Base de dados : MedCarib
Pesquisa : D01.339.387 [Categoria DeCS]
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  1 / 8 MedCarib  
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Fotocópia
Id: 17382
Autor: Oyekan, Adebayo O(aut).
Título: The suppression by lipopolysaccharide of cytochrome P450-dependent renal vasodilation in the rat is mediated by nitric oxide
Fonte: European journal of pharmacology;277(2-3):123-132, April 24, 1995. graf.
Idioma: en.
Resumo: The isolated perfused kidney of the rat was used to examine the hypothesis that lipopolysaccharide-induced nitric oxide (NO) production inhibits cytochrome P450-dependent vasodilation. The vasodilator responses to arachidonic acid and bradykinin were examined as the response to arachidonic acid is wholly dependent, and that to bradykinin partly dependent on cytochrome P450 metabolism. In endotoxin-treated rats, the vasodilator response to arachidonic acid was inhibited, and those to bradykinin and acetylcholine were enhanced. Following treatment with phenobarbitone, the inducer of certain isoforms of cytochrome P450 enzymes, the vasodilator effects of all three agonists,especially that of arachidonic acid were amplified. Lipopolysaccharide inhibited the effect of phenobarbitone on the vasodilator effect of arachidonic acid and bradykinin but enhanced that of acetylcholine. The effect of lipopolysaccharide was antagonized by haemoglobin, a NO antagonist, and N (omega)- nitro-L-arginine, an inhibitor of NO synthase, suggesting that the inhibitory effect of lipopolysaccharide on arachidonic acid- and bradykinin-induced vasodilation was mediated by NO/NO synthase. N(omega)-Nitro-L-arginine enhanced vasodilation induced by arachidonic acid while that induced by bradykinin or acetylcholine was reduced, implying that endogenous NO inhibits vasodilator cytochrome P450 metabolites in the rat kidney. Pretreatment with dexamethasone, an inhibitor of inducible NO synthase, resulted in inhibition of the lipopolysaccharide modulation of arachidoni acid-induced vasodilation, suggesting that the inducible NO synthase is the target of the inhibitory effect of lipopolysaccharide. The inhibitory effect of lipopolysaccharide was mimicked by nitroprusside, the L-arginine-independent NO donor, and by L-arginine, the biosynthetic precusor of NO ...
Responsável: TT5 - Médical Sciences Library
TT5; W1, EU72E


  2 / 8 MedCarib  
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Fotocópia
Id: 2400
Autor: McGrowder, Donavan; Ragoobirsingh, Dalip; Dasgupta, Tara P.
Título: The hyperglycaemic effect of S-nitroso-glutathione via the release of nitric oxide
Fonte: WEST INDIAN MED. J;46(1(Suppl.1)):31-2, Feb. - Mar. 1997.
Idioma: En.
Conferência: Apresentado em: 3rd Annual Postgraduate Course and International Conference, Ocho Rios, Feb.27 - Mar.2 1997.
Resumo: Nitric oxide is a pathogenic factor of inflammatoryislet cell death in Type I diabetes. Insulin-Dependent Diabetes Mellitus (IDDM) is mediated by an autoimmune mechanism or inflammatory process that is characterized by destruction of beta cells. Incubation of pancreatic islet cells with activated macrophages, which release large amounts of nitric oxide, causes the death of the islet cells. When the cells are exposed to the nitric oxide donor, sodium nitroprusside, lysis of the cells occur in a concentration and time-dependent manner. In this study we investigated the pharmacological activity of S-nitroso-glutathione (GSNO), a carrier of nitric oxide on blood glucose levels in dogs, and measured the plasma nitrate/nitrite concentration in the dog serum after the administration of GSNO using an automated method. The blood glucose level was measured using the glucose oxidase assay. S-nitroso-glutathione elicited a dose-dependent increase in blood glucose levels which was paralleled with an increase in nitrate/nitrite production. The blood glucose levels at 2.0 hrs and 2.5 hrs of the Oral Glucose Tolerance Test (OGTT) were significantly higher in dogs administered with GSNO than those of the controls (p<0.05). Post-prandial blood glucose levels in dogs administered with 35 mg per kg body weight of GSNO were 7.2 + 0.9mmol/l and 7.1 + 0.7mmol/l, compared with 4.8 + 0.2mmol/l and 4.6 + 0.2mmol/l in controls. The hyperglycaemic effect was more pronounced on adminstration of 35 mg per kg body weight of GSNO and ascorbic acid. Post-prandial blood glucose levels in the dogs after administration of 50 mg per body weight, at 2.0 hrs and 2.5 hrs were 9.2 + 0.7mmol/l and 9.3 + 0.3mmol/l, respectively. The basal nitrate/nitrite concentration was 12.4 + 0.4umol. On administration of 35 mg per kg body weight of GSNO, there was a 35 - 60 percent increase in the plasma nitrate/nitrite concentration. The plasma nitrate/nitrite concentration at 2.0 hrs to 2.5 hrs ranged from 16.8 + 1.0umol. The plasma nitrate/nitrite concentration increase by 100 percent on administration of 50 mg per kg of GSNO. This study confirms that S-nitroso-glutathione is a hyperglycaemic compound which affects the blood glucose levels in dogs. The hyperglycaemic effects can be caused by the nitric oxide action on the pancreatic islet cells (AU).
Responsável: JM3.1 - Médical Library
JM3.1; R18.W4


  3 / 8 MedCarib  
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Fotocópia
Id: 2309
Autor: McGrowder, Donavan; Ragoobirsingh, Dalip; Dasgupta, Tara P.
Título: The hyperglycaemic effect of s-nitroso-glutathione via the release of nitric oxide - abstract
Fonte: WEST INDIAN MED. J;46(Suppl 2):22, Apr. 1997.
Idioma: En.
Conferência: Apresentado em: Commonwealth Caribbean Medical Research Council 42nd Scientific Meeting, St. Maarten, Apr. 16 - 19 1997.
Resumo: Recent evidence suggests that nitric oxide (NO) is an important factor in both inflammatory-induced and streptozotocin-induced diabetes. In this study we investigated the pharmacological activity of S-nitroso-glutathoine (GNSO), a carrier of NO, on blood glucose level in 10 mongrel dogs, and measured their plasma nitrate concentration after the administration of GSNO. S-nitroso-glutathoine elicited a dose-dependent increase in blood glucose level (15 - 102 percent) which was paralled with an increase in nitrate production. The blood glucose levels at 2.0 and 2.5 hrs in an Oral Glucose Tolerance Test were significantly higher in dogs administered with GNSO than those of the controls (p<0.05). There was also a significant increase in plasma nitrate on administration of GSNO (35 - 100 percent). The plasma nitrate concentrations from 0.5hr to 2.5hrs were significantly higher compared to the controls (p<0.05). The hyperglycaemic effect of GSNO was enhanced with the co-adminstration of ascorbic acid. This resulted in 5 - 30 percent increase in blood glucose concentration. The blood glucose levels at 2hrs in dogs after the co-administration of 35mg kg of GSNO (P<0.05). The data from this study showed that persistent hyperglycemia can be an unwanted side effect of GSNO administration and that the glucose concentration should be closely monitored when this drug is used to treat patients(AU)
Responsável: JM3.1 - Médical Library
JM3.1; R18.W4


  4 / 8 MedCarib  
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Fotocópia
Id: 1550
Autor: McGrowder, Donavan; Ragoobirsingh, Dalip; Dasgupta, Tara P.
Título: Decreased insulin binding to erythrocytes and mononuclear leucocytes in normal dogs administered with S-nitroso- glutathione
Fonte: West Indian med. j;47(suppl. 1):30-1, Mar. 5-8, 1998.
Idioma: En.
Resumo: Nitric oxide is a pathogenic factor of inflammatory islet cell death in type 1 diabetes. An early event in the pathogenesis of insulin-dependent diabetes mellitus (IDDM) is intraislet accumulation of activated macrophages. Their secretory products such as nitric oxide (NO) are found to play a crucial role in islet destruction. Macrophage activity and progressive islet cell destruction persist during a long period of chronic inflammatory events preceding diabetes, suggesting the presence of nitric oxide contributing to continued immunostimulation. It has been shown previously that the nitric oxide donor, S-nitrosoglutathione (GSNO) caused persistent postprandial hyperglycaemia in normal healthy dogs at 35 and 50mg/kg. parallel with an increase in plasma nitrate concentration and decrease in insulin secretion. This study was designed to investigate differences in cellular binding of insulin in dogs administered with the GSNO. A time course assay of insulin binding, to isolate erythrocytes and mononuclear leucocytes from dog administered with GSNO, was done during the oral glucose tolerance test (OFTT). The erthrocyte receptor assay performed was the methodology used by Ghambir et al (1977). A modification was also done for mononuclear leucocytes insulin binding assay. The plasma glucose levels were measured by the glucose oxidase method, while the insulin levels were determined by radio-immunoassay. The results of these studies show that erythrocytes and mononuclear leucocytes from dogs administered with GSNO have decreased ability to bind insulin when compared to erythrocytes and mononuclear leucocytes from the controls. In dogs administered with GSNO, there was less binding of erythrocytes and mononuclear leucocytes, 44 percent and 29 percent respectively, when compared to the bound free ratio value of the controls. The data also shows that erythrocytes and mononuclear leucocytes from dogs administered with GSNO have 256 and 10.7x10 insulin receptor sites per cell, respectively, compared with 296 and 18.4x10 per cell for the control (P<0.05). Competitive inhibition studies using unlabelled insulin indicate that the affinity of insulin for its receptor on erythrocytes from dogs administered with GSNO was also significantly different from the controls, while that of mononuclear leucocytes from both group was comparable.(AU)
Responsável: JM3.1 - Médical Library
JM3.1; R18.W4


  5 / 8 MedCarib  
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Fotocópia
Id: 1246
Autor: McGrowder, Donavan; Ragoobirsingh, Dalip; Dasgupta, Tara P.
Título: The effect of nitric oxide released from s-nitroso-glutathoine on glucagon and insulin in dogs
Fonte: West Indian med. j;48(Suppl. 1):24-5, Mar. 7, 1999.
Idioma: En.
Resumo: Nitric oxide (NO), a potent modulator of cellular function, and NO donors have been useful tools in both experimental and clinical setting. Low molecular weight thiols such as cysteine and glutathoine were proposed to act as NO-carriers. The study was undertaken to investigate the pharmacological activity of the NO donor, S-nitrosoglutathoine (GSNO), on the plasma glucose and on the gluco-regulatory hormones, insulin and glucagon in healthy normoglycaemic dogs. Plasma glucose levels were measured by the glucose oxidase method, while the insulin and glucagon levels were determined by radioimmunoassay. In healthy normoglycaemic dogs, administration of 50 mg/kg GSNO caused an increase in post-prandial plasma glucose levels. The plasma glucose levels were significantly (p<0.05) elevated at 1.5 hr, 2.0 hr and 2.5 hr of the oral glucose tolerance test. These values were significantly higher than those obtained for the controls. The increase in glucose level was associated with a significant decrease in insulin levels and increase in glucagon levels (p<0.05). The fasting insulin level was 8.0 ± 0.3 IU/ml in the control. The insulin level increased to a maximum of 34.0 ± 0.3 IU/ml 1.5 hr post-prandial, and then decreased to 12.4 ± 0.4 IU/ml after 2.5 hr. On administration of 50 mg/kg GSNO, the insulin level increased to a maximum of 23.0 ± 0.6 IU/,l after 1.5 hr post-prandial and then decreased to 17.0 ± 0.4 IU/ml after 2.5 hr. The blood glucagon levels increased from 40.0 ± 0.3 pg/ml to 53.0 ± 0.3 pg/ml after 1 hr in controls. In dogs administered with GSNO, the blood glucagon level increases to a maximum level of 80.0 ± 0.5 pg/ml 1.5hr post-prandial. These results suggest that in healthy normoglycaemic dogs, nitric oxide released from GSNO caused a transient increase in post-prandial plasma glucose levels, inhibited glucose stimulated insulin secretion and elevated glucagon levels.(AU)
Responsável: JM3.1 - Médical Library
JM3.1; R18.W4


  6 / 8 MedCarib  
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Fotocópia
Id: 1141
Autor: Kissoon, Niranjan.
Título: Measurement of lung inflammation in asthmatics - reason for optimism
Fonte: West Indian med. j;49(1):9-11, Mar. 2000.
Idioma: En.
Resumo: It is recognized that bronchial asthma is an inflammatory disease. However, aggressive anti-inflammatory therapy is not guided by the degree of lung inflammation. This is of particular concern in children in whom over-aggressive therapy with corticosteroid may lead to growth retardation. Analysis of breath exhaled nitric oxide levels may be an indirect measurement of lung inflammation. Since exhaled nitric oxide levels and inflammation decrease after steroid therapy, measurement of exhaled nitric oxide levels may provide a rationale for optimization of steroid therapy and possible reduction of side effects. Measurement of exhaled nitric oxide levels is not available for routine use but may be so in the near future. This will likely herald a new dawn in the management of asthma, a disease with increasing frequency, mortality and morbidity.(Au)
Responsável: JM3.1 - Médical Library
JM3.1; R18.W4


  7 / 8 MedCarib  
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Fotocópia
Id: 1006
Autor: Deneuville, M; Claire, M.
Título: Vasoactive alterations in lower limb subcutaneous resistive arteries from Caribbean patients with atherosclerosis
Fonte: West Indian med. j;49(Suppl 2):17, Apr. 2000.
Idioma: En.
Resumo: OBJECTIVE: This study was performed to investigate the endothelium-dependent relaxation and contractile responses to endothelin-1 in subcutaneous resistive arteries from Caribbean patients with advanced atherosclerotic femoro-crural arterial disease. DESIGN AND METHODS: Small subcutaneous arteries (inner diameter 200 um) from control subjects (n=8) and atherosclerotic patients (n=8) were dissected from fat biopsies obtained at routine vascular surgery and mounted in vitro on a wire-myograph measuring parietal tension under isometric conditions. RESULTS: Acetylcholine-induced relaxation (10-6 M) was significantly reduced in pre-contracted arteries from atherosclerotic patients (24 + or - 16 percent vs 17 percent in control, p<0.001). Smooth muscle relaxation to sodium nitroprusside was comparable in both groups. Contractions elicited by endothelin-1 (10-9 M) were significantly lower and almost suppressed in both the atherosclerotic group (1.2 + or - 0.8 Kpa) and in the hypertensive subgroup of control subjects (n=4, 1.2= 0r - 1.2 Kpa) comparatively to normotensive control subjects (12.3 + or - 6.9 Kpa, p<0.001). Contractile responses induced by endothelin-1 at higher concentrations (10-8 - 10-7 M), noradrenaline and hyperosmolar potassium were comparable in both groups. CONCLUSIONS: These data suggest a specific impairment of both endothelium-dependent relaxation and contractility in lower limb subcutaneous resistive arteries from Caribbean patients with atherosclerotic femoro-crural arterial disease. These changes in vessels which largely determine proximal vascular resistance may contribute to ischaemic complications in this vascular bed including skin ulcerations and gangrene.(Au)
Responsável: JM3.1 - Médical Library
JM3.1; R18.W4


  8 / 8 MedCarib  
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Fotocópia
Id: 885
Autor: Bissoon, D; Ramchandani, N; Monteil, Michele A; Carrington, C. V. F.
Título: Nitric oxide levels in children with febrile illnesses - Poster abstract
Fonte: West Indian med. j;49(suppl. 2):60-1, Apr. 2000.
Idioma: En.
Resumo: OBJECTIVE: To determine nitric oxide (NO) levels in children with febrile illness and to investigate its prognostic value in early dengue virus infections. DESIGN AND METHOD: A pilot case control study was conducted from September 1998 to March 1999 at the Eric Williams Medical Sciences Complex, Priority Care Facility (PCF), in Trinidad. Serum NO concentrations were measured in children <12 years presenting with febrile illnesses in the absence of clinically significant bacterial infection. RESULTS: Of 59 blood samples collected, there were 22 from individuals diagnoses as virally induced gastroenteritis (VGE), with 31 non-specific viral illnesses (VI), and 6 viral infections associated with upper-respiratory tract infection (URTI-VI). The mean (NO) in all cases was above normal (11.9 uM SD 5.9) 81.17 uM in VGE, 41.30 uM in VI and 57.83 uM in URTI-VI. Krushkal-Wallis test revealed that there was a significant difference (p = 0.007) between all three means and that the mean (NO) for VGE was significantly higher (p = 0.003) than that of VI. CONCLUSIONS: The degree of elevation of NO varies between viral illnesses in children and its potential as a rapid prognostic marker warrants further investigation.(AU)
Responsável: JM3.1 - Médical Library
JM3.1; R18.W4



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