proteins can be divided into 4 groups by their biological function: (1) Energy metabolism and mitochondrial function related proteins; (2) oxidative stress-induced proteins; (3) cytoskeletal Proteins; (4) other proteins. The findings show that the myocardial protective effects of verapamil in the myocardial damage process are related to the recovery of energy supply as well as antioxidative stress property.

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Cardiac Sarcoplasmic Reticular Function in Rats with Chronic Heart Failure Following Myocardial Infarction

Cited by 22 publications

References 0 publications

Cardiac contractile dysfunction in J2N-k cardiomyopathic hamsters is associated with impaired SR function and regulation

Cardiac contractile dysfunction in J2N-k cardiomyopathic hamsters is associated with impaired SR function and regulation

Baroreflex function in conscious rats submitted to iron overload

Proteome analysis of differential protein expression in infarcted rat heart after verapamil treatment

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