Search

To investigate the effect of lisinopril on cardiac remodeling induced by smoking.Rats were allocated into 3 groups: group CON (n=8): control; group CSE (n=8): cigarette smoke exposure; group CSE-LIS (n=8): exposed to tobacco smoke and treated with lisinopril.After 2 months, the tail systolic pressure was lower in CSE-LIS (CON=116 +/-27 mm Hg, CSE=126+/-16, CSE-LIS=89+/-12; P.001). CSE animals showed higher left ventricular systolic diameter (CON=8.25+/-2.16 mm/kg, CSE=11.5+/-1.3, CSE-LIS=9.27+/-2.00; P=.009) and myocyte cross-sectional area (CON=245+/-8 microm2, CSE=260+/-17, CSE-LIS=238+/-12; P=.01) than CON and CSE-LIS. The ejection fraction (CON =0.91+/-0.02, CSE=0.86+/-0.02, CSE-LIS=0.92+/-0.03; P=.002) and fractional shortening (CON=55.7+/-4.41%, CSE=48.7+/-3.43, CSE-LI=58.2+/-7.63; P=.006) were lower in CSE group than CON and CSE-LIS. CSE and CSE-LIS animals showed higher collagen amounts (CON=3.49+/-0.95%, CSE= 5.01+/-1.58, CSE-LIS=5.27+/-0.62; P=.009) than CON. CON group showed a higher connexin 43 amount in the intercalated disc (CON=3.70+/-0.38, CSE=2.13+/-0.53; CSE-LIS=2.17+/-0.73; P=.004) than CSE and CSE-LIS. There were no differences in IFN-gamma or TNF-alpha cardiac levels among the groups.Lisinopril attenuated both morphologic and functional abnormalities induced by exposure to tobacco smoke. In addition, this effect was associated with diminished blood pressure, but not alterations in connexin 43 distribution, cytokine production or collagen amount.

The role of the adrenergic system on ventricular remodeling induced by cigarette smoking is unknown.To investigate the influence of propranolol on ventricular remodeling induced by exposure to tobacco smoke.Rats were divided into three groups: 1) C, n=10--control group; 2) F, n=10--animals exposed to tobacco smoke; 3) BB, n=10--animals receiving propranolol and exposed to tobacco smoke (40 mg/kg/day). After 2 months, the animals underwent echocardiographic and morphometric analyses. One-way ANOVA (mean +/- standard deviation) or the Kruskal-Wallis test (median and interquartile interval) was used.Group BB showed a lower heart rate than group F (C = 358 +/- 74 bpm, F = 374 +/- 53 bpm, BB = 297 +/- 30; P = 0.02). Group F showed greater end-diastolic diameters (C = 18.6 +/- 3.4 mm/kg, F = 22.8 +/- 1.8 mm/kg, BB = 21.7 +/- 1.8 mm/kg; P = 0.003) and left ventricular (LV) end-systolic diameters (C = 8.6 +/- 2.1 mm/kg, F = 11.3 +/- 1.3 mm/kg, BB = 9.9 +/- 1.2 mm/kg; P = 0.004), adjusted for body weight (BW) and a tendency towards a lower ejection fraction (C = 0.90 +/- 0.03, F = 0.87 +/- 0.03, BB =0.90 +/- 0.02; P = 0.07) than group C. Group BB showed a tendency towards a lower LV/BW ratio than group F (C = 1.94 (1.87 - 1.97), F = 2.03 (1.9-2.1) mg/g, BB = 1.89 (1.86-1.94); P = 0.09).Administration of propranolol attenuated some of the variables of ventricular remodeling induced by the exposure to tobacco smoke in rats.

We investigated the effects of length of exposure to tobacco smoke on the cardiac remodeling process induced by exposure to cigarette smoke in rats.Rats were separated into 4 groups: nonsmoking (NS)2 (n=25; control animals not exposed to tobacco smoke for 2 months), smoking (S)2 (n=22; rats exposed to smoke from 40 cigarettes/d for 2 months), NS6 (n=18; control animals not exposed to tobacco smoke for 6 months), and S6 (n=25; rats exposed to smoke from 40 cigarettes/d for 6 months). All animals underwent echocardiographic, isolated heart, and morphometric studies. Data were analyzed with a 2-way analysis of variance.No interaction among the variables was found; this suggests that length of exposure to tobacco smoke did not influence the effects of exposure to smoke. Values for left ventricular diastolic diameter/body weight and left atrium/body weight were higher (p=0.023 and p=0.001, respectively) in smoking (S2 and S6) than in nonsmoking animals (NS2 and NS6). Left ventricular mass index was higher (p=0.048) in smoking than in nonsmoking animals. In the isovolumetrically beating ventricle, peak systolic pressure was higher (p=0.034) in smoking than in nonsmoking animals. Significantly higher values were found for left ventricular weight (p=0.017) and right ventricular weight (p=0.001) adjusted for body weight in smoking as opposed to nonsmoking animals. Systolic pressure was higher (p=0.001) in smoking (128+/-14 mm Hg) than in nonsmoking animals (112+/-11 mm Hg).Length of exposure to cigarette smoke did not influence cardiac remodeling caused by exposure to smoke in rats.

The mechanisms involved in the biggest remodeling caused by the post-infarct beta-carotene are unknown.To analyze the role of lipoperoxidation in the ventricular remodeling after infarct of the myocardium in rats supplemented with beta-carotene.Rats were infarcted and divided into two groups: C (control) and BC (500mg/kg/regimen). After six months, echocardiogram and biochemical evaluation were performed. The t test was used, with 5% significance.The animals from BC group presented highest means of the diastolic (C = 1.57 +/- 0.4 mm(2)/g, BC = 2.09 +/- 0.3 mm(2)/g; p0.001) and systolic (C = 1.05 +/- 0.3 mm(2)/g, BC = 1.61 +/- 0.3 mm(2)/g; p0.001) areas of LV, which were adapted according to the rat's body weight. The systolic function of LV, evaluated by the area variation fraction, was lower in the animals supplemented with beta-carotene (C = 31.9 +/- 9.3%, BC = 23.6 +/- 5.1%; p = 0.006). The animals supplemented with beta-carotene presented higher values of the E/A relation (C = 2.7 +/- 2.5, BC = 5.1 +/- 2.8; p = 0.036). No differences were found between the groups concerning the cardiac levels of the GSH (C = 21 +/- 8 nmol/mg of protein, BC = 37 +/- 15 nmol/mg of protein; p = 0.086), GSSG (C = 0.4 (0.3-0.5) nmol/g of protein, BC = 0.8 (0.4-1.0; p = 0.19) of protein; p = 0.246) and lipoperoxides (C = 0.4 +/- 0.2 nmol/mg of tissue, BC = 0.2 +/- 0.1 nmol/mg of tissue; p = 0.086).The highest remodeling in infarcted rats supplemented with beta-carotene does not depend on the lipoperoxidation.

To analyze the effects of beta-carotene on the ventricular remodeling process following myocardial infarction (MI) in rats exposed to cigarette smoke.After acute myocardial infarction (AMI), the animals were divided into four groups: 1) Group C, 24 animals that were given standard diet; 2) Group BC, 26 animals that were given beta-carotene; 3) Group ECS, 26 animals that were given standard diet and were exposed to cigarette smoke; and 4) Group BC+ECS, 20 animals that were given beta-carotene and were exposed to cigarette smoke. After six months, a morphofunctional study was performed. We used a 5% significance level.As regards diastolic areas (DA) and systolic areas (SA), the values for the BC group were higher than those for the C group. If DA/body weight (BW) and SA/BW are considered, the values for group BC+ECS were higher than the values for group C. As regards the fractional area change, we observed significant differences between ECS (lower values) and C (higher values) and between BC (lower values) and C (higher values). Differences between groups regarding infarction size were not observed. The ECS group presented higher values for myocyte cross-section area (MCA) than control animals. Additionally, the BC+ECS group presented higher MCA values than the BC, ECS and C groups.After myocardial infarction, smoking and beta-carotene intensified the heart remodeling process; harmful effects of the remodeling process were heightened when the two treatments were used in conjunction.

To evaluate the differences between three methods for the measurement of experimental infarction in rats in comparison to the traditional method.Histological analysis of the infarction area (AREA), histological analysis of the internal cavity perimeter (PER) and echocardiogram analysis of the internal perimeter (ECHO) were compared to the traditional method (histological analysis of the epicardial and endocardial circumferences of the infarction region - CIR). Repeated ANOVA measurements were used in conjunction with the Dunn multiple comparison test, the Bland and Altman concordance method and the Spearman correlation test. Significance was established as p0.05.The data of 122 animals were analyzed, 3 to 6 months after the infarction. Infarction size assessments revealed differences between CIR and the other three methods (p0.001): CIR = 42.4% (35.9-48.8), PER = 50.3% (39.1-57.0), AREA = 27.3% (20.2-34.3), ECHO = 46.1% (39.9-52.6). Therefore, measurement by area underestimated the infarct size by 15%, whereas the echocardiogram and histological internal perimeter measurements overestimated the infarct size by 4% and 5%, respectively. In relation to ECHO and PER, even though the difference between the methods was only 1.27%, the concordance interval ranged from 24.1% to -26.7%, suggesting a low level of concordance between the methods. In relation to associations, statistically significant correlations were found between: CIR and PER (r = 0.88 and p0.0001); CIR and AREA (r = 0.87 and p0.0001) and CIR and ECHO (r = 0.42 and p0.0001).Despite the high level of correlation, there was a low level of concordance between the methods to define infarct size.

To determine the cardiac structural and functional alterations caused by cigarette smoke exposure in rats.The animals were randomly distributed into the following 2 groups: 1) smokers (S), comprising 10 animals exposed to cigarette smoke at a rate of 40 cigarettes/day; and 2) control (C), comprising 10 animals not exposed to cigarette smoke. After 4 months, the animals underwent morphological and functional study with echocardiography. The variables studied were analyzed by use of the t test or the Mann-Whitney test.The smoking rats had a greater left atrium (S=4.2+/-0.7 mm; C=3.5+/-0.6 mm; P0.05), and greater left ventricular diastolic (S=7.9+/-0.7 mm; C=7.2+/-0.5 mm; P0.05) and systolic (S=4.1+/-0.5; C=3.4+/-0.5; P0.05) diameters. The left ventricular mass index was greater in the smoking animals (S=1.5 mg/kg+/-0.2; C=1.3 mg/kg+/-0.2; P0.05), and the ejection fraction (S=0.85+/-0.03; C=0.89+/-0.03; P0.05) and the shortening fraction (S=47.8%+/-3.7; C=52.7%+/-4.6; P0.05) were greater in the control group. No differences were observed in the diastolic transmitral flow variables (E wave, A wave, and E/A ratio).Chronic cigarette smoke exposure results in cardiac remodeling with a decrease in ventricular functional capacity.