Direct Effects of Colchicine on Myocardial Function

Cicogna, Antônio Carlos; Robinson, Kathleen G.; Conrad, Chester H.; Singh, Krishna; Squire, Robyn; Okoshi, Marina Politi; Bing, O.

doi:10.1161/01.hyp.33.1.60

Cited by 48 publications

(26 citation statements)

References 31 publications

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“…In this study, rats from MI-C and MI-NAC groups had similar infarct sizes, approximately 48%, which is considered large. Heart failure diagnosis was based on observation of clinical and pathologic features [24,25] and confirmed by the greater right ventricle and lung weights in MI-C than Sham group. N -acetylcysteine did not modify these variables.…”

Section: Discussionmentioning

confidence: 99%

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Influence of N-Acetylcysteine on Oxidative Stress in Slow-Twitch Soleus Muscle of Heart Failure Rats

Martinez

Bonomo

Guizoni

et al. 2015

Cell Physiol Biochem

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Background: Chronic heart failure is characterized by decreased exercise capacity with early exacerbation of fatigue and dyspnea. Intrinsic skeletal muscle abnormalities can play a role in exercise intolerance. Causal or contributing factors responsible for muscle alterations have not been completely defined. This study evaluated skeletal muscle oxidative stress and NADPH oxidase activity in rats with myocardial infarction (MI) induced heart failure. Methods and Results: Four months after MI, rats were assigned to Sham, MI-C (without treatment), and MI-NAC (treated with N-acetylcysteine) groups. Two months later, echocardiogram showed left ventricular dysfunction in MI-C; NAC attenuated diastolic dysfunction. In soleus muscle, glutathione peroxidase and superoxide dismutase activity was decreased in MI-C and unchanged by NAC. 3-nitrotyrosine was similar in MI-C and Sham, and lower in MI-NAC than MI-C. Total reactive oxygen species (ROS) production was assessed by HPLC analysis of dihydroethidium (DHE) oxidation fluorescent products. The 2-hydroxyethidium (EOH)/DHE ratio did not differ between Sham and MI-C and was higher in MI-NAC. The ethidium/DHE ratio was higher in MI-C than Sham and unchanged by NAC. NADPH oxidase activity was similar in Sham and MI-C and lower in MI-NAC. Gene expression of p47^phox was lower in MI-C than Sham. NAC decreased NOX4 and p22^phox expression. Conclusions: We corroborate the case that oxidative stress is increased in skeletal muscle of heart failure rats and show for the first time that oxidative stress is not related to increased NADPH oxidase activity.

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Section: Discussionmentioning

confidence: 99%

“…Tachypnea/labored respiration was the clinical finding. Pathologic findings included pleuropericardial effusion, left atrial thrombi, pulmonary congestion (lung weight-to-body weight (BW) ratio >2 standard deviation above sham group mean), and right ventricular hypertrophy (right ventricle weight-to-BW ratio >0.8 mg/g) [24,25]. …”

Section: Methodsmentioning

confidence: 99%

Influence of N-Acetylcysteine on Oxidative Stress in Slow-Twitch Soleus Muscle of Heart Failure Rats

Martinez

Bonomo

Guizoni

et al. 2015

Cell Physiol Biochem

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“…At the time of euthanasia, we determined the presence or absence of congestive HF by assessing lung congestion (lung weight/body weight ratio > 2 standard deviations above Sham group mean) and right ventricular hypertrophy (right ventricle weight-to-body weight ratio greater than 0.8 mg/g) [34,35,36]. After euthanasia, the infarcted rats were subdivided in two groups: 1) MI/HF- rats with no evidence of HF (n=10), and 2) MI/HF+ rats with right ventricular hypertrophy and lung congestion (n=10).…”

Section: Methodsmentioning

confidence: 99%

Heart Failure-Induced Diaphragm Myopathy

Lima

Martinez

Damatto

et al. 2014

Cell Physiol Biochem

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Background: Intracellular signaling pathways involved in skeletal myosin heavy chain (MyHC) isoform alterations during heart failure (HF) are not completely understood. We tested the hypothesis that diaphragm expression of mitogen-activated protein kinases (MAPK) and myogenic regulatory factors is changed in rats with myocardial infarction (MI) induced HF. Methods: Six months after MI rats were subjected to transthoracic echocardiography. After euthanasia, infarcted rats were subdivided in MI/HF- group (with no HF evidence; n=10), and MI/HF+ (with right ventricular hypertrophy and lung congestion; n=10). Sham-operated rats were used as controls (n=10). MyHC isoforms were analyzed by electrophoresis. Statistical analysis: ANOVA and Pearson correlation. Results: MI/HF- had left cardiac chambers dilation with systolic and diastolic left ventricular dysfunction. Cardiac injury was more intense in MI/HF+ than MI/HF-. MyHC I isoform percentage was higher in MI/HF+ than MI/HF-, and IIb isoform lower in MI/HF+ than Sham. Left atrial diameter-to-body weight ratio positively correlated with MyHC I (p=0.005) and negatively correlated with MyHC IIb (p=0.02). TNF-a serum concentration positively correlated with MyHC I isoform. Total and phosphorylated ERK was lower in MI/HF- and MI/HF+ than Sham. Phosphorylated JNK was lower in MI/HF- than Sham. JNK and p38 did not differ between groups. Expression of NF-κB and the myogenic regulatory factors MyoD, myogenin, and MRF4 was similar between groups. Conclusion: Diaphragm MyHC fast-to-slow shift is related to cardiac dysfunction severity and TNF-a serum levels in infarcted rats. Reduced ERK expression seems to participate in MyHC isoform changes. Myogenic regulatory factors and NF-κB do not modulate diaphragm MyHC distribution during chronic HF.

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“…Intrinsic cardiac contractile performance was evaluated by studying isolated LV papillary muscle (27). Briefly, rats were anes-thetized intraperitoneally with 50 mg/kg pentobarbital sodium and sacrificed; their hearts were quickly removed and placed in oxygenated Krebs-Henseleit solution at 28ºC.…”

Section: Functional Studymentioning

confidence: 99%

<a name="home"></a>Effect of unsaturated fatty acids on myocardial performance, metabolism and morphology

Pinotti

Silva

Sugizaki

et al. 2006

Braz J Med Biol Res

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Diets rich in saturated fatty acids are one of the most important causes of atherosclerosis in men, and have been replaced with diets rich in unsaturated fatty acids (UFA) for the prevention of this disorder. However, the effect of UFA on myocardial performance, metabolism and morphology has not been completely characterized. The objective of the present investigation was to evaluate the effects of a UFA-rich diet on cardiac muscle function, oxidative stress, and morphology. Sixty-day-old male Wistar rats were fed a control (N = 8) or a UFArich diet (N = 8) for 60 days. Myocardial performance was studied in isolated papillary muscle by isometric and isotonic contractions under basal conditions after calcium chloride (5.2 mM) and ß-adrenergic stimulation with 1.0 µM isoproterenol. Fragments of the left ventricle free wall were used to study oxidative stress and were analyzed by light microscopy, and the myocardial ultrastructure was examined in left ventricle papillary muscle. After 60 days the UFA-rich diet did not change myocardial function. However, it caused high lipid hydroperoxide (176 ± 5 vs 158 ± 5, P < 0.0005) and low catalase (7 ± 1 vs 9 ± 1, P < 0.005) and superoxide-dismutase (18 ± 2 vs 27 ± 5, P < 0.005) levels, and discrete morphological changes in UFA-rich diet hearts such as lipid deposits and mitochondrial membrane alterations compared to control rats. These data show that a UFA-rich diet caused myocardial oxidative stress and mild structural alterations, but did not change mechanical function.

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Direct Effects of Colchicine on Myocardial Function

Cited by 48 publications

References 31 publications

Influence of N-Acetylcysteine on Oxidative Stress in Slow-Twitch Soleus Muscle of Heart Failure Rats

Influence of N-Acetylcysteine on Oxidative Stress in Slow-Twitch Soleus Muscle of Heart Failure Rats

Heart Failure-Induced Diaphragm Myopathy

<a name="home"></a>Effect of unsaturated fatty acids on myocardial performance, metabolism and morphology

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