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1.
Atherosclerosis ; 204(2): 544-8, 2009 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-19013573

RESUMO

OBJECTIVE: Circulating endothelial progenitor cells (EPCs) play a critical role in maintaining the integrity of vascular vessels. The number of EPCs inversely correlates with the number of atherosclerotic risk factors. Although nonpharmacological treatment represents the first approach to the primary prevention of atherosclerotic diseases, little is known about the effects of diet on EPCs. We investigated the effect of a dietary intervention with vegetables that are commonly eaten in Okinawa on the number of EPCs. METHODS AND RESULTS: Forty-five healthy young women were employed and randomized to a dietary intervention group (n=24) or a control group (n=21). Subjects in the intervention group received typical Okinawan vegetables through home-parcel delivery for 2 weeks. After the dietary intervention, urinary potassium and magnesium excretion increased only in the intervention group and changes were greater than in the control group (p=0.007, 0.010, respectively). The consumption of total vegetables correlated with changes in both urinary potassium and magnesium excretion. Serum folic acid increased and plasma homocysteine decreased in both groups but the change was significant only in the intervention group. The EPCs number significantly increased in the intervention group but did not in the control group. An inverse correlation was observed between EPC number and plasma homocysteine level (r=-0.272, p=0.016). Changes in the EPC number inversely correlated with changes in both serum total cholesterol and low-density lipoprotein cholesterol level (r=-0.555, p=0.0002; r=-0.626, p<0.0001, respectively). CONCLUSIONS: The consumption of vegetables increased the number of circulating EPCs; this change might be associated with a homocysteine-lowering effect.


Assuntos
Dieta , Células Endoteliais/fisiologia , Células-Tronco/fisiologia , Verduras , Adulto , Biomarcadores/sangue , Biomarcadores/urina , Contagem de Células , Colesterol/sangue , LDL-Colesterol/sangue , Feminino , Ácido Fólico/sangue , Homocisteína/sangue , Humanos , Japão , Magnésio/urina , Potássio/urina , Espécies Reativas de Oxigênio/sangue , Adulto Jovem
2.
Hypertens Res ; 31(2): 353-61, 2008 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-18360056

RESUMO

Thiazolidinediones, which stimulate peroxisome proliferator-activated receptor gamma, have been shown to prevent cardiovascular injury. However, little is known about their effects on salt-sensitive hypertension. We thus investigated whether or not pioglitazone affects left ventricular (LV) hypertrophy in Dahl salt-sensitive rats, then compared its effects to those of an angiotensin II receptor blocker, candesartan. Rats were used at 16 weeks of age after they had been fed either a low-salt (0.3%; DSL) or high-salt (8%; DSH) diet for 10 weeks; some of the DSH rats were treated with pioglitazone (10 mg/kg/day) or candesartan (4 mg/kg/day). Both drugs decreased the elevated blood pressure in DSH rats, although it was still higher than in DSL rats. Both drugs decreased plasma insulin levels, but neither affected plasma glucose levels. The thiobarbituric acid reactive substance level in the LV was decreased by both drugs. LV hypertrophy evaluated by echocardiography in DSH rats was nearly normalized by both drugs, whereas only candesartan decreased LV diameter. In histological analysis, both drugs ameliorated LV fibrosis and myocardial cell hypertrophy. Both drugs decreased elevated gene expression levels of transforming growth factor-beta1 and collagen type I, although the pioglitazone action was slightly modest. The metalloproteinase activity was increased in DSH rats, but both drugs decreased this level. Taken together, these findings indicate that pioglitazone reduced LV hypertrophy and fibrosis in salt-sensitive hypertension. Improvement in blood pressure, insulin level, and oxidative stress may be associated with this beneficial action of pioglitazone.


Assuntos
Hipertensão/complicações , Hipertrofia Ventricular Esquerda/tratamento farmacológico , Hipoglicemiantes/farmacologia , Miocárdio/patologia , Tiazolidinedionas/uso terapêutico , Animais , Benzimidazóis/farmacologia , Compostos de Bifenilo , Glicemia/análise , Fibrose , Masculino , Metaloproteinases da Matriz/genética , Miocárdio/metabolismo , Miócitos Cardíacos/patologia , Tamanho do Órgão/efeitos dos fármacos , Pioglitazona , RNA Mensageiro/análise , Ratos , Ratos Endogâmicos Dahl , Sístole/efeitos dos fármacos , Tetrazóis/farmacologia
3.
Intern Med ; 41(10): 864-6, 2002 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-12413011

RESUMO

A 33-year-old woman was referred from an outside dialysis clinic to our hospital because of severe abdominal pain during hemodialysis. She had been on chronic hemodialysis for the past 11 years due to chronic glomerulonephritis. Nafamostat mesilate was used as an anticoagulant for hemodialysis, because it was during her menstrual period with hypermenorrhea. On admission, she had no abdominal pain or gynecological abnormalities. On the second day, she had similar abdominal pain during hemodialysis with nafamostat mesilate in our dialysis unit. The abdominal pain disappeared within 60 minutes after discontinuing the hemodialysis. We re-started dialysis using heparin instead of nafamostat mesilate and she had no symptoms. The titer of total immunoglobulin E was high. The drug lymphocyte stimulation test was positive for nafamostat mesilate and antigen specific immunoglobulin E to nafamostat mesilate was highly positive in her blood. Although an allergic reaction to nafamostat mesilate is a rare complication, it should be one of the differential diagnoses of abdominal pain occurring during hemodialysis.


Assuntos
Dor Abdominal/induzido quimicamente , Anticoagulantes/efeitos adversos , Hipersensibilidade a Drogas/etiologia , Guanidinas/efeitos adversos , Dor Abdominal/terapia , Adulto , Benzamidinas , Hipersensibilidade a Drogas/terapia , Feminino , Fibrinolisina/antagonistas & inibidores , Glomerulonefrite/terapia , Hemodiálise no Domicílio/efeitos adversos , Humanos , Imunoglobulina E/sangue , Ativação Linfocitária/fisiologia
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