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Biomedical subjects

E Samols

Publications and source records attributed to E Samols.

At least 55 records · Page 3Linked to original sources
PubMed1985

Role of intrapancreatic ganglia in regulation of periodic insular secretions.

The regulatory system responsible for insulin oscillations from the in vitro pancreas is unknown. To test the hypothesis that intrapancreatic ganglia are the pacemaker or driver of the oscillations, combined nicotinic, muscarinic, and adrenergic antagonists were infused. Combined muscarinic, alpha- and beta-adrenergic, and presynaptic nicotinic receptor blockade (beta-bungarotoxin) was without effect on oscillations. The infusion of the postsynaptic nicotinic receptor antagonists, hexamethonium, alpha-bungarotoxin (ATX), or curarine, significantly altered the preinfusion oscillatory pattern of insulin release by reducing the period. Nicotine-stimulated insulin release was inhibited by ATX on a background of atropine, phentolamine, and beta-bungarotoxin. Propranolol decreased nicotine-stimulated insulin release, which was further reduced by ATX. These data support the theory that nicotinic receptors may be present pre- and postsynaptically at the ganglionic level and presynaptically on sympathetic nerve axons. We propose that ganglionic nicotinic receptors may be regulatory and that ganglia may serve as the pacemaker to regulate pancreatic hormone oscillations.

Animals↗
PubMed1982

Medical x-ray exposure of the human embryo and fetus.

In a period of 2 yr. 6 pregnant women who were not aware that they were pregnant at the time of radiological examination of their abdomen and pelvis, wanted to know the radiation dose received by their embryo or fetus. Radiation dose estimate to the embryo or fetus was made by performing dosimetry with a phantom and the equipment utilized for the actual procedure. The dose to the embryo or fetus varied between less than 50 mrads and 3.52 rads when fluoroscopy was also performed. As the radioimmunoassay test now enables immediate, (same day) detection of pregnancy after day 21 of the menstrual cycle, it is reasonable to recommend that (1) the test be performed in all patients whose pregnancy status is uncertain and (2) that a positive result will ensure minimization of any necessary diagnostic radiation dose. The risk to the embryo or fetus is discussed.

Costs and Cost Analysis↗
PubMed1982

Radiation exposure in nuclear cardiovascular studies.

Nuclear cardiovascular studies are being introduced in almost every Nuclear Medicine Department. The number of studies performed per week is increasing very rapidly. The physical characteristics including the specific gamma ray constant for radionuclides used in cardiovascular studies are listed. The radiation dose estimates to different organs of a patient administered with 201Tl and 99mTc radiopharmaceuticals are shown. The radiation levels measured around patients administered with 201Tl chloride, 99mTc HSA (human serum albumin), and 99mTc-MDP (methylene diphosphonate) are within the permissible limits. Radiation doses to different organs from nuclear cardiovascular studies are less than those associated with fluoroscopy, particularly cardiac catheterization. However, the gonadal doses received from cardiac catheterization and angiocardiography are considerably lower than nuclear cardiovascular studies.

Cardiovascular Diseases↗
PubMed1982

Abolition of dopaminergic insulin secretion by beta-adrenergic antagonism.

To determine whether the insulinotropic effects of dopamine were mediated through the adrenergic system, dogs were infused with dopamine before or after various combinations of adrenergic and cholinergic blockade. Plasma glucose levels did not change significantly throughout the individual experiments, although cardiovascular effects from both blockade and dopamine infusion were demonstrated. The pronounced in vivo insulinotropic effects of dopamine were abolished by beta-adrenergic blockade with propranolol and all subsequent combinations of propranolol, phentolamine, and atropine. These results contrast with the in vitro suppression of insulin by dopamine, which is abolished by alpha-adrenergic blockade by phentolamine. Therefore, it may be concluded that the prevention of dopamine effects on insulin secretion by adrenergic antagonism is evidence that dopamine exerts its effects on the B cell directly or indirectly through the adrenergic system.

Adrenergic beta-Antagonists↗
PubMed1981

Autonomic function and control of pancreatic somatostatin.

In the canine pancreas alpha and beta adrenergic receptors exist on D cells with alpha stimulation inhibiting and beta stimulation increasing somatostatin release. There are no dopaminergic receptors on D cells. Stimulation of muscarinic receptors causes mild inhibition of somatostatin secretion. Autonomic receptors on the D cell may be physiologically stimulated in vivo via local ganglionic and/or central autonomic drivers.

Animals↗
PubMed1980

Reinterpretation of the effect of haloperidol and ethanol on insulin secretion.

We were unable to confirm the report of haloperidol induced dose-dependent inhibition of insulin and glucagon release from the isolated canine pancreas. The possibility that the inhibition was caused by ethanol, previously used as the solvent for haloperidol, was tested. Infusion of ethanol at increasing concentrations (15.8 to 252 mmol/l) caused a progressive inhibition of insulin (-17 +/- 1 to -69 +/- 2%) and glucagon (-13 +/- 3 to -67 +/- 3%) secretion, using a perfusate containing 200 mg/dl glucose and 2.65 mmol/l calcium. Haloperidol (5 to 20 mumol/l) dissolved in ethanol (252 mmol/l) did not augment the inhibitory effects of ethanol. At a low calcium concentration (1.3 mmol/l) ethanol further inhibited insulin secretion (-83 +/- 2%) with no additional inhibition by 20 mumol/l haloperidol (-80 +/- 3%). At a high calcium concentration (8.8 mmol/l) the inhibitory effect of ethanol on insulin or glucagon secretions was diminished and variable. This strongly suggests that the inhibition of insulin and glucagon secretion previously attributed to haloperidol was caused by the ethanol solvent.

Animals↗
PubMed1980

Sustained oscillations of insulin, glucagon, and somatostatin from the isolated canine pancreas during exposure to a constant glucose concentration.

Canine pancreata were perfused in vitro to examine whether hormone cycles could be demonstrated without hepatic or central nervous influence. Insulin, glucagon, and somatostatin demonstrated regular sustained cyclic secretion from the in vitro canine pancreas. Oscillations were noted for over 200 min during the infusion of a constant glucose concentration. Insulin demonstrated a 10-min period with a range of 8-12 min/cycle. Somatostatin had a 10-min period with a range of 8-11 min. Glucagon had a period of 8.6 min with range of 6-10 min. These periods do not allow glucagon to be consistently 90 degrees out of phase with insulin and somatostatin. When glucose was increased from 88 to 200 mg/dl, insulin cycles persisted but on an elevated base line, demonstrating that cycles react to glucose changes but are not dependent upon them. Cycles were disrupted by infusions of dopamine, apomorphine, epinephrine, and acetylcholine, but were reestablished. Autonomic blockade by both single and combined infusions of atropine (cholinergic), propranolol, and dibenzyline (adrenergic) had no effect on cycles. These results suggest that, in vitro, there is an intrinsic rhythm of hormone secretion by the pancreas despite a constant glucose level. The production of in vitro cycles requires the presence of a driving oscillator or pacemaker within the pancreas and the coordination of islets by pace-maker-islet communication, presumably by a non-adrenergic neural system. In vitro oscillations may Indicate that the pancreas is the driver or Zeitgeber of in vivo glucose-insulin cycles.

Animals↗
PubMed1980

Low T4 and low FT4I in seriously ill patients: concise communication.

Of 128 euthyroid hospitalized patients with nonthyroidal illnesses (NTI), 33% had a low total thyroxine (T4). Forty-three percent of the latter patients had a low free thyroxine index. In euthyroid patients with NTI, free T4 was, with rare exceptions, within the range for well euthyroid controls. The free T4, as determined by two different radioimmunoassays, was diagnostically low in 34 of 37 hypothyroid patients without NTI. However, in hypothyroid patients with NTI, the free T4 determination was less informative. Only four of ten patients had a low free T4 by the Corning test, and none of ten were low by the Clinical Assays test. Our data suggest that patients with NTI frequently have low T4 and low FT4I, despite being euthyroid. Low free T4 strongly suggests hypothyroidism, but normal free T4 in patients with NTI does not exclude hypothyroidism.

Critical Care↗
PubMed1979

Low-dose versus high-dose insulin therapy for diabetic ketoacidosis.

The effects of low-dose continuous insulin therapy were compared to those of high-dose subcutaneous and intravenous insulin therapy in six episodes of diabetic ketoacidosis. Time for correction of acidosis, ketosis, and hyperglycemia were similar for both regimens. The high-dose method required more exogenous glucose and supplemental potassium to avoid hypoglycemia and/or hypokalemia during treatment. Levels of cortisol, human growth hormone, and glucagon, initially elevated in most patients, showed a progressive decline with both modes of therapy. Plasma insulin remained remarkably stable during both treatment regimens, but remained within the physiologic range only in patients receiving low-dose therapy. Our study suggest that either modality is effective in the treatment of diabetic ketoacidosis.

Adult↗
PubMed1979

Adrenergic modulation of pancreatic A, B, and D cells alpha-Adrenergic suppression and beta-adrenergic stimulation of somatostatin secretion, alpha-adrenergic stimulation of glucagon secretion in the perfused dog pancreas.

The effects of adrenergic substances on pancreatic insular secretions were studied in a completely isolated canine pancreas with exclusion of the duodenum from the perfusion circuit. To ensure adequate blockade, blockers were infused before agonists. A dose range of beta-receptor blockade was tested, and putative alpha-adrenergic effects were confirmed by combined alpha- and beta-adrenergic receptor blockade.beta-Adrenergic agonism (2 ng/ml isoproterenol) induced a mean integrated increase of 79+/-20% in somatostatin secretion, whereas glucagon and insulin secretion were increased by 185+/-45 and 495+/-146%, respectively. The stimulations of D, A, and B cells were abolished by propranolol.alpha-Adrenergic agonism (10 ng/ml epinephrine) after beta-adrenergic blockade) moderately decreased somatostatin (-37+/-7%) secretion, moderately increased glucagon (91+/-19%), and markedly decreased insulin (-85+/-3%) release. Similar effects on D-, A-, and B-cell secretion were induced with 2 ng/ml epinephrine or 10 ng/ml norepinephrine after beta-adrenergic blockade. The alpha-adrenergic effects on the D and A cell were abolished by either phentolamine or by phenoxybenzamine. This study showed that there are indeed alpha-adrenergic receptors on A cells and that the secretion of glucagon, a "stress" hormone, was stimulated either by alpha- or beta-adrenergic receptor agonism. D-cell secretion, like that of the B cell, was inhibited by alpha-adrenergic agonism and was stimulated by beta-adrenergic agonism. However, beta-adrenergic-induced changes in D-cell secretion were smaller in magnitude than those of B-cell secretion.

Adrenergic alpha-Agonists↗
PubMed1979

Somatostatin and pancreatic polypeptide secretion: effects of glucagon, insulin, and arginine.

The isolated perfused canine pancreas with duodenal exclusion was used to examine islet hormone output in response to arginine and exogenous glucagon and insulin. Exogenous glucagon (100 ng/ml) stimulated insulin and somatostatin secretion, which occurred in a biphasic pattern. The insulin response to glucagon was markedly enhanced by increased perfusate glucose, unlike the somatostatin response, which was little affected. The insulin and somatostatin responses were seen between 15 and 45 s after the glucagon stimulus. Pancreatic polypeptide secretion was uninfluenced by exogenous glucagon. Biphasic release of glucagon, somatostatin, and pancreatic polypeptide was evoked by 10 mM arginine, the responses first being apparent within less than 30 s. Exogenous insulin (50 mU/ml) infused for 10 min had no statistically significant effect on glucagon, somatostatin, or pancreatic polypeptide secretion. This study suggests that these four islet hormones may all be involved in the dynamic mechanisms of nutrient metabolism. In addition, potential intra-islet paracrine effects are identified.

Animals↗
PubMed1978

Automated data processing and radioassays.

Radioassays include (1) radioimmunoassays, (2) competitive protein-binding assays based on competition for limited antibody or specific binding protein, (3) immunoradiometric assay, based on competition for excess labeled antibody, and (4) radioreceptor assays. Most mathematical models describing the relationship between labeled ligand binding and unlabeled ligand concentration have been based on the law of mass action or the isotope dilution principle. These models provide useful data reduction programs, but are theoretically unfactory because competitive radioassay usually is not based on classical dilution principles, labeled and unlabeled ligand do not have to be identical, antibodies (or receptors) are frequently heterogenous, equilibrium usually is not reached, and there is probably steric and cooperative influence on binding. An alternative, more flexible mathematical model based on the probability or binding collisions being restricted by the surface area of reactive divalent sites on antibody and on univalent antigen has been derived. Application of these models to automated data reduction allows standard curves to be fitted by a mathematical expression, and unknown values are calculated from binding data. The vitrues and pitfalls are presented of point-to-point data reduction, linear transformations, and curvilinear fitting approaches. A third-order polynomial using the square root of concentration closely approximates the mathematical model based on probability, and in our experience this method provides the most acceptable results with all varieties of radioassays. With this curvilinear system, linear point connection should be used between the zero standard and the beginning of significant dose response, and also towards saturation. The importance is stressed of limiting the range of reported automated assay results to that portion of the standard curve that delivers optimal sensitivity. Published methods for automated data reduction of Scatchard plots for radioreceptor assay are limited by calculation of a single mean K value. The quality of the input data is generally the limiting factor in achieving good precision with automated as it is with manual data reduction. The major advantages of computerized curve fitting include: (1) handling large amounts of data rapidly and without computational error; (2) providing useful quality-control data; (3) indicating within-batch variance of the test results; (4) providing ongoing quality-control charts and between assay variance.

Electronic Data Processing↗
PubMed1978

Management of chlorpropamide-induced hypoglycemia with diazoxide.

Diazoxide, as demonstrated by the case we present, may be of substantial value in abolishing hypoglycemia and in preventing its recurrence. The mainstay of treatment for the patient with chlorpropamide toxicity is the constant close monitoring of clinical and laboratory parameters and the correction of hypoglycemia by administration of exogenous glucose when necessary. However, the need for exogenous glucose is reduced with the concomitant use of diazoxide. We therefore suggest that diazoxide should be considered as a part of the routine treatment of sulfonylurea-induced hypoglycemia.

Aged↗
PubMed1977

Hyperkalemia due to selective hypoaldosteronism.

Hyperkalemia secondary to hyporeninemic hypoaldosteronism with a normal glucocorticoid function was diagnosed in a 47-year-old man with moderate renal insufficiency. Mineralocorticoid administration corrected the hyperkalemia. A probable explanation for hyporeninemia and hypoaldosteronism in this syndrome is that the primary defect is an inability to release renin and the resultant angiotensin deficiency leads to an aldosterone deficiency.

Acidosis↗