Cardiac hypertrophy is a common pathological process of various cardiovascular diseases and eventually develops into heart failure. This paper was aimed to study the different pathological characteristics exhibited by different mouse strains after hypertrophy stimulation. Two mouse strains, A/J and FVB/nJ, were treated with isoproterenol (ISO) by osmotic pump to induce cardiac hypertrophy. Echocardiography was performed to monitor heart morphology and function. Mitochondria were isolated from hearts in each group, and oxidative phosphorylation function was assayed in vitro. The results showed that both strains showed a compensatory enhancement of heart contractile function after 1-week ISO treatment. The A/J mice, but not the FVB/nJ mice, developed significant cardiac hypertrophy after 3-week ISO treatment as evidenced by increases in left ventricular posterior wall thickness, heart weight/body weight ratio, cross sectional area of cardiomyocytes and cardiac hypertrophic markers. Interestingly, the heart from A/J mice contained higher mitochondrial DNA copy number compared with that from FVB/nJ mice. Functionally, the mitochondria from A/J mice displayed faster O
Animals ; Cardiomegaly/chemically induced* ; Heart Failure ; Isoproterenol/toxicity* ; Mice ; Mitochondria ; Myocytes, Cardiac/metabolism*

Antipsychotic Agents/adverse effects* ; Heart Failure/chemically induced* ; Humans ; Syncope

OBJECTIVE: This article investigated the changes of some biochemical markers and cardiac function in chronic heart failure (CHF), and provided the basis for the diagnosis of CHF. METHODS: New Zealand rabbit CHF model was established using adriamycin (ADR). Twenty New Zealand rabbits were randomly divided into model group (=15) and control group (=5), injected with ADR and saline solution the ear vein respectively, 2 times a week, lasting for 8 weeks. After that, myocardial enzymes, carotid artery pressure, echocardiogram (ECG) and phonocardiogram (PCG) of all New Zealand rabbits were detected and recorded. RESULTS: Compared with control group, all parameters of the model group were changed significantly (<0.05). CONCLUSIONS CHF leads to myocardial damage in New Zealand rabbits, decreased systolic and diastolic function, cardiac reserve index can be used to assess cardiac function.
Animals ; Biomarkers ; analysis ; Blood Pressure ; Carotid Arteries ; physiopathology ; Chronic Disease ; Doxorubicin ; Electrocardiography ; Heart Failure ; chemically induced ; physiopathology ; Myocardium ; enzymology ; Phonocardiography ; Rabbits ; Random Allocation

OBJECTIVETo investigate the effects of Xinfuli Granule (XG) on cardiomyocyte apoptosis in rats with adriamycin-induced dilated cardiomyopathy (DCM).

METHODSSeventy-two male SD rats were randomly divided into 6 groups, i.e., the normal control group, the model group, the irbesartan group, the low dose XG group, the medium dose XG group, and the high dose XG group. The DCM heart failure rat model was established using peritoneal injection of ADR. Equal volume of normal saline was injected to those in the normal control group, once per week for 6 consecutive weeks. The medication was started from the 5th week by gastrogavage. XG was dispensed into 0.5 g/mL suspension with distilled water. The XG was administered at the daily dose of 0.675 g/kg, 1.350 g/kg, and 2.700 g/kg to those in the low dose XG group, the medium dose XG group, and the high dose XG group, respectively. Irbesartan was administered to rats in the irbesartan group at the daily dose of 50 mg/kg. Equal volume of normal saline was administered to those in the normal control group and the model group by gastrogavage, once in the morning for 4 consecutive weeks. Myocardial apoptosis was measured by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL), and the expressions of the Bcl-2 and Bax protein of cardiomyocytes were measured by immunohistochemical assay.

RESULTSCompared with the normal control group, the cardiomyocyte apoptosis rate and Bax expression level obviously increased, but the expression of Bcl-2 and the Bcl-2/Bax ratio decreased significantly in the model group (P < 0.05). Compared with the model group, the expression of Bax and the Bcl-2/Bax ratio increased significantly in the high dose XG group and the irbesartan group (P < 0.01). The Bax expression level obviously decreased in all groups except the normal control group (P < 0.01).

CONCLUSIONSXG could obviously attenuate cardiomyocyte apoptosis in the adriamycin-induced DCM rats, and reverse the occurrence and development of heart reconstruction. The underlying mechanism might be related to regulating and controlling the expressions of Bax and Bcl-2.

Animals ; Apoptosis ; drug effects ; Cardiomyopathy, Dilated ; chemically induced ; complications ; Doxorubicin ; adverse effects ; Drugs, Chinese Herbal ; pharmacology ; Heart Failure ; chemically induced ; pathology ; Male ; Myocytes, Cardiac ; drug effects ; metabolism ; Rats ; Rats, Sprague-Dawley

Animals ; Animals, Newborn ; Chronic Disease ; Daunorubicin ; adverse effects ; Disease Models, Animal ; Heart Failure ; chemically induced ; Rats ; Rats, Sprague-Dawley

Acute amiodarone toxicity after a single dose of intravenous amiodarone is very rarely seen. We report the case of a 64-year-old Chinese man who presented with atrial fibrillation and fluid overload due to congestive cardiac failure. He was treated with a single bolus dose of intravenous amiodarone, after which he developed elevated serum transaminases, coagulopathy, thrombocytopenia and acute renal failure. His parameters returned to normal after 25 days and his recovery was uneventful.
Acute Kidney Injury ; chemically induced ; Amiodarone ; adverse effects ; Anti-Arrhythmia Agents ; adverse effects ; Atrial Fibrillation ; drug therapy ; Blood Coagulation Disorders ; chemically induced ; Heart Failure ; complications ; drug therapy ; Humans ; Male ; Middle Aged ; Thrombocytopenia ; chemically induced ; Transaminases ; blood ; Treatment Outcome

OBJECTIVETo investigate the changes of cholinergic nerves in doxorubicin (DOX)-induced rat failing heart and tumor necrosis factor-α (TNF-α) in the heart tissue and serum.

METHODSAdult Sprague-Dawley rats were randomized into control (n=10) and DOX-induced chronic heart failure (CHF) groups (n=15), and in the latter group, the rats were given intraperitoneal injections of 2.5 mg/kg DOX once a week for 6 weeks, with a total cumulative dose of 15 mg/kg. The control rats were injected with normal saline (1 ml/week). Karnovsky-Roots histochemical staining combined with point counting was used to demonstrate the distribution of cholinergic nerves in the heart. The expression levels of TNF-α in the heart tissue and serum were determined with ELISA.

RESULTSPositively stained cholinergic nerves were found in all the rat hearts in the two groups, but in CHF group, the point counts of cholinergic nerves were significantly lower than that of the control group (P<0.01). Compared with the control rats, those with DOX-induced CHF showed elevated levels of TNF-α both in the heart tissue and in the serum (P<0.01).

CONCLUSIONIn rats with DOX-induced CHF, the parasympathetic nervous system is down-regulated in the failing heart, and the diminished cholinergic anti-inflammatory pathway may play an important role in the progression of CHF.

Animals ; Cholinergic Agents ; pharmacology ; Cholinergic Fibers ; drug effects ; Doxorubicin ; pharmacology ; Heart ; drug effects ; innervation ; Heart Failure ; chemically induced ; metabolism ; Male ; Myocardium ; metabolism ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo study the effects and mechanism of Buzhong Yiqi decoction on adriamycin-induced acute myocardial injury in rats.

METHOD50 rats were randomly divided to five groups: control group, heart failure group, low dose Buzhong Yiqi decoction, high dose Buzhong Yiqi decoction and captopril group. Adriamycin was injected into the latter four groups to built a model of heart failure. Then, the effects of different doses of Buzhong Yiqi decoction on hemodynamics, cardiac tissue histological changes, antioxidant capacity and apoptosis of the damaged hearts were studied.

RESULTAdriamycin led to myocardial fiber swelling and fracture, Buzhong Yiqi decoction could reduce myocardial lesions. Buzhong Yiqi decoction could also improve heart antioxidant capacity and inhibit adriamycin-induced cardiomyocyte apoptosis.

CONCLUSIONBuzhong Yiqi decoction could significantly ease adriamycin induced heart failure in rats, and the mechanism is related to anti-oxidation and inhibiting apoptosis.

Animals ; Antibiotics, Antineoplastic ; toxicity ; Doxorubicin ; toxicity ; Drugs, Chinese Herbal ; pharmacology ; Heart Failure ; chemically induced ; prevention & control ; Male ; Nitric Oxide ; biosynthesis ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; blood ; Ventricular Function, Left ; drug effects

BACKGROUNDMaintenance of normal cardiac function is controlled by the autonomic nervous system. In congestive heart failure (CHF), sympathetic nerve denervation is increasingly recognized. The sympathetic fiber density depends on the balance between neurotrophins and neural guidance molecules. Semaphorin 3A (sema3a), a secreted neural guidance factor, is a well characterized member of the newly found semaphorin family. It can induce sympathetic growth cone collapse and axon repulsion. We conducted this study to investigate cell sources of sema3a in the heart, the expression level of sema3a in CHF and discuss the possible role of sema3a in CHF.

METHODSRats were divided into four groups: 30 days control group rats, 30 days CHF rats, 60 days control group rats, 60 days CHF rats. The heart failure model was induced by injection of isoproterenol (ISO) 340 mg/kg continuously two days. All animals underwent echocardiography and haemodynamics measurements. Cardiac expression of sema3a was determined by real time polymerase chain reaction (RT-PCR) and Western blotting analysis. Immunohistochemical analysis was used to determine the cell source of sema3a in the heart.

RESULTSIsoproterenol induced 30 days and 60 days CHF rats displayed left ventricular dilation, systolic and diastolic function decrease. Sema3a was secreted by the cardiocytes and increased significantly in 30 days and 60 days CHF rats compared with the controls (RT-PCR: 30 days group: 0.32 ± 0.05 vs. 0.58 ± 0.06, P < 0.01; 60 days group: 0.34 ± 0.08 vs. 0.71 ± 0.07, P < 0.01. Western blotting: 30 days group: 0.25 ± 0.10 vs. 0.46 ± 0.10, P < 0.05; 60 days group: 0.29 ± 0.10 vs. 0.55 ± 0.16, P < 0.01. Immunohistochemical analysis: 30 days group: 2.91 ± 0.20 vs. 5.31 ± 0.30, P < 0.01; 60 days group: 2.94 ± 0.30 vs. 5.80 ± 0.30, P < 0.01).

CONCLUSIONSSema3a was expressed in the heart by cardiocytes. Increased expression of sema3a may partly account for sympathetic denervation in CHF; modulation of this pathway may prove beneficial in heart failure sympathetic remodeling.

Animals ; Blotting, Western ; Echocardiography ; Heart Failure ; chemically induced ; metabolism ; Hemodynamics ; drug effects ; Immunohistochemistry ; Isoproterenol ; toxicity ; Male ; Myocardium ; metabolism ; Rats ; Rats, Wistar ; Real-Time Polymerase Chain Reaction ; Semaphorin-3A ; genetics ; metabolism

Antitubercular Agents ; adverse effects ; Chronic Disease ; Heart Failure ; complications ; Humans ; Isoniazid ; adverse effects ; Male ; Middle Aged ; Rhabdomyolysis ; chemically induced ; etiology