Biomedical subjects

Antonio Carlos Cicogna

Publications and source records attributed to Antonio Carlos Cicogna.

14 recordsLinked to original sources

PubMed2008

Cardiac hemangioma of the right atrium.

Primary cardiac tumors are rare, with an incidence range between 0.001% and 0.030% at autopsy. Recent technical advances have facilitated diagnosis and surgical treatment of such lesions. Patients with a resectable tumor usually have a good prognosis, but patients with an unresectable tumor may have a poor prognosis. This report shows a case of right atrial hemangioma growing like an extracardiac mass, with cardiac tamponade the only clinical presentation.

Adult↗

PubMed2006

[Echocardiographic criteria for the definition of ventricular dysfunction severity in aortic banded rats].

OBJECTIVE: The purpose of this study was to identify echocardiographic parameters that allow distinguishing different levels of cardiac dysfunction in aortic banded rats. METHODS: Wistar male rats (90-100 g) were subjected to aortic banding (n=23) or a sham operation (n=12). The following echocardiographic parameters were evaluated and used to group rats into groups with similar characteristics using cluster analysis: absolute values and after normalization to body weight of left ventricular end-diastolic diameter (LVDD) and left atrial systolic diameter; left ventricular end-systolic diameter (LVSD); LV weight to body weight ratio (LVW/BW); three indexes of left ventricular shortening (endocardial fractional shortening, EFS; midwall FS, MFS; and posterior wall shortening velocity, (PWSV). RESULTS: The cluster analysis could group aortic banded rats into two groups: mild (n=13) and severe (n=9) stage of heart failure. There was no overlapping among the values of the 95% confidence interval of the following parameters between the two groups: LVDD, LVSD, EFS, MFS, LVW/BW, and PWSV. CONCLUSION: It is feasible to distinguish two groups of aortic banded rats according to the level of cardiac dysfunction using those echocardiographic parameters. This allows to perform longitudinal studies in homogeneous groups of rats with aortic banding and cardiac dysfunction.

Animals↗

PubMed2006

Heart failure alters MyoD and MRF4 expressions in rat skeletal muscle.

Heart failure (HF) is characterized by a skeletal muscle myopathy with increased expression of fast myosin heavy chains (MHCs). The skeletal muscle-specific molecular regulatory mechanisms controlling MHC expression during HF have not been described. Myogenic regulatory factors (MRFs), a family of transcriptional factors that control the expression of several skeletal muscle-specific genes, may be related to these alterations. This investigation was undertaken in order to examine potential relationships between MRF mRNA expression and MHC protein isoforms in Wistar rat skeletal muscle with monocrotaline-induced HF. We studied soleus (Sol) and extensor digitorum longus (EDL) muscles from both HF and control Wistar rats. MyoD, myogenin and MRF4 contents were determined using reverse transcription-polymerase chain reaction while MHC isoforms were separated using polyacrylamide gel electrophoresis. Despite no change in MHC composition of Wistar rat skeletal muscles with HF, the mRNA relative expression of MyoD in Sol and EDL muscles and that of MRF4 in Sol muscle were significantly reduced, whereas myogenin was not changed in both muscles. This down-regulation in the mRNA relative expression of MRF4 in Sol was associated with atrophy in response to HF while these alterations were not present in EDL muscle. Taken together, our results show a potential role for MRFs in skeletal muscle myopathy during HF.

Animals↗

PubMed2006

Heart failure alters matrix metalloproteinase gene expression and activity in rat skeletal muscle.

Heart failure is associated with a skeletal muscle myopathy with cellular and extracellular alterations. The hypothesis of this investigation is that extracellular changes may be associated with enhanced mRNA expression and activity of matrix metalloproteinases (MMP). We examined MMP mRNA expression and MMP activity in Soleus (SOL), extensor digitorum longus (EDL), and diaphragm (DIA) muscles of young Wistar rat with monocrotaline-induced heart failure. Rats injected with saline served as age-matched controls. MMP2 and MMP9 mRNA contents were determined by RT-PCR and MMP activity by electrophoresis in gelatin-containing polyacrylamide gels in the presence of SDS under non-reducing conditions. Heart failure increased MMP9 mRNA expression and activity in SOL, EDL and DIA and MMP2 mRNA expression in DIA. These results suggest that MMP changes may contribute to the skeletal muscle myopathy during heart failure.

Animals↗

PubMed2005

Exercise training increases myocardial inotropic response in food restricted rats.

This study evaluated the effects of exercise training on myocardial function and ultrastructure of rats submitted to different levels of food restriction (FR). Male Wistar-Kyoto rats, 60 days old, were submitted to free access to food, light FR (20%), severe FR (50%) and/or to swimming training (one hour per day with 5% of load, five days per week for 90 days). Myocardial function was evaluated by left ventricular papillary muscle under basal condition (calcium 1.25 mM), and after extracellular calcium elevation to 5.2 mM and isoproterenol (1 microM) addition. The ultrastructure of the myocardium was examined in the papillary muscle. The training effectiveness was verified by improvement of myocardial metabolic enzyme activities. Both 20% and 50% food restriction protocols presented minor body and ventricular weights gain. The 20%-FR, in sedentary or trained rats, did not alter myocardial function or ultrastructure. The 50%-FR, in sedentary rats, caused myocardial dysfunction under basal condition, decreased response to inotropic stimulation, and promoted myocardial ultrastructural damage. The 50%-FR, in exercised rats, increased myocardial dysfunction under basal condition but increased response to inotropic stimulation although there was myocardial ultrastructural damage. In conclusion, the exercise training in severe restriction caused marked myocardial dysfunction at basal condition but increased myocardial response to inotropic stimulation.

3-Hydroxyacyl CoA Dehydrogenases↗

PubMed2005

Myocardial dysfunction induced by food restriction is related to morphological damage in normotensive middle-aged rats.

Previous works from our laboratory have revealed that food restriction (FR) promotes discrete myocardial dysfunction in young rats. We examined the effects of FR on cardiac function, in vivo and in vitro, and ultrastructural changes in the heart of middle-aged rats. Twelve-month-old Wistar-Kyoto rats were fed a control (C) or restricted diet (daily intake reduced to 50% of the control group) for 90 days. Cardiac performance was studied by echocardiogram and in isolated left ventricular (LV) papillary muscle by isometric contraction in basal condition, after calcium chloride (5.2 mM) and beta-adrenergic stimulation with isoproterenol (10(-6) M). FR did not change left ventricular function, but increased time to peak tension, and decreased maximum rate of papillary muscle tension development. Inotropic maneuvers promoted similar effects in both groups. Ultrastructural alterations were seen in most FR rat muscle fibers and included, absence and/or disorganization of myofilaments and Z line, hyper-contracted myofibrils, polymorphic and swollen mitochondria with disorganized cristae, and a great quantity of collagen fibrils. In conclusion, cardiac muscle sensitivity to isoproterenol and elevation of extracellular calcium concentration is preserved in middle-aged FR rats. The intrinsic muscle performance depression might be related to morphological damage.

Aging↗

PubMed2005

[Effects of the prolonged inhibition of the angiotensin-converting enzyme on the morphological and functional characteristics of left ventricular hypertrophy in rats with persistent pressure overload].

OBJECTIVE: To assess the effects of lisinopril (L) on mortality (M) rate and congestive heart failure (CHF), and the characteristics of geometrical myocardial remodeling and left ventricular function in rats with supravalvular aortic stenosis (SAS). METHODS: Some Wistar rats underwent SAS or the simulated surgery (CG, n=10). After 6 weeks, the animals were randomized to receive lisinopril (LG, n=30) or no treatment (SG, n=73) for 15 weeks. Cardiac remodeling was assessed in the sixth and 21st weeks after the surgical procedures through concomitant echocardiographic, hemodynamic, and morphological studies. RESULTS: The M were 53.9% and 16.7% in SG and LG, respectively; the incidence of CHF was 44.8% and 20%, in SG and LG, respectively, (P<0.05). At the end of the experiment, the values of LV systolic pressure in SG and LG were equivalent and significantly greater than those in CG; (P<0.05) and did not differ from those observed 6 weeks after the surgical procedures. The values of LV diastolic pressure in SG were greater than those in LG; (P<0.05), and both were greater than those in CG; (P<0.05). The same behavior was observed with the following variables: E/A ratio; mass index; sectional area of the myocytes; and LV hydroxyproline content. Left ventricular shortening percentage was similar in CG and LG; (P>0.05), and both were greater than those in SG; (P<0.05). Similar results were obtained with the values of the positive and negative first derivate of LV pressure. CONCLUSION: In rats with SAS, the treatment with L reduced M rate and ICC and had beneficial effects on geometrical myocardial remodeling and left ventricular function.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2004

Follow-up study of morphology and cardiac function in rats undergoing induction of supravalvular aortic stenosis.

OBJECTIVE: To characterize the follow-up of an experimental model of left ventricular hypertrophy (LVH) induced by supravalvular ascending aortic stenosis in young rats. METHODS: Wistar rats were submitted to thoracotomy and aortic stenosis was created by placing a clip on the ascending aorta (AoS group, n=12). Age-matched control animals underwent a sham operation (C group, n=12). Cardiac function was analysed by echocardiograms performed 6, 12, and 21 weeks after aortic banding. Myocardial morphological features and myocardial hydroxyproline concentration (HOP) were evaluated 2, 6, 12, and 21 weeks after surgery in additional animals. RESULTS: Aortic banding promoted early concentric LVH and a progressive increase in HOP. Under light microscopy, we observed myocyte hypertrophy and wall thickening of the intramural branches of the coronary arteries due to medial hypertrophy. Cardiac function was supranormal after 6 weeks (percentage of fractional shortening - EAo6: 70.3 +/- 10.8; C6: 61.3 +/- 5.4; p<0.05), and depressed in the last period. Diastolic dysfunction was detected after 12 weeks (ratio of early-to-late filling velocity - EAo12: 4.20 +/- 3.25; C12: 1.61 +/- 0.16; p<0.05). CONCLUSION: Ascending aortic stenosis promotes concentric LVH with myocardial fibrosis and minimal histological changes. According to the period of evaluation, cardiac function may be improved, normal, or depressed. The model is suitable and useful for studies on pathophysiology and treatment of the different phases of cardiac hypertrophy.

Analysis of Variance↗

PubMed2004

Improved systolic ventricular function with normal myocardial mechanics in compensated cardiac hypertrophy.

There is still controversy about the relation between changes in myocardial contractile function and global left ventricular (LV) performance during stable concentric hypertrophy. To clarify this, we analyzed LV function in vivo and myocardial mechanics in vitro in rats with pressure overload-induced cardiac hypertrophy. Male Wistar rats (70 g) underwent ascending aortic stenosis for 8 weeks (group AAS, n = 9). LV performance was assessed by transthoracic echocardiography under anesthesia. Myocardial function was studied in isolated papillary muscle preparations during isometric contraction. The data were compared with age- and sex-matched sham-operated rats (group C, n = 9). LV weight-to-body weight ratio (C: 2.13 +/- 0.14 mg/g; AAS: 3.24 +/- 0.44 mg/g), LV relative wall thickness (C: 0.18 +/- 0.02; AAS: 0.33 +/- 0.09), and LV fractional shortening (C: 54 +/- 5%; AAS: 70 +/- 8%) were increased in group AAS (P < 0.05). Echocardiographic analysis also indicated a significant association (r = 0.74; P < 0.001) between the percent fractional shortening index and LV relative wall thickness. The performance of AAS isolated muscle revealed that active tension (C: 6.6 +/- 1.7 g/mm2; AAS: 6.5 +/- 1.5 g/mm2) and maximum rate of tension development (C: 69 +/- 21 g/mm2/s; AAS: 69 +/- 18 g/mm2/s) were not significantly different from group C (P > 0.05). In conclusion, compensated pressure-overload myocardial hypertrophy is associated with preserved myocardial function and increased ventricular performance. The improved LV function might be due to the ventricular remodeling characterized by an increased relative wall thickness.

Animals↗

PubMed2004

Impact of the training program on lipid profile and cardiac health.

The aim of this study was to investigate the effects of training programs on serum lipid profile and myocardial oxidative stress. Male Wistar rats (2 mo-old) were divided into three groups (n = 8): sedentary (S), loadless trained (T) and trained-overload 2% body weight (TL). T and TL were trained through swimming for 9 weeks. T and TL rats had increased myocardial lipoperoxide (TBA) and lipid hydroperoxide (HP), whereas HP was higher in TL than in T animals. Superoxide dismutase (SOD) activities were lowest in TL. Myocardial glutathione peroxidase (GSH-Px) was lower in TL than in T and S rats. TL decreased HDL-cholesterol and increased LDL-cholesterol. The serum lactate dehydrogenase and TBA were increased, while SOD and GSH-Px activities were decreased in TL rats. Loadless training was able to improve HDL-cholesterol and to reduce LDL-cholesterol. In conclusion, the loadless training program induced beneficial effects on lipid profile, while overload training induced dyslipidemic profile that was associated with serum oxidative stress. The overload training program was deleterious relative to loadless training program, increasing myocardial oxidative stress.

Animals↗

PubMed2003

Behavior of cardiac variables in animals exposed to cigarette smoke.

OBJECTIVE: To assess the behavior of cardiac variables in animals exposed to cigarette smoke. METHODS: Two groups of Wistar rats were studied as follows: control group (C), comprising 28 animals; and smoking group (S), comprising 23 animals exposed to cigarette smoke for 30 days. Left ventricular cardiac function was assessed in vivo with transthoracic echocardiography, and myocardial performance was analyzed in vitro in preparations of isolated left ventricular papillary muscle. The cardiac muscle was assessed in isometric contractions with an extracellular calcium concentration of 2.5 mmol/L. RESULTS: No statistical difference was observed in the values of the body variables of the rats and in the mechanical data obtained from the papillary muscle between the control and smoking groups. The values of left ventricular systolic diameter were significantly greater in the smoking animals than in the control animals (C=3.39 +/- 0.4 mm and S=3.71 +/- 0.51 mm, P=0.02). A significant reduction was observed in systolic shortening fraction (C=56.7 +/- 4.2% and S=53.5 +/- 5.3%, P=0.02) and in ejection fraction (C=0.92 +/- 0.02 and S=0.89 +/- 0.04, P=0.01). CONCLUSION: The rats exposed to cigarette smoke had a reduction in left ventricular systolic function, although their myocardial function was preserved.

Animals↗

PubMed2003

Ventricular remodeling induced by retinoic acid supplementation in adult rats.

Retinoic acid (RA) plays a role in regulating cardiac geometry and function throughout life. The aim of this study was to analyze the cardiac effects of RA in adult rats. Wistar rats were randomly allocated to a control group (n = 18) receiving standard rat chow and a group treated with RA (n = 14) receiving standard rat chow supplemented with RA for 90 days. All animals were evaluated by echocardiography, isolated papillary muscle function, and morphological studies. Whereas the RA-treated group developed an increase in both left ventricular (LV) mass and LV end-diastolic diameter, the ratio of LV wall thickness to LV end-diastolic diameter remained unchanged when compared with the control group. In the isolated papillary muscle preparation, RA treatment decreased the time to peak developed tension and increased the maximum velocity of isometric relengthening, indicating that systolic and diastolic function was improved. Although RA treatment produced an increase in myocyte cross-sectional area, the myocardial collagen volume fraction was similar to controls. Thus our study demonstrates that small physiological doses of RA induce ventricular remodeling resembling compensated volume-overload hypertrophy in rats.

Animals↗

PubMed2003

Myosin heavy chain expression and atrophy in rat skeletal muscle during transition from cardiac hypertrophy to heart failure.

The purpose of this investigation was to determine whether changes in myosin heavy chain (MHC) expression and atrophy in rat skeletal muscle are observed during transition from cardiac hypertrophy to chronic heart failure (CHF) induced by aortic stenosis (AS). AS and control animals were studied 12 and 18 weeks after surgery and when overt CHF had developed in AS animals, 28 weeks after the surgery. The following parameters were studied in the soleus muscle: muscle atrophy index (soleus weight/body weight), muscle fibre diameter and frequency and MHC expression. AS animals presented decreases in both MHC1 and type I fibres and increases in both MHC2a and type IIa fibres during late cardiac hypertrophy and CHF. Type IIa fibre atrophy occurred during CHF. In conclusion, our data demonstrate that skeletal muscle phenotype changes occur in both late cardiac hypertrophy and heart failure; this suggests that attention should be given to the fact that skeletal muscle phenotype changes occur prior to overt heart failure symptoms.

Animals↗

PubMed2002

Volume overload influence on hypertrophied myocardium function.

The aim of this study was to demonstrate that hypertrophied cardiac muscle is more sensitive to volume-overload than normal cardiac muscle. We assessed the mechanical function of isolated left ventricular papillary muscle from male spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar-Kyoto rats (WKY) submitted to volume overload caused by aortocaval fistula (ACF) for 30 days. Muscles were perfused with Krebs-Henseleit solution at 28 degrees C and studied isometrically at a stimulation rate of 0.2 Hz. The ACF increased the right and left ventricular weight-to-body weight ratio in WKY rats; it also promoted right ventricular hypertrophy and further increased the basal hypertrophy in the left ventricle from SHR. The arterial systolic pressure was greater in SHR than in WKY rats, and decreased with ACF in both groups. Developed tension (DT) and maximum rate of DT (+dT/dt) were greater in the SHR-control than in the WKY-control (P < 0.05); the time from peak tension to 50% relaxation (RT 1/2) was similar in these animals. ACF did not change any parameters in the SHR group and increased the resting tension in the WKY group. However, the significant difference observed between myocardial contraction performance in WKY-controls and SHR-controls disappeared when the SHR-ACF and WKY-controls were compared. Furthermore, RT 1/2 increased significantly in the SHR-ACF in relation to the WKY-controls. In conclusion, the data lead us to infer that volume-overload for 30 days promotes more mechanical functional changes in hypertrophied muscle than in normal cardiac muscle.

Animals↗