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Biomedical subjects

D E Potter

Publications and source records attributed to D E Potter.

At least 91 records · Page 5Linked to original sources
PubMed1980

Treatment of end-stage renal disease in children: a 15-year experience.

From 1964-1979, 154 children 1 to 16 years of age with end-stage renal disease (ESRD) were treated in a regional pediatric dialysis and transplant program. The incidence of ESRD was 1.6 per million total population per year. The survival rate of children undergoing dialysis for an average of 10 months was 93%. After living donor kidney transplantation (LD), patients survival rates in 60 children were 89% at 5 years, 83% at 10 years, and 74% at 15 years. After cadaver donor kidney transplantation (CD), patient survival rates in 85 children were 70% at 5 and 10 years. LD kidney survival was 71% at 5 years, 55% at 10 years, and 40% at 15 years, whereas CD kidney survival was 43% at 5 years and 31% at 10 years. The survival of first and second transplants was similar. Patient and kidney survival have improved since 1972. The survival rate of 26 children 1 to 5 years of age was 46%, but patients with Wilms' tumor accounted for most of the deaths. We attribute these favorable long-term results in children to an integrated program of dialysis and transplantation with special pediatric facilities.

Adolescent↗
PubMed1980

Comparative metabolic and cardiovascular effects of carbuterol, isoproterenol, metaproterenol and salbutamol in the baboon.

The metabolic and cardiovascular responses to two bronchiolar selective beta-adrenergic drugs, carbuterol (CAR) and salbutamol (SAL), were compared with isoproterenol (ISO) and metaproterenol (MET) in fasted, anesthetized baboons. ISO was more active than the selective beta-adrenergic drugs in elevating plasma levels of glucose, lactate, free fatty acids, insulin, and glucagon. Moreover, ISO was more active in increasing heart rate and respiratory rate and in depressing diastolic blood pressure. Although ISO was shown to have greater activity than CAR, MET, and SAL, the bronchiolar selective drugs (CAR and SAL) did produce significant changes in plasma levels of metabolic substrates and pancreatic hormones and in cardiovascular measurements at higher dose rates.

Adrenergic beta-Agonists↗
PubMed1980

Catecholamine-induced hyperglycemia in dogs: independence from alterations in pancreatic hormone release.

Although isoproterenol is a very effective hyperglycemic agent in dogs, other species such as rats, baboons and man are resistant to this effect. In each of these species catecholamines exert pronounced effects on insulin and glucagon release from the pancreas. In man, baboons, and rats catecholamine-induced alterations in pancreatic hormone release indirectly influence the hyperglycemic response to these amines: glucagon release supports and insulin release limits hyperglycemic responses. In contrast, the present study demonstrates that in dogs catecholamine-induced hyperglycemic responses are relatively independent of concurrent alterations in pancreatic hormone release. In dogs isoproterenol produces hyperglycemia equal to or greater than responses to epinephrine despite large increases in insulin release produced by isoproterenol. Moreover, catecholamine-induced hyperglycemia is not significantly altered when insulin and glucagon release are blocked with somatostatin.

Animals↗
PubMed1980

Acute pretreatment with pyrazole and ethanol: effects on glucose-induced changes in insulin and glucagon.

Ethanol suppressed, in a dose-related manner, glucose-induced insulin (IRI) release and thus delayed the disappearance of glucose from the blood of rats. Pretreatment with pyrazole, an alcohol dehydrogenase inhibitor, exacerbated the effect of ethanol on IRI release, glucose tolerance and glucagon (IRG) release. These results suggest that ethanol produces glucose intolerance by inhibiting glucose-induced IRI release and by augmenting IRG release. Moreover, these findings indicate that ethanol does not have to be metabolized completely in order to produce these effects.

Animals↗
PubMed1980

Effect of ethanol on basal and arginine-stimulated plasma levels of glucose, insulin and glucagon in fasted unanesthetized rabbits.

Plasma glucose, insulin (IRI) and glucagon (IRG) levels were determined in fasting unanesthetized rabbits following pretreatment of either saline or ethanol (1.5 g/kg p.o.) and i.v. infusion of either saline or arginine (10 mg/kg/min for 30 min). Ethanol lowered plasma glucose and IRI levels but raised IRG levels in rabbits infused with saline. Arginine-induced hyperglycemia and hyperinsulinemia were markedly suppressed by ethanol so that any further increase expected by the infusion of arginine was minimized. Thus, ethanol not only alters basal levels of IRI, IRG and glucose but also suppresses arginine-stimulated levels as well.

Animals↗
PubMed1979

Effects of adrenergic drugs on aqueous cAMP and cGMP and intraocular pressure.

The following variously selective adrenergic agonists were tested for their effects on the concentration of adenosine 3',5' cyclic monophosphate and guanosine 3',5- cyclic monophosphate in the aqueous humor of treated and fellow eyes of rabbits one hour after topical unilateral application (2 mg, base): Epinephrine (alpha, beta 1.beta 2), phenylephrine alpha), isoproterenol (beta 1, beta 2), tazolol (beta 1) and terbutaline (beta 2). All drugs produced a significant increase in cAMP in the treated eyes and all but terbutaline produced a significant increase in the fellow eye. Terbutaline alone caused an increased in cGMP although a similar dose of pilocarpine, a cholinergic agonist, was ineffective in changing cGMP levels. We conclude that (1) diverse adrenoceptor stimulation can increase cAMP, but (2) not necessarily in direct relation to an agent's hypotension induced by pilocarpine is not accompanied by an increase in aqueous cGMP.

Administration, Topical↗
PubMed1979

Effect of beta-adrenergic drugs on plasma glucose and glucagon in Japanese quail: a preliminary report.

The present study was conducted to determine the effects of beta-adrenergic stimulation on plasma glucose and glucagon (IRG) levels in Japanese quail. Isoproterenol, epinephrine and three relatively selective beta-adrenoceptor agonists (terbutaline, salbutamol and reproterol) produced dose-related hyperglycemia and hypoglucagonemia. This study demonstrates that beta-adrenoceptor agonists produce hyperglycemia in birds as they do in mammals, but that the rise in plasma glucose in birds, unlike mammals, is accompanied by a profound fall in plasma IRG levels.

Adrenergic beta-Agonists↗
PubMed1979

The influence of endogenous glucagon release on hyperglycemic responses to catecholamines in normal fed and diabetic rats.

The present study provides evidence that changes in glucagon secretion are influential in determining the hyperglycemic activity of catecholamines in normal and diabetic rats. In normal fed rats, epinephrine (EPI) stimulated large increments in glucagon release and inhibited insulin secretion. In contrast, the modest hyperglycemic activity of isoproterenol (ISO) in normal fed rats correlated with its weak glucagon-releasing activity and its strong insulin-releasing activity. In alloxan-diabetic rats, the augmented hyperglycemic response to ISO was accompanied by larger increments in plasma glucagon levels than the catecholamine produced in normal fed rats. When glucagon release was inhibited by a concurrent infusion of somatostatin, the hyperglycemic responses of normal fed rats to EPI were reduced by approximately 67%. ISO-induced hyperglycemia in alloxan-diabetic rats was even more sensitive to inhibition by somatostatin since this response was reduced by approximately 90% when glucagon release was inhibited by somatostatin. These findings indicate that more than half of the hyperglycemic response to EPI in normal fed rats and nearly all of the hyperglycemia produced by ISO in diabetic rats result from increased glucagon release. Moreover, the impotence of ISO as a hyperglycemic agent in normal fed rats is probably due to insulin release which tends to suppress glucagon release.

Animals↗
PubMed1979

Alterations in arginine-induced pancreatic hormone release: influence of acute and chronic exposure to ethanol.

Acute oral administration of ethanol (150 and 750 mg/100g) to fasted rats produced dose-related inhibition of arginine-induced insulin (IRI) release, an elevation of plasma glucagon (IRG) levels and minor effects on blood glucose. In contrast, chronic consumption of ethanol for 10 weeks augmented arginine-induced hyperglycemia and hperinsulinemia. Thus, acute ethanol administration decreased plasma IRI levels at both doses, presumably by suppressing beta cell function; whereas, function of the alpha cell and plasma IRG levels were increased, but only by the high dose of ethanol. In these experiments the effects exerted by ethanol on the pancreatic endocrine responses to arginine infusion varied according to: dose of ethanol administered; duration of exposure to ethanol; and state of nourishment of the subjects.

Animals↗
PubMed1978

Avascular necrosis of bone after renal transplantation.

Avascular necrosis (AN) of bone developed in 11 of 100 children who received renal transplants from 1964 to 1977. Bones involved were femoral heads, 14; femoral condyles, 12; tall, two; and carpal naviculars, two. Seven children with symptomatic AN of the femoral heads were treated with limited weight bearing; three subsequently required arthroplasty, and degenerative joint disease developed in one. The AN at other joints healed clinically but not roentgenographically. Although the prevalence of AN decreased after 1967 coincident with a decrease in prednisone dose, children with AN received the same cumulative prednisone dose as children in a control group. Serum phosphorus levels were different in the AN and control groups, but other indexes of hyperparathyroidism were similar. The relative contributions of prednisone therapy and hyperparathyroidism to the development of AN could not be delineated.

Adolescent↗
PubMed1978

Statural growth of children with renal disease.

Growth retardation occurs in 35 to 65% of children with kidney disease. It is especially common in children with congenital diseases of the kidney, anomalies, and inherited disorders. Acquired disease, however, also may impair growth, particularly where renal function (GFR) is below 25 ml/min/1.73 m2. Therapy used in renal disease, notably prednisone, also impairs growth. Chronic dialysis therapy, both hemodialysis and peritoneal, are associated with poor growth. Several specific changes in renal disease are associated with growth failure. These include, in addition to azotemia, acidosis, hyposthenuria, renal osteodystrophy, endocrine disorders and resistance to hormone action, and nutritional disturbances.

Body Height↗
PubMed1978

Measurement of growth in children with renal insufficiency.

The serial measurement of stature, weight, skin-fold thickness, mean arm circumference, skeletal maturity, and where appropriate, stage of sexual development are recommended as suitable indices for assessing growth in children with kidney disease. Methods of expressing the data for evaluating the individual child are generally used methods. Emphasis is given to relating stature to bone age in evaluating growth potential. Methods for comparing growth rates in groups of children are less well-developed. Using standard deviation scores is recommended for comparing stature in two groups of children or in the same child observed at the end of two different regimens. Weight using ideal weight-for-height as reference from a group of children can be treated statistically. Data of skinfold thickness and arm circumference from two groups can be handled statistically only when the groups are comparable in age and sex.

Anthropometry↗
PubMed1978

Catecholamine-induced changes in plasma glucose, glucagon and insulin in rabbits: effects of somatostatin.

The present study was conducted to determine if glucagon release is involved in the hyperglycemic response to epinephrine and isoproterenol in the fasted and fed, unanesthetized rabbit. Epinephrine produced dose-related increases in plasma glucose and glucagon levels in fed and fasted rabbits whereas isoprotereol produced modest hyperglycemia without hyperglucagonemia. Infusion of somatostatin suppressed epinephrine-induced glucagon release and this was correlated with a 50% reduction in the hyperglycemic response. These data suggest that epinephrine-induced glucagon release is the primary reason for the difference in hyperglycemic activity between epinephrine and isoproterenol in the unanesthetized rabbit.

Animals↗
PubMed1978

Role of glucagon in the hyperglycemic response to catecholamines in fasted baboons.

The hyperglycemic activities of epinephrine (EPI) and isoproterenol (ISO) in baboons correlated with their ability to increase plasma glucagon (IRG) levels relative to insulin (IRI). EPI inhibited IRI release and produced greater increases in plasma glucose and IRG than did ISO. ISO increased plasma IRI levels more than IRG. Infusion of somatostatin blocked IRG release and inhibited hyperglycemic responses to EPI by approximately 50%. These findings indicate that, as in man, IRG release contributes significantly to the hyperglycemic effects of catecholamines in baboons. The baboon thus appears to be a suitable model for predicting effects of drugs on glucose homeostasis in humans.

Animals↗