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Katashi Okoshi

Publications and source records attributed to Katashi Okoshi.

At least 19 recordsLinked to original sources
PubMed2006

Myocardial contractile dysfunction contributes to the development of heart failure in rats with aortic stenosis.

OBJECTIVES: To analyze the potential contribution of contractility state and ventricular geometry to the development of heart failure in rats with aortic stenosis. METHODS: Rats were divided into three groups: compensated aortic stenosis (AS, n=11), heart failure AS (n=12) and control rats (C, n=13). RESULTS: After 21 weeks, failing AS rats presented higher systolic (C=36.6+/-3.1, AS=78.6+/-4.8*, failing AS=104.6+/-7.8*(dagger)) and diastolic meridian stress (C=6.9+/-0.4, AS=20.1+/-1.1*, failing AS=43.2+/-3.2*(dagger)), hydroxyproline (C=3.6+/-0.7 mg/g, AS=6.6+/-0.6* mg/g, failing AS=9.2+/-1.4*(dagger) mg/g) and cross-sectional area (C=338+/-25 microm2, AS=451+/-32* microm2, failing AS=508+/-36*(dagger) microm2), in comparison with control and compensated AS animals (*p<0.05 vs. control, (dagger)p<0.05 vs. AS). In the isometric contraction study, considering the time from peak tension to 50% relaxation (RT50), the relative variation responses, following post-rest contraction and increase in Ca2+ concentration, were higher in failing AS than compensated AS animals. In contrast, following post-rest contraction, compensated AS group presented higher values of the peak developed tension (DT) than failing AS group. Following beta-adrenergic stimulation, control animals presented higher values of +dT/dt and -dT/dt than AS animals. In addition, failing AS animals presented higher TPT values than compensated AS animals. CONCLUSION: Myocardial contractile dysfunction contributes to the development of heart failure in rats with aortic stenosis.

Animals↗
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

Association between atherosclerotic aortic plaques and left ventricular hypertrophy in patients with cerebrovascular events.

BACKGROUND AND PURPOSE: The purpose of this research was to evaluate whether an association exists between the presence of atherosclerotic plaque in the thoracic aorta and left ventricular hypertrophy (LVH) in patients with a cerebrovascular event. METHODS: We included 116 consecutive patients (79 men; mean age, 62+/-12.4 years) with previous history of stroke or transient ischemic attack in a cross-sectional study. Transthoracic echocardiogram was performed to diagnose LVH and transesophageal echocardiogram for the detection of atheromas of the thoracic aorta. Continuous variables were analyzed by Student t or Mann-Whitney tests and categorized variables by Goodman test. From the significant association of LVH and age with atheromatous disease of the aorta, an adjustment to the multivariate logistic model was made using high blood pressure history or age as covariates. All of the statistical tests were carried out at a level of 5% significance. RESULTS: Almost half of the patients (43.1%) presented atherosclerotic lesions in the aorta. LVH was present in 90.0% of patients with plaque and in only 30.3% of patients without plaque. Using high blood pressure as a covariate, the risk of patients with LVH presenting atherosclerotic plaque in the aorta was 18.23-fold greater than the risk for patients without LVH (95% CI, 5.68 to 58.54; P<0.0001). Adding age into the model, the risk increased to 26.36 (95% CI, 7.14 to 97.30; P<0.0001). CONCLUSIONS: LVH detected by conventional echocardiogram is associated with high risk of atherosclerotic plaque in the aorta and would be used as a criterion for indication of transesophageal echocardiography in patients with previous stroke or transient ischemic attack LVH.

Adult↗
PubMed2005

Beta-carotene supplementation attenuates cardiac remodeling induced by one-month tobacco-smoke exposure in rats.

OBJECTIVE: The objectives were to analyze the cardiac effects of exposure to tobacco smoke (ETS), for a period of 30 days, alone and in combination with beta-carotene supplementation (BC). RESEARCH METHODS AND PROCEDURES: Rats were allocated into: Air (control, n = 13); Air + BC (n = 11); ETS (n = 11); and BC + ETS (n = 9). In Air + BC and BC + ETS, 500 mg of BC were added to the diet. After three months of randomization, cardiac structure and function were assessed by echocardiogram. After that, animals were euthanized and morphological data were analyzed post-mortem. One-way and two-way ANOVA were used to assess the effects of ETS, BC and the interaction between ETS and BC on the variables. RESULTS: ETS presented smaller cardiac output (0.087 +/- 0.001 vs. 0.105 +/- 0.004 l/min; p = 0.007), higher left ventricular diastolic diameter (19.6 +/- 0.5 vs. 18.0 +/- 0.5 mm/kg; p = 0.024), higher left ventricular (2.02 +/- 0.05 vs. 1.70 +/- 0.03 g/kg; p < 0.001) and atrium (0.24 +/- 0.01 vs. 0.19 +/- 0.01 g/kg; p = 0.003) weight, adjusted to body weight of animals, and higher values of hepatic lipid hydroperoxide (5.32 +/- 0.1 vs. 4.84 +/- 0.1 nmol/g tissue; p = 0.031) than Air. However, considering those variables, there were no differences between Air and BC + ETS (0.099 +/- 0.004 l/min; 19.0 +/- 0.5 mm/kg; 1.83 +/- 0.04 g/kg; 0.19 +/- 0.01 g/kg; 4.88 +/- 0.1 nmol/g tissue, respectively; p > 0.05). Ultrastructural alterations were found in ETS: disorganization or loss of myofilaments, plasmatic membrane infolding, sarcoplasm reticulum dilatation, polymorphic mitochondria with swelling and decreased cristae. In BC + ETS, most fibers showed normal morphological aspects. CONCLUSION: One-month tobacco-smoke exposure induces functional and morphological cardiac alterations and BC supplementation attenuates this ventricular remodeling process.

Animals↗
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

[Blockade of renin-angiotensin system attenuates cardiac remodeling in rats undergoing aortic stenosis].

OBJECTIVE: To assess the role of the AT1 receptor blocker and the angiotensin-converting enzyme inhibitor in cardiac remodeling induced by aortic stenosis in rats. METHODS: Wistar rats were divided into the following 4 groups: 1) C--control (n=13); 2) AoS--aortic stenosis (n=11); 3) LIS--AoS treated with lisinopril, 20 mg/kg/day (n=11); and 4) LOS--AoS treated with losartan, 40 mg/kg/day (n=9). The treatments were initiated 3 days before surgery. After 6 weeks, the animals underwent echocardiographic study, and quantification of the hydroxyproline (HOP) concentration and the left ventricular (LV) myocyte cross-sectional area (CSA). RESULTS: Aortic stenosis induced an increase in left ventricular wall thickness. The LIS and LOS groups showed no difference as compared with the control group. The AoS and LIS rats had greater left atrial diameters than the control rats did, while no difference was observed in the LOS animals. The AoS animals had greater values of shortening percentage than control animals did. This fact was modified with neither LIS nor LOS. The cross-sectional area of the animals in the AoS group was greater than that in the control group. However, treatment with LOS and LIS attenuated the AoS-induced increase in area. Aortic stenosis caused an increase in HOP concentration, while the LOS group showed no difference as compared with the control group. CONCLUSION: Blockade of the renin-angiotensin system with AT1 blocker and ACEI may attenuate the development of heart hypertrophy, but only the blockade of AT1 receptors attenuates left ventricular interstitial fibrosis.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2005

Heterozygous knockout of neuregulin-1 gene in mice exacerbates doxorubicin-induced heart failure.

Neuregulins and their erbB receptors are essential for cardiac development and postulated to be cardioprotective in the presence of injury in the postnatal heart. We tested the hypothesis that the development of doxorubicin-induced cardiotoxicity in vivo is more severe in mice with heterozygous knockout of the neuregulin-1 gene (NRG-1(+/-)) compared with wild-type mice (WT). Three-month old NRG-1(+/-) and WT mice were injected with a single dose of doxorubicin (20 mg/kg ip). Survival was analyzed by the Kaplan-Meier approach. Left ventricular (LV) function and signaling pathways were analyzed 4 days after treatment. Fifteen days after treatment, survival was significantly lower in doxorubicin-treated NRG-1(+/-) mice (NRG-1(+/-)-Dox) compared with doxorubicin-treated WT mice (WT-Dox) (15% vs. 33%, P < 0.01). LV mass was significantly lower in NRG-1(+/-)-Dox but not in WT-Dox compared with nontreated animals. LV systolic pressure and LV midwall fractional shortening were significantly lower in NRG-1(+/-)-Dox compared with WT-Dox mice. LV protein levels of NRG-1, erbB2, and erbB4 receptors were similar in WT-Dox and NRG-1(+/-)-Dox mice. However, levels of phosphorylated erbB2, Akt, and ERK-1/2 were significantly decreased in NRG-1(+/-)-Dox compared with WT-Dox mice. A significant decrease in phosphorylated P70S6K levels was also observed in NRG-1(+/-)-Dox compared with nontreated NRG-1(+/-) mice. These results demonstrate that heterozygous knockout of the neuregulin-1 gene worsens survival and LV function in the presence of doxorubicin-induced cardiac injury in vivo. This is associated with the depression of activation of the erbB2 receptor as well as Akt, p70S6K, and ERK-1/2 pathways.

Animals↗
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↗
PubMed2005

[The early administration of growth hormone results in deleterious effects on ventricular remodeling after acute myocardial infarction].

OBJECTIVE: To assess the effect of growth hormone (GH) on myocardial remodeling in infarcted rats. METHODS: This study comprised 24 Wistar rats divided into 3 groups as follows: 1) AMI-GH group--comprising 8 rats that underwent infarction and were treated with GH; 2) AMI group--comprising 8 rats that underwent infarction and received only the diluent of the GH solution; and 3) control group (C group)--comprising 8 rats that underwent simulated infarction. After 30 days, the animals underwent functional study through echocardiography, and the changes in myocardial contractility of the isolated left ventricular (LV) papillary muscle were studied. RESULTS: The echocardiography identified an increase in the diastolic (C=7.32+/-0.49; AMI=8.50+/-0.73; AMI-GH=9.34+/-0.73; P<0.05) and systolic (C=3.38+/-0.47, AMI=5.16+/-1.24; AMI-GH=5.96+/-1.54; P<0.05) diameters (mm) in the LV of the infarcted animals. The AMI-GH group animals had a lower ejection fraction (%) (C=0.9+/-0.03; AMI=0.76+/-0.12; AMI-GH= 0.72+/- 0.14; P<0.05 for C vs AMI-GH) compared with those in controls. The study of the isolated left ventricular papillary muscle showed that the AMI-GH group had changes (C=1.50+/-0.59; AMI=1.28+/-0.38; AMI-GH=1.98+/-0.41; P<0.05 for C vs AMI-GH) only in the tension at rest (TR - g/mm2) and in the time delta for a 50% decrease in the tension developed (TR50, ms) after stimulation with calcium (C=23.75+/-9.16; AMI=-16.56+/-14.82; AMI-GH=-4.69+/-8.39; P<0.05 for C vs AMI-GH) and in the delta of tension developed (TD, g/mm2) after stimulation with isoproterenol (C=0.99+/-0.17; AMI=0.54+/-0.62; AMI-GH=0.08+/-0.75; P<0.05 for C vs AMI-GH) compared with those in control animals. CONCLUSION: The early administration of GH in the experimental infarction model in rats may result in adverse effects on the process of ventricular remodeling.

Animals↗
PubMed2004

Neuregulins regulate cardiac parasympathetic activity: muscarinic modulation of beta-adrenergic activity in myocytes from mice with neuregulin-1 gene deletion.

BACKGROUND: Neuregulins are required for maintenance of acetylcholine receptor-inducing activity of nicotinic receptors in neurons and skeletal muscle, but effects of neuregulins on muscarinic receptors are not known. In the normal heart, parasympathetic activation counterbalances beta-adrenergic activation. To test the hypothesis that neuregulins modify parasympathetic function in the heart, we studied cardiomyocytes from mice heterozygous for neuregulin-1 gene deletion (NRG-1+/-) and examined the effects of beta-adrenergic stimulation on contractility in the presence and absence of the muscarinic agonist carbachol. METHODS AND RESULTS: We evaluated contraction and intracellular Ca2+ transients ([Ca2+]i) in left ventricular (LV) myocytes loaded with Fluo-3 from NRG-1+/- and wild-type (WT) mice. Under baseline conditions (0.5 Hz, 1.5 mmol/L [Ca2+]o, 25 degrees C), characteristics of myocyte contraction/relengthening and systolic/diastolic [Ca2+]i were not different between WT and NRG-1+/- mice. The steady-state increases in fractional shortening (FS) and peak-systolic [Ca2+]i in response to isoproterenol were similar in both groups. In WT myocytes stimulated with isoproterenol, carbachol decreased FS, peak-systolic [Ca2+]i, and cAMP levels. In NRG-1+/- myocytes, carbachol did not attenuate either FS or peak-systolic [Ca2+]i, associated with the failure to decrease cAMP levels. Investigation of muscarinic receptor signaling showed no difference of LV protein levels of muscarinic M2 receptors or G protein Galpha(i1,2), Galpha(i3), and Galpha(o) subunits. CONCLUSIONS: Cardiomyocytes deficient in neuregulin signaling are unable to adequately counterbalance beta-adrenergic activation by inhibitory parasympathetic activity. This mechanism may contribute to the known increased risk of heart failure in injured human hearts when neuregulin signaling is suppressed.

Adrenergic beta-Agonists↗
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

Aldosterone directly stimulates cardiac myocyte hypertrophy.

BACKGROUND: Clinical and experimental studies suggest that aldosterone modulates myocardial hypertrophy. From in vivo studies, it is not possible to distinguish between direct actions on myocyte growth and effects of mechanical load. In this study we tested the hypothesis that aldosterone induces myocyte hypertrophy in low-density, serum-free cultures of neonatal rat ventricular myocytes. METHODS AND RESULTS: Hypertrophy was quantified by [(14)C]-phenylalanine incorporation and confocal microscopic assessment of myocyte surface area. Aldosterone caused a 27% increase in protein incorporation (EC(50) = 40 nmol/L) and a 29% increase in myocyte surface area compared with the vehicle control. This response was associated with increased mRNA levels of atrial natriuretic factor, alpha- and beta-myosin heavy chain measured by RNase protection assay, and it was suppressed by the mineralocorticoid receptor blocker spironolactone. Analysis of early signaling events showed that aldosterone stimulation acutely translocated protein kinase C (PKC)-alpha to the membrane fraction and increased the levels of phosphorylated ERK1/2 and JNK. PD 98059, an inhibitor of the ERK activator MEK (mitogen-activated protein kinase kinase) and bisindolylmaleimide I, an inhibitor of PKC activation, each blocked aldosterone-stimulated hypertrophy. CONCLUSION: Aldosterone directly stimulates hypertrophy in neonatal rat ventricular myocytes. The growth response is dependent on the mineralocorticoid receptor and is associated with activation of ERK, JNK, and PKC-alpha.

Aldosterone↗
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↗
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

Influence of fluid volume variations on the calculated value of the left ventricular mass measured by echocardiogram in patients submitted to hemodialysis.

The left ventricular mass (LVM) measurement is of major importance for renal patients, as ventricular hypertrophy is an important prognostic index. The echocardiogram of the ventricular mass is larger before than it is after hemodialysis, which can confuse data interpretation. The aim of this work is to study the influence of alterations in fluid volume on the variations in measurements of ventricular mass observed during the course of a hemodialysis. Sixteen patients with chronic renal insufficiency in hemodialysis were evaluated at the Dialysis Unit of the University Hospital-UNESP, Botucatu, São Paulo State. The left ventricular mass was calculated from echocardiograms taken before and after hemodialysis and simultaneous ultra-filtration (12 patients: UF GROUP) and before and after hemodialysis isovolemic phase with sequential ultra-filtration (10 patients: ISO GROUP). Six of these patients were submitted to measurements of left ventricular mass before and after hemodialysis in both isovolemic and simultaneous ultra-filtration procedures. In the UF group, there was significant reduction in the following parameters before and after dialysis: diastolic diameter from 54.0 +/- 6.0mm to 45.6 +/- 7.6mm; left ventricular mass from 342 +/- 114 g to 265 +/- 117 g; and its respective index (IMVE) from 214 +/- 68 g/m2 to 168 +/- 71 g/m2. The ISO group showed no statistically significant variation. The behavior of the variables of six patients submitted to both observations confirm these results. In conclusion, the variations in echocardiogram measurements of the left ventricula mass relating to hemodialysis appear to be induced by alterations of the volemic condition.

Adolescent↗
PubMed2002

Ventricular remodeling and diastolic myocardial dysfunction in rats submitted to protein-calorie malnutrition.

The effects of protein-calorie malnutrition (PCM) on heart structure and function are not completely understood. We studied heart morphometric, functional, and biochemical characteristics in undernourished young Wistar rats. They were submitted to PCM from birth (undernourished group, UG). After 10 wk, left ventricle function was studied using a Langendorff preparation. The results were compared with age-matched rats fed ad libitum (control group, CG). The UG rats achieved 47% of the body weight and 44% of the left ventricular weight (LVW) of the CG. LVW-to-ventricular volume ratio was smaller and myocardial hydroxyproline concentration was higher in the UG. Left ventricular systolic function was not affected by the PCM protocol. The myocardial stiffness constant was greater in the UG, whereas the end-diastolic pressure-volume relationship was not altered. In conclusion, the heart is not spared from the adverse effects of PCM. There is a geometric alteration in the left ventricle with preserved ventricular compliance despite the increased passive myocardial stiffness. The systolic function is preserved.

Animals↗