Cardioprotective effects of Amiodarone in a rat model of epilepsy‐induced cardiac dysfunction

Ischemia followed by reperfusion in the presence of polymorphonuclear leukocytes (PMNs) results in cardiac dysfunction. C-peptide, a cleavage product of proinsulin to insulin processing, induces nitric oxide (NO)-mediated vasodilation. NO is reported to attenuate cardiac dysfunction caused by PMNs after ischemia-reperfusion (I/R). Therefore, we hypothesized that C-peptide could attenuate PMN-induced cardiac dysfunction. We examined the effects of C-peptide in isolated ischemic (20 min) and reperfused (45 min) rat hearts perfused with PMNs. C-peptide (70 nmol/kg iv) given 4 or 24 h before I/R significantly improved coronary flow ( P < 0.05), left ventricular developed pressure (LVDP) ( P < 0.01), and the maximal rate of development of LVDP (+dP/d t max) compared with I/R hearts obtained from rats given 0.9% NaCl ( P < 0.01). N G-nitro-l-arginine methyl ester (l-NAME) (50 μmol/l) blocked these cardioprotective effects. In addition, C-peptide significantly reduced cardiac PMN infiltration from 183 ± 24 PMNs/mm2 in untreated hearts to 44 ± 10 and 58 ± 25 PMNs/mm2 in hearts from 4- and 24-h C-peptide-treated rats, respectively. Rat PMN adherence to rat superior mesenteric artery exposed to 2 U/ml thrombin was significantly reduced in rats given C-peptide compared with rats given 0.9% NaCl ( P < 0.001). Moreover, C-peptide enhanced basal NO release from rat aortic segments. These results provide evidence that C-peptide can significantly attenuate PMN-induced cardiac contractile dysfunction in the isolated perfused rat heart subjected to I/R at least in part via enhanced NO release.

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Early cardiac dysfunction is rescued by upregulation of SERCA2a pump activity in a rat model of metabolic syndrome

Acta Physiologica ◽

10.1111/j.1748-1716.2012.02420.x ◽

2012 ◽

Vol 205 (3) ◽

pp. 381-393 ◽

Cited By ~ 14

Author(s):

Z. Miklós ◽

P. Kemecsei ◽

T. Bíró ◽

R. Marincsák ◽

B. I. Tóth ◽

...

Keyword(s):

Metabolic Syndrome ◽

Rat Model ◽

Cardiac Dysfunction ◽

Pump Activity

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Cardioprotective Effects of 20(S)-Ginsenoside Rh2 against Doxorubicin-Induced CardiotoxicityIn VitroandIn Vivo

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2012/506214 ◽

2012 ◽

Vol 2012 ◽

pp. 1-8 ◽

Cited By ~ 14

Author(s):

Hongbo Wang ◽

Pengfei Yu ◽

Haitao Gou ◽

Jianqiao Zhang ◽

Mei Zhu ◽

...

Keyword(s):

Rat Model ◽

A549 Cells ◽

H9c2 Cell ◽

Protective Agent ◽

Protective Effects ◽

Ginsenoside Rh2 ◽

Cardioprotective Effects ◽

Heart Injury

Doxorubicin (DOX) is considered as one of the best antineoplastic agents. However, its clinical use is restricted by its associated cardiotoxicity, which is mediated by the production of reactive oxygen species. In this study, 20(S)-ginsenoside Rh2 (Rh2) was explored whether it had protective effects against DOX-induced cardiotoxicity.In vitrostudy on H9C2 cell line, as well asin vivoinvestigation in one mouse and one rat model of DOX-induced cardiomyopathy, was carried out. The results showed that pretreatment with Rh2 significantly increased the viability of DOX-injured H9C2 cells. In the mouse model, Rh2 could suppress the DOX-induced release of the cardiac enzymes into serum and improved the occurred pathological changes through ameliorating the decreased antioxidant biomolecules and the cumulated lipid peroxidation malondialdehyde in heart tissues. In the rat model, Rh2 could attenuate the change of ECG resulting from DOX administration. Furthermore, Rh2 enhanced the antitumor activity of DOX in A549 cells. Our findings thus demonstrated that Rh2 pretreatment could effectively alleviate heart injury induced by DOX, and Rh2 might act as a novel protective agent in the clinical usefulness of DOX.

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