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Metabolism ; 30(1): 18-26, Jan. 1981.
Artigo em Inglês | MedCarib | ID: med-12087


The possibility that insufficient glucose production or availability of gluconeogenic substrates could account for fasting hypoglycemia was investigated in three children with epinephrine deficiency. Each had been born the smaller of discordant identical twins, and the unaffected twins served as controls. Fasting plasma glucose production was measured by constant infusion of U-[13]C-glucose under steady-state conditions and was compared with availability of potential glucose sources estimated from respiratory calorimetry and excretory nitrogen. The average rate of glucose production was 2.6 mg/kg/min in the affected twins after they became symptomatic and 2.9 mg/kg/min in the control twins after comparable fasting. Plasma alanine was lower in the affected twins during this interval (average: 0.11 mM versus 0.16 mM), but not earlier prior to decreased plasma glucose; alanine correlated with plasma glucose in a similar way in both groups (r = 0.77). Plasma urea production was 0.30 versus 0.15 mg urea N/kg/min. The calculated availability of potential gluconeogenic amino acids was 1.2 versus 0.6 mg/kg/min. Availability of glycerol, estimated from respiratory calorimetry was 0.4 mg/kg/min in both groups. In two of the twin pairs, net oxidation of carbohydrate (glycogen) was, by design, relatively small under these conditions (0.1 and 0.4 mg/kg/min in the affected and control twins, respectively). Gluconeogenesis therefore accounted for the majority of glucose production. The unaccounted remaining major gluconeogenic source is assumed to be recycled substrates from unoxidized pyruvate. Infusion of excess alanine in these two pairs increased plasma glucose and glucose production similarly in both the affected and control twins. This change was associated with an abnormally large increase in plasma alanine. In the third twin pair, net oxidation of carbohydrate was greater in the affected twin (1.8 versus 1.3 mg/kg/min) and possible glucose sources exceeded total glucose production during hypoglycemia. Earlier during fasting, net oxidation of carbohydrate in this twin was 5.8 mg/kg/min versus 3.1 mg/kg/min in the control. Plasma glucose production measured simultaneously was 4.3 versus 3.8 mg/kg/min, being less than the rate of carbohydrtae oxidation in the affected twin. It is concluded that the abnormal fasting metabolism observed in these children with decreased epinephrine was not primarily a consequence of deficient glucose production or lack of potential gluconeogenic substrates. Initial persistent oxidation of glycogen and subsequent increased utilization of protein during hypoglycemia indicate failure to conserve these limited net sources of pyruvate(AU)

Humanos , Gravidez , Pré-Escolar , Criança , Masculino , Feminino , Peso ao Nascer , Glicemia/biossíntese , Epinefrina/diagnóstico , Hipoglicemia/metabolismo , Gêmeos , Gêmeos Monozigóticos , Alanina/sangue , Aminoácidos/metabolismo , Jejum , Gluconeogênese , Glicogênio/metabolismo , Cinética , Oxirredução , Ureia/sangue
Metabolism ; 30(1): 6-17, 1981. tab, gra
Artigo em Inglês | MedCarib | ID: med-3530


The possible role of epinephrine deficiency in abnormal utilization of energy sources during fasting was investigated in three pairs of discordant identical twins with recurrent fasting hypoglycemia. The hypoglycemic twins, ages 2, 8 and 9 years, each had beens smaller at birth. Defective epinephrine responsiveness to hypoglycemia was established by administration of 2-deoxyglucose, 50 mg/kg, i.v. In the control twins, this resulted in a rapid increase of plasma glucose (+39 mg/100 ml), free fatty acids (+0.3 mM), and urinary epinephrine (+224 ng/mg creatine). These changes did not occur in the affected twins. Fasting metabolism in the epinephrine-deficient twins was compared to the unaffected twins as controls. Oxidation of carbohydrate and fat were estimated from hourly measurements of oxygen consumption and carbon dioxide production, and utilization of protein was determined from nitrogen excretion. PLasma glucose decreased more rapidly in the affected twins during the 8 hours prior to appearance of symptoms. During this period, carbohydrate was oxidized more rapidly than in the controls (average: 3.1 versus 1.7 mg/kg/min). Plasma á-hydroxybutyrate and free fatty acids was frequently less in relation to glucose. Symptoms occurred when the sum of both glucose and á-hydroxybutyrate was lower than in the controls. Urinary epinephrine excretion increased from an average baseline of 18 to a maximum of 134 ng/mg creatinine in the control twins. The average maximum urinary epinephrine reached in the deficient twins was only 51 ng/mg creatinine, in spite of lower glucose. Plasma insulin decreased in relation to glucose below 40 mg/100 ml in the control twins (r = 0.65), but this did not occur in the deficient twins (r = -0.38). Cortisol and growth hormone responses were similar in the two groups. THerefore, the consequences of inability to increase epinephrine when availability of glucose became acutely limiting were inappropriate persistent oxidation of carbohydrate, decreased circulating alternate substrates from fat, and lack of suppression of insulin. (AU)

Pré-Escolar , Feminino , Humanos , Masculino , Doenças em Gêmeos , Metabolismo Energético , Epinefrina/deficiência , Jejum , Gêmeos , Gêmeos Monozigóticos , Hipoglicemia/metabolismo , Peso ao Nascer , Glicemia/metabolismo , Carboidratos/metabolismo , Desoxiglucose/diagnóstico , Epinefrina/urina , Ácidos Graxos não Esterificados/sangue , Hidroxibutiratos/sangue , Oxirredução
West Indian med. j ; 13(4): 276, Dec. 1964.
Artigo em Inglês | MedCarib | ID: med-7390


Adrenaline and Noradrenaline both caused a contraction of the vas deferens. However, adrenaline was a more potent stimulant than noradrenaline. Isoprenaline by itself had no effect on the vas deferens, but it modified the stimulatory effect of subsequent administered adrenaline and noradrenaline. In small doses isoprenaline lessened and in large doses it potentiated the stimulating effect of the other two amines, the degree of inhibition by isoprenaline being greater on noradrenaline than on adrenaline. It was suggested that isoprenaline acted by inhibiting alpha adrenergic receptors in small concentrations, stimulating them in large concentrations and not by stimulating Beta receptors as is presently believed (AU)

21003 , Cobaias , Técnicas In Vitro , Aminas/efeitos adversos , Ducto Deferente/efeitos dos fármacos , Cobaias , Epinefrina , Norepinefrina , Isoproterenol
West Indian med. j ; 13(1): 38-53, Mar. 1964.
Artigo em Inglês | MedCarib | ID: med-10632


The use of B-thiopropionic acid for the stabilisation of the flourescence of the final solutions in the trihydroxyindole method of analysis of adrenaline and noradrenaline is described. Reliable plasma analysis with a methodological error of about ñ0.1 ng may be achieved using this thio-acid, and the Turner 111 flourometer (AU)

Epinefrina/análise , Norepinefrina/análise , Plasma/análise
J Pediatr ; 59(6): 836-47, Dec. 1961. tab, gra
Artigo em Inglês | MedCarib | ID: med-3580


Blood ketone, blood glucose and plasma NEFA concentrations after a 24 hour fast werre studied in 181 infants and children from birth to 12 years of age. The same measurements following epinephrine injections were made in 89 infants and children from birth to 14 years. It was found that infants under 36 hours were more resistant to ketosis on fasting than infants 2 to 6 days of age whose ketosis became almost as severe as that of subjects aged 1 week to 4 years. The difference in response between these two newborn groups was found to be associated with large stores of liver glycogen in the younger group. Infants under 36 hours did not appear to have any impairment of fat catabolism as indicated by a progressive rise in blood ketone levels on more extended fasts and by their normal NEFA elevation after epinephrine. Subjects 1 week to 4 years of age developed more ketosis on fasting than did older children. It was shown that this was not related to differences in excretion or utilization of ketone bodies, indicating that variation in ketone production was the factor responsible. Blood sugar levels below 40 mg. percent occurred in 45 of 123 subjects under 6 months of age who were fasted for 24 hours. With one exception, blood sugar below this level was not found in subjects over 7 months of age(AU)

Humanos , Lactente , Criança , Glicemia , Cetonas , Ácidos Graxos não Esterificados , Jejum , Epinefrina/administração & dosagem , Metabolismo Energético , Ingestão de Energia , Cetose , Desenvolvimento Infantil , Doenças do Recém-Nascido , Transtornos da Nutrição do Lactente , Glicemia/metabolismo
West Indian med. j ; 6(4): 272-84, Dec. 1957.
Artigo em Inglês | MedCarib | ID: med-12842


Since 1924 the incidence of malaria fever after operations has been investigated. These researches can be divided in two different periods, that is, from 1924 to, roughly, 1947, when malaria was endemic and hyperendemic in British Guiana, and from 1947 up to now, when the extensive anti-malarial campaign carried out by Dr. G. Giglioli has eradicated this disease completely from this colony. In the first period, out of the total of 14,027 operations, 3,445 were performed on patients who had suffered from malaria some time or another prior to operation. In 13.5 per cent of these cases, post-operative malaria fever was registered, but this percentage varied considerably when this category of patients had been subdivided in various groups according to the finding at the physical and clinical examinations, in relation to the malaria history. No cases of similar post-operative fever were registered in the 10,582 cases of operations in non-malaria subjects. During the second period of time 14,124 operations have been performed in the same class of patients as during the first period and only five cases of post-operative malarial fever have been registered, and all five in patients admitted from the Brazilian district with a typical history of recent attacks of malaria. Age, sex, race and nature of the operation did not influence the incidence of malaria, but the form of anaesthesia was of great importance. Spinal and local anaesthesia were associated with the highest incidence of post-operative malaria and particularly with attacks occurring a few hours post-operatively. It is postulated that adrenaline in the anaesthetic solution or the stress of the operation induced contraction of the spleen with the release of malaria parasites into the blood streams. (AU)

Humanos , Malária , Complicações Pós-Operatórias , Anestesia Local/efeitos adversos , Raquianestesia/efeitos adversos , Epinefrina/efeitos adversos , Guiana , Grupos Étnicos