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1.
Mol Biol Rep ; 38(7): 4343-6, 2011 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-21110105

RESUMO

Cystic Fibrosis (CF) is an autosomal recessive disease, caused by mutations in the Cystic Fibrosis Transmembrane Regulator gene (CFTR). The most frequent mutation in CF is ΔF508. The disease is clinically characterized by elevated concentrations of sweat chlorides and abnormally thick mucus. It affects organs such as lung, pancreas, gastrointestinal and reproductive tract. Women with CF commonly present delayed puberty and amenorrhea due to malnutrition. Our objective was to screen the presence of ΔF508 mutation in 24 women with altered fertility. Nine of these women presented reduced fertility without a known cause, four showed polycystic ovaries and two had early menopause. One woman with early menopause was a carrier of the ΔF508 mutation. Our study demonstrates that it is possible that the frequency of CF mutations among patients with altered fertility may be higher than expected. Previous data showed that fibrocystic women can show reduced fertility, maternal mortality associated with pregnancy and increased incidence of spontaneous abortion. We therefore recommend that women with reduced fertility undertake genetic tests for a better evaluation of pregnancy risks and clinical monitoring.


Assuntos
Regulador de Condutância Transmembrana em Fibrose Cística/genética , Fibrose Cística/genética , Fertilidade/genética , Testes Genéticos , Mutação/genética , Adulto , Brasil , Feminino , Humanos , Reação em Cadeia da Polimerase , Gravidez
2.
Braz J Med Biol Res ; 30(5): 679-87, 1997 May.
Artigo em Inglês | MEDLINE | ID: mdl-9283639

RESUMO

An increase in angiotensin-converting enzyme (ACE) activity has been observed in the heart after myocardial infarction (MI). Since most studies have been conducted in chronically infarcted individuals exhibiting variable degrees of heart failure, the present study was designed to determine ACE activity in an earlier phase of MI, before heart failure development. MI was produced in 3-month old male Wistar rats by ligation of the anterior branches of the left coronary artery, control rats underwent sham surgery and the animals were studied 7 or 15 days later. Hemodynamic data obtained for the anesthetized animals showed normal values of arterial blood pressure and of end-diastolic pressure in the right and left ventricular cavities of MI rats. Right and left ventricular (RV, LV) muscle and scar tissue homogenates were prepared to determine ACE activity in vitro by measuring the velocity of His-Leu release from the synthetic substrate Hyp-His-Leu. ACE activity was corrected to the tissue wet weight and is reported as nmol His-Leu g-1 min-1. No significant change in ACE activity in the RV homogenates was demonstrable. A small nonsignificant increase of ACE activity (11 +/- 9%; P > 0.05) was observed 7 days after MI in the surviving left ventricular muscle. Two weeks after surgery, however, ACE activity was 46 +/- 11% (P < 0.05) higher in infarcted rats compared to sham-operated rats. The highest ACE activity was demonstrable in the scar tissue homogenate. In rats studied two weeks after surgery, ACE activity in the LV muscle increased from 105 +/- 7 nmol His-Leu g-1 min-1 in control hearts to 153 +/- 11 nmol His-Leu g-1 min-1 (P < 0.05) in the remaining LV muscle of MI rats and to 1051 +/- 208 nmol His-Leu g-1 min-1 (P < 0.001) in the fibrous scar. These data indicate that ACE activity increased in the heart after infarction before heart failure was demonstrable by hemodynamic measurements. Since the blood vessels of the scar drain to the remaining LV myocardium, the high ACE activity present in the fibrous scar may increase the angiotensin II concentration and decrease bradykinin in the cardiac tissues surrounding the infarcted area. The increased angiotensin II in the fibrous scar may contribute to the reactive fibrosis and hypertrophy in the left ventricular muscle surviving infarction.


Assuntos
Ventrículos do Coração/enzimologia , Infarto do Miocárdio/enzimologia , Peptidil Dipeptidase A/metabolismo , Angiotensina II/metabolismo , Animais , Pressão Sanguínea/fisiologia , Peso Corporal/fisiologia , Frequência Cardíaca/fisiologia , Masculino , Ratos , Ratos Wistar , Sistema Renina-Angiotensina/fisiologia
3.
Braz J Med Biol Res ; 32(3): 355-60, 1999 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-10347796

RESUMO

The excessive stimulation of beta-adrenergic receptors in the heart induces myocardial hypertrophy. There are several experimental data suggesting that this hypertrophy may also depend, at least partially, on the increase of local production of angiotensin II secondary to the activation of the cardiac renin-angiotensin system. In this study we investigated the effects of isoproterenol on the activity of angiotensin-converting enzyme (ACE) in the heart and also in the aorta and plasma. Male Wistar rats weighing 250 to 305 g were treated with a dose of (+/-)-isoproterenol (0.3 mg kg-1 day-1, N = 8) sufficient to produce cardiac hypertrophy without deleterious effects on the pumping capacity of the heart. Control rats (N = 7) were treated with vehicle (corn oil). The animals were killed one week later. ACE activity was determined in vitro in the four cardiac chambers, aorta and plasma by a fluorimetric assay. A significant hypertrophy was observed in both ventricular chambers. ACE activity in the atria remained constant after isoproterenol treatment. There was a significant increase (P < 0.05) of ACE activity in the right ventricle (6.9 +/- 0.9 to 8.2 +/- 0.6 nmol His-Leu g-1 min-1) and in the left ventricle (6.4 +/- 1.1 to 8.9 +/- 0.8 nmol His-Leu g-1 min-1). In the aorta, however, ACE activity decreased (P < 0.01) after isoproterenol (41 +/- 3 to 27 +/- 2 nmol His-Leu g-1 min-1) while it remained unchanged in the plasma. These data suggest that ACE expression in the heart can be increased by stimulation of beta-adrenoceptors. However, this effect is not observed on other local renin-angiotensin systems, such as the aorta. Our data also suggest that the increased sympathetic discharge and the elevated plasma concentration of catecholamines may contribute to the upregulation of ACE expression in the heart after myocardial infarction and heart failure.


Assuntos
Agonistas Adrenérgicos beta/farmacologia , Aorta/efeitos dos fármacos , Aorta/enzimologia , Isoproterenol/farmacologia , Miocárdio/enzimologia , Sistema Renina-Angiotensina/efeitos dos fármacos , Sistema Renina-Angiotensina/fisiologia , Angiotensina II/metabolismo , Inibidores da Enzima Conversora de Angiotensina/metabolismo , Animais , Átrios do Coração/efeitos dos fármacos , Ventrículos do Coração/efeitos dos fármacos , Masculino , Plasma/efeitos dos fármacos , Ratos , Ratos Wistar
4.
Arq Bras Cardiol ; 69(2): 101-10, 1997 Aug.
Artigo em Português | MEDLINE | ID: mdl-9567332

RESUMO

PURPOSE: To determine angiotensin converting enzyme (ACE) activity in the heart of infarcted rats and to investigate the effects of captopril and losartan on the post-infarction remodeling process. METHODS: Myocardial infarction (MI) was produced in Wistar rats by ligature of the left coronary artery. Control rats (Con) underwent a sham surgery. MI and Con rats remained untreated or were treated with captopril (30 mg/kg/day) or losartan (15 mg/kg/day) for 30 days. ACE activity was determined in right (RV) and left ventricular (LV) muscles and in the scar tissue. The effects of captopril therapy was also investigated in the hydroxiproline (OH-Pro) and protein in RV and LV. RESULTS: ACE activity increased 25% in the RV and 70% in the remaining LV muscle. The highest ACE activity was found in the scar tissue, where it was 4.5 times the value of the LV muscle (420 +/- 68 vs 94 +/- 8 nmoles/g/min; P < 0.01). An increase of the end-diastolic pressure and of the muscle mass was found in the RV and LV of MI rats. Captopril and losartan treatments were equally efficient to attenuate these parameters in both ventricles. Captopril also reduced the total OH-Pro content in the RV and LV muscles. The Prot concentration was significantly reduced in the myocardium of MI rats, an effect enhanced by captopril therapy. CONCLUSION: The AII concentration in the blood draining from the scar to the surrounding muscle is probably high. It is likely that this elevated local generation of AII contributes to hypertrophy and to collagen deposition. The effects of ACE inhibitors on remodeling are likely to depend on the reduction of the locally generated AII.


Assuntos
Inibidores da Enzima Conversora de Angiotensina/farmacologia , Anti-Hipertensivos/farmacologia , Captopril/farmacologia , Ventrículos do Coração/efeitos dos fármacos , Coração/fisiologia , Losartan/farmacologia , Infarto do Miocárdio/fisiopatologia , Peptidil Dipeptidase A/fisiologia , Angiotensina II , Animais , Ventrículos do Coração/química , Hemodinâmica/efeitos dos fármacos , Hidroxiprolina/análise , Masculino , Proteínas/análise , Ratos , Ratos Endogâmicos , Ratos Wistar , Vasoconstritores
6.
Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;30(5): 679-87, May 1997. tab, graf
Artigo em Inglês | LILACS | ID: lil-196683

RESUMO

An increase in angiotensin-converting enzyme (ACE) activity has been observed in the heart after myocardial infarction (MI). Since most studies have been conducted in chronically infarcted individuals exhibiting variable degrees of heart failure, the present study was designed to determine ACE activity in an earlier phase of MI, before heart failure development. MI was produced in 3-month old male Wistar rats by ligation of the anterior branches of the left coronary artery, control rats underwent sham surgery and the animals were studied 7 or 15 days later. Hemodynamic data obtained for the anesthetized animals showed normal values of arterial blood pressure and of end-diastolic pressure in the right and left ventricular cavities of MI rats. Right and left ventricular (RV, LV) muscle and scar tissue homogenates were prepared to determine ACE activity in vitro by measuring the velocity of His-Leu release from the synthetic substrate Hyp-His-Leu. ACE activity was corrected to the tissue wet weight and is reported as nmol His-Leu g(-1) min(-1). No significant change in ACE activity in the RV homogenates was demonstrable. A small nonsignificant increase of ACE activity (11 + 9 percent; P>0.05) was observed 7 days after MI in the surviving left ventricular muscle. Two weeks after surgery, however, ACE activity was 46 + 11 percent (P<0.05) higher in infarcted rats compared to sham-operated rats. The highest ACE activity was demosntrable in the scar tissue homogenate. In rats studied two weeks after surgery, ACE activity in the LV muscle increased from 105 + 7 nmol His-Leu g(-1) min (-1) in control hearts to 153 + 11 nmol His-Leu g(-1) min(-1) (P<0.05) in the remaining LV muscle of MI rats and to 1051 + 208 nmol His-Leu g(-1) min(-1) (P<0.001) in the fibrous scar. These data indicate that ACE activity increased in the heart after infarction before heart failure was demonstrable by hemodynamic measurements. Since the blood vessels of the scar drain to the remaining LV myocardium, the high ACE activity present in the fibrous scar may increase the angiotensin II concentration and decrease bradykinin in the cardiac tissues surrounding the infarcted area. The increased angiotensin II in the fibrous scar may contribute to the reactive fibrosis and hypertrophy in the left ventricular muscle surviving infarction.


Assuntos
Ratos , Animais , Masculino , Angiotensina II/metabolismo , Ventrículos do Coração/fisiopatologia , Infarto do Miocárdio/fisiopatologia , Peptidil Dipeptidase A/metabolismo , Sistema Renina-Angiotensina/fisiologia , Pressão Sanguínea/fisiologia , Peso Corporal/fisiologia , Frequência Cardíaca/fisiologia , Ratos Wistar
7.
Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;32(3): 355-60, Mar. 1999.
Artigo em Inglês | LILACS | ID: lil-230465

RESUMO

The excessive stimulation of beta-adrenergic receptors in the heart induces myocardial hypertrophy. There are several experimental data suggesting that this hypertrophy may also depend, at least partially, on the increase of local production of angiotensin II secondary to the activation of the cardiac renin-angiotensin system. In this study we investigated the effects of isoproterenol on the activity of angiotensin-converting enzyme (ACE) in the heart and also in the aorta and plasma. Male Wistar rats weighing 250 to 305 g were treated with a dose of (ñ)-isoproterenol (0.3 mg kg-1 day-1, N = 8) sufficient to produce cardiac hypertrophy without deleterious effects on the pumping capacity of the heart. Control rats (N = 7) were treated with vehicle (corn oil). The animals were killed one week later. ACE activity was determined in vitro in the four cardiac chambers, aorta and plasma by a fluorimetric assay. A significant hypertrophy was observed in both ventricular chambers. ACE activity in the atria remained constant after isoproterenol treatment. There was a significant increase (P<0.05) of ACE activity in the right ventricle (6.9 = 0.9 to 8.2 = 0.6 nmol His-Leu g-1 min-1) and in the left ventricle (6.4 ñ 1.1 to 8.9 ñ 0.8 nmol His-Leu g-1 min-1). In the aorta, however, ACE activity decreased (P<0.01) after isoproterenol (41 = 3 to 27 = 2 nmol His-Leu g-1 min-1) while it remained unchanged in the plasma. These data suggest that ACE expression in the heart can be increased by stimulation of beta-adrenoceptors. However, this effect is not observed on other local renin-angiotensin systems, such as the aorta. Our data also suggest that the increased sympathetic discharge and the elevated plasma concentration of catecholamines may contribute to the upregulation of ACE expression in the heart after myocardial infarction and heart failure


Assuntos
Animais , Masculino , Ratos , Agonistas Adrenérgicos beta/farmacologia , Inibidores da Enzima Conversora de Angiotensina/metabolismo , Aorta/enzimologia , Isoproterenol/farmacologia , Miocárdio/enzimologia , Sistema Renina-Angiotensina/fisiologia , Angiotensina II/metabolismo , Aorta/efeitos dos fármacos , Átrios do Coração/efeitos dos fármacos , Ventrículos do Coração/efeitos dos fármacos , Plasma/efeitos dos fármacos , Ratos Wistar , Sistema Renina-Angiotensina/efeitos dos fármacos
8.
Arq. bras. cardiol ; Arq. bras. cardiol;40(2): 111-113, 1983. tab
Artigo em Português | LILACS | ID: lil-13962

RESUMO

Foram estudados 20 pacientes assintomaticos, sedentarios, do sexo masculino, submetidos a um programa de condicionamento fisico por 4 meses. A prescricao de exercicios foi feita segundo o proposto por Balke em 1974. Foram analisados: frequencia cardiaca de repouso, frequencia cardiaca maxima, pressao arterial em repouso, consumo de oxigenio, tempo de esforco e carga maxima atingida. Ficaram evidenciadas as adaptacoes organicas consequentes ao condicionamento fisico, caracterizadas por reducao significativa de frequencia cardiaca de repouso e de esforco para uma determinada carga, queda de valores tensionais, elevacao do consumo maximo de oxigenio e aumento da capacidade de desenvolver trabalho, determinado pela aptidao do individuo em alcancar maiores valores de carga (watts), antes de atingir a fadiga muscular


Assuntos
Humanos , Masculino , Adulto , Pessoa de Meia-Idade , Educação Física e Treinamento , Exercício Físico , Aptidão Física , Hemodinâmica
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