Chlorpropamide: A sulfonylurea hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. (From Martindale, The Extra Pharmacopoeia, 30th ed, p277)Flushing: A transient reddening of the face that may be due to fever, certain drugs, exertion, stress, or a disease process.Demeclocycline: A TETRACYCLINE analog having a 7-chloro and a 6-methyl. Because it is excreted more slowly than TETRACYCLINE, it maintains effective blood levels for longer periods of time.Suppositories: Medicated dosage forms that are designed to be inserted into the rectal, vaginal, or urethral orifice of the body for absorption. Generally, the active ingredients are packaged in dosage forms containing fatty bases such as cocoa butter, hydrogenated oil, or glycerogelatin that are solid at room temperature but melt or dissolve at body temperature.Chlorothiazide: A thiazide diuretic with actions and uses similar to those of HYDROCHLOROTHIAZIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p812)Diabetes Insipidus: A disease that is characterized by frequent urination, excretion of large amounts of dilute URINE, and excessive THIRST. Etiologies of diabetes insipidus include deficiency of antidiuretic hormone (also known as ADH or VASOPRESSIN) secreted by the NEUROHYPOPHYSIS, impaired KIDNEY response to ADH, and impaired hypothalamic regulation of thirst.Erythema: Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of causes.Tolbutamide: A sulphonylurea hypoglycemic agent with actions and uses similar to those of CHLORPROPAMIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p290)Blood Glucose: Glucose in blood.Sulfonylurea CompoundsElectronic Mail: Messages between computer users via COMPUTER COMMUNICATION NETWORKS. This feature duplicates most of the features of paper mail, such as forwarding, multiple copies, and attachments of images and other file types, but with a speed advantage. The term also refers to an individual message sent in this way.Diabetes Mellitus, Type 1: A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence.Food Dispensers, Automatic: Mechanical food dispensing machines.Diabetes Mellitus: A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.Diabetes Mellitus, Type 2: A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.Postal Service: The functions and activities carried out by the U.S. Postal Service, foreign postal services, and private postal services such as Federal Express.Internet: A loose confederation of computer communication networks around the world. The networks that make up the Internet are connected through several backbone networks. The Internet grew out of the US Government ARPAnet project and was designed to facilitate information exchange.Insulin: A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).Hypoglycemic Agents: Substances which lower blood glucose levels.Glucose: A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.Hypoglycemia: A syndrome of abnormally low BLOOD GLUCOSE level. Clinical hypoglycemia has diverse etiologies. Severe hypoglycemia eventually lead to glucose deprivation of the CENTRAL NERVOUS SYSTEM resulting in HUNGER; SWEATING; PARESTHESIA; impaired mental function; SEIZURES; COMA; and even DEATH.Ultraviolet Rays: That portion of the electromagnetic spectrum immediately below the visible range and extending into the x-ray frequencies. The longer wavelengths (near-UV or biotic or vital rays) are necessary for the endogenous synthesis of vitamin D and are also called antirachitic rays; the shorter, ionizing wavelengths (far-UV or abiotic or extravital rays) are viricidal, bactericidal, mutagenic, and carcinogenic and are used as disinfectants.DNA Repair: The reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule which contained damaged regions. The major repair mechanisms are excision repair, in which defective regions in one strand are excised and resynthesized using the complementary base pairing information in the intact strand; photoreactivation repair, in which the lethal and mutagenic effects of ultraviolet light are eliminated; and post-replication repair, in which the primary lesions are not repaired, but the gaps in one daughter duplex are filled in by incorporation of portions of the other (undamaged) daughter duplex. Excision repair and post-replication repair are sometimes referred to as "dark repair" because they do not require light.Centrifugation, Isopycnic: A technique used to separate particles according to their densities in a continuous density gradient. The sample is usually mixed with a solution of known gradient materials and subjected to centrifugation. Each particle sediments to the position at which the gradient density is equal to its own. The range of the density gradient is usually greater than that of the sample particles. It is used in purifying biological materials such as proteins, nucleic acids, organelles, and cell types.Cricetinae: A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.DNA Damage: Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS.CHO Cells: CELL LINE derived from the ovary of the Chinese hamster, Cricetulus griseus (CRICETULUS). The species is a favorite for cytogenetic studies because of its small chromosome number. The cell line has provided model systems for the study of genetic alterations in cultured mammalian cells.Unconsciousness: Loss of the ability to maintain awareness of self and environment combined with markedly reduced responsiveness to environmental stimuli. (From Adams et al., Principles of Neurology, 6th ed, pp344-5)Tablets: Solid dosage forms, of varying weight, size, and shape, which may be molded or compressed, and which contain a medicinal substance in pure or diluted form. (Dorland, 28th ed)Candy: Sweet food products combining cane or beet sugars with other carbohydrates and chocolate, milk, eggs, and various flavorings. In the United States, candy refers to both sugar- and cocoa-based confections and is differentiated from sweetened baked goods; elsewhere the terms sugar confectionary, chocolate confectionary, and flour confectionary (meaning goods such as cakes and pastries) are used.Patient Acceptance of Health Care: The seeking and acceptance by patients of health service.Agropyron: A plant genus of the family POACEAE. The common name of wheatgrass is also used for other plants in the family.Nesidioblastosis: An inherited autosomal recessive syndrome characterized by the disorganized formation of new islets in the PANCREAS and CONGENITAL HYPERINSULINISM. It is due to focal hyperplasia of pancreatic ISLET CELLS budding off from the ductal structures and forming new islets of Langerhans. Mutations in the islet cells involve the potassium channel gene KCNJ11 or the ATP-binding cassette transporter gene ABCC8, both on CHROMOSOME 11.Pathology, Clinical: A subspecialty of pathology applied to the solution of clinical problems, especially the use of laboratory methods in clinical diagnosis. (Dorland, 28th ed.)Pancreatic Diseases: Pathological processes of the PANCREAS.Hyperinsulinism: A syndrome with excessively high INSULIN levels in the BLOOD. It may cause HYPOGLYCEMIA. Etiology of hyperinsulinism varies, including hypersecretion of a beta cell tumor (INSULINOMA); autoantibodies against insulin (INSULIN ANTIBODIES); defective insulin receptor (INSULIN RESISTANCE); or overuse of exogenous insulin or HYPOGLYCEMIC AGENTS.Pancreatectomy: Surgical removal of the pancreas. (Dorland, 28th ed)Poison Control Centers: Facilities which provide information concerning poisons and treatment of poisoning in emergencies.Poisoning: A condition or physical state produced by the ingestion, injection, inhalation of or exposure to a deleterious agent.Information Centers: Facilities for collecting and organizing information. They may be specialized by subject field, type of source material, persons served, location, or type of services.Gas PoisoningNational Health Planning Information Center (U.S.): A center in the HEALTH RESOURCES ADMINISTRATION Division of Planning Methods and Technology which provides access to current information on health planning and resources development.Poisons: Substances which, when ingested, inhaled, or absorbed, or when applied to, injected into, or developed within the body in relatively small amounts may, by their chemical action, cause damage to structure or disturbance of function. (From Dorland, 27th ed)

X-ray structure of the FimC-FimH chaperone-adhesin complex from uropathogenic Escherichia coli. (1/73)

Type 1 pili-adhesive fibers expressed in most members of the Enterobacteriaceae family-mediate binding to mannose receptors on host cells through the FimH adhesin. Pilus biogenesis proceeds by way of the chaperone/usher pathway. The x-ray structure of the FimC-FimH chaperone-adhesin complex from uropathogenic Escherichia coli at 2.5 angstrom resolution reveals the basis for carbohydrate recognition and for pilus assembly. The carboxyl-terminal pilin domain of FimH has an immunoglobulin-like fold, except that the seventh strand is missing, leaving part of the hydrophobic core exposed. A donor strand complementation mechanism in which the chaperone donates a strand to complete the pilin domain explains the basis for both chaperone function and pilus biogenesis.  (+info)

A systematic review of drug induced ocular reactions in diabetes. (2/73)

AIMS: To conduct a systematic review of drug induced adverse ocular effects in diabetes to determine if this approach identified any previously unrecognised adverse drug effects; to make a preliminary assessment of the feasibility of this approach in identifying adverse drug reactions; and to assess the current accessibility of this information to prescribing physicians. METHODS: Literature search of online biomedical databases. The search strategy linked eye disorders with adverse drug reactions and diabetes. Source journals were classified as medical, pharmaceutical, diabetes related, or ophthalmological. It was determined whether the reactions identified were recorded in drug datasheets and the British National Formulary. RESULTS: 63 references fulfilled the selection criteria, of which 45 were considered to be relevant to the study. The majority of these were case reports but cross sectional surveys, case-control and cohort studies, and review articles were also identified. 61% of the reactions were not recorded in the British National Formulary and 41% were not recorded in the datasheets. 55% appeared in specialist ophthalmology journals. CONCLUSIONS: This is a feasible approach to the identification of adverse drug reactions. Adverse reactions not listed in the most commonly used reference sources were found. The majority were published in specialist ophthalmology journals which might not be seen by prescribing physicians.  (+info)

Chlorpropamide upregulates antidiuretic hormone receptors and unmasks constitutive receptor signaling. (3/73)

The mechanism by which chlorpropamide (CP) treatment promotes antidiuresis is unknown. CP competitively inhibited antidiuretic hormone (ADH) binding and adenylyl cyclase (AC) stimulation (inhibition constants K(i) and K'(i) of 2.8 mM and 250 microM, respectively) in the LLC-PK(1) cell line. CP (333 microM) increased the apparent K(a) of ADH for AC activation (0.31 vs. 0.08 nM) without affecting a maximal response, suggesting competitive antagonism. Because CP lowers "basal" AC activity and the AC activation-ADH receptor occupancy relationship (A-O plots), it is an ADH inverse agonist. Twenty-four-hour CP exposure (100 microM) upregulated the ADH receptors without affecting affinity. This lowered K(a) and increased basal AC activity and maximal response (1. 86 vs. 1.35 and 14.9 vs. 10.6 fmol cAMP. min(-1). 10(3) cells(-1), n = 6, P<0.05). NaCl, which potentiates ADH stimulation, also increased basal AC activity. This, together with the CP-ADH inverse agonism and increased basal AC activity at higher receptor density, unmasks constitutive receptor signaling. The CP-ADH inverse agonism explains receptor upregulation and predicts the need for residual ADH with functional isoreceptors for CP-mediated antidiuresis. This could be why CP ameliorates partial central diabetes insipidus but not nephrogenic diabetes insipidus.  (+info)

Inhibition of CFU-E/BFU-E by 3'-azido-3'-deoxythymidine, chlorpropamide, and protoporphirin IX zinc (II): a comparison between direct exposure of progenitor cells and long-term exposure of bone marrow cultures. (4/73)

Erythropoiesis occurs in two stages: proliferation amplifies cell number, and differentiation stimulates the acquisition of the functional properties of red blood cells. The erythroid colony-forming unit (CFU-E) amplifies the differentiation process in response to erythropoietic stress in vitro, whereas the burst-forming unit (BFU-E), which is not particularly sensitive to erythropoietin stimulation, gives rise to the CFU-E and, when stimulated, produces morphologically-identifiable erythroid colonies. The aim of this work was to evaluate the toxic effects of the antiviral agent, 3'-azido-3'-deoxythymidine (AZT), the antidiabetic drug, chlorpropamide (CLP), and the heme-analogous compound, protophorphirin IX zinc (II) (ZnPP), on the proliferation of erythroblastic progenitors by using human umbilical-cord blood cells and murine progenitors from long-term bone marrow cultures. All these agents may interfere with the hemopoietic process, causing myelotoxicity as an adverse effect via different mechanisms. Our results showed selective toxicity of the three drugs on the erythroid progenitors (IC(50): AZT 0.35 +/- 0.13 microM, ZnPP 23.34 +/- 1.16 microM, CLP 1.07 +/- 0.27 mM), with respect to the myeloid progenitors (IC(50): AZT 0.8 microM, ZnPP 103.9 +/- 3.9 microM and CLP > 2800 microM). The IC(50) values were well correlated with peak plasma levels reached in vivo by the drugs. There was a marked similarity between the drug sensitivities of the human and murine progenitors but differences in toxicity exerted by the drugs on the basis of the time of exposure. Drug treatment of long-term cultures, followed by the clonogenic assay of progenitors collected from them in the absence of the drugs, generally resulted in a lower hematotoxicity.  (+info)

Investigation of hypoglycemic properties of rectal suppositories with chlorpropamide. (5/73)

Rectal suppositories with chlorpropamide and suppositories with chlorpropamide in the dispersion system with urea were prepared. Witepsol H15 and H19 and a polyoxyethyleneglycol mixture were used as bases. Rabbits were tested for blood-glucose level. The animals have been administered with prepared suppositories and commercial tablets. It was found that the suppositories prepared on the basis Witepsol H 15 with the dispersed chlorpropamide caused a much higher decrease of blood-glucose level than commercial tablets.  (+info)

Crystal doping aided by rapid expansion of supercritical solutions. (6/73)

The purpose of this study was to test the utility of rapid expansion of supercritical solution (RESS) based cocrystallizations in inducing polymorph conversion and crystal disruption of chlorpropamide (CPD). CPD crystals were recrystallized by the RESS process utilizing supercritical carbon dioxide as the solvent. The supercritical region investigated for solute extraction ranged from 45 to 100 degrees C and 2000 to 8000 psi. While pure solute recrystallization formed stage I of these studies, stage II involved recrystallization of CPD in the presence of urea (model impurity). The composition, morphology, and crystallinity of the particles thus produced were characterized utilizing techniques such as microscopy, thermal analysis, x-ray powder diffractometry, and high-performance liquid chromatography. Also, comparative evaluation between RESS and evaporative crystallization from liquid solvents was performed. RESS recrystallizations of commercially available CPD (form A) resulted in polymorph conversion to metastable forms C and V, depending on the temperature and pressure of the recrystallizing solvent. Cocrystallization studies revealed the formation of eutectic mixtures and solid solutions of CPD + urea. Formation of the solid solutions resulted in the crystal disruption of CPD and subsequent amorphous conversion at urea levels higher than 40% wt/wt. Consistent with these results were the reductions in melting point (up to 9 degrees C) and in the DeltaH(f) values of CPD (up to 50%). Scanning electron microscopy revealed a particle size reduction of up to an order of magnitude upon RESS processing. Unlike RESS, recrystallizations from liquid organic solvents lacked the ability to affect polymorphic conversions. Also, the incorporation of urea into the lattice of CPD was found to be inadequate. In providing the ability to control both the particle and crystal morphologies of active pharmaceutical ingredients, RESS proved potentially advantageous to crystal engineering. Rapid crystallization kinetics were found vital in making RESS-based doping superior to conventional solvent-based cocrystallizations.  (+info)

Effect of sulfonylureas on triglyceride metabolism in the rat liver: possible role of the lysosomes in hepatic lipolysis. (7/73)

It has been suggested previously that chlorpropamide and other hypoglycemic sulfonylureas interfere with hepatic triglyceride breakdown. Since ketogenesis from endogenous hepatic lipid stores is a measure of hepatic triglyceride hydrolysis, ketogenesis derived from endogenous lipids as well as ketogenesis derived from exogenously added isotopic oleate was determined in isolated hepatocytes from fasted rats in an attempt to identify the nature of the direct effects of sulfonylureas on hepatic lipid metabolism. Ketogenesis from endogenous lipids was inhibited by 1 mM chlorpropamide, while ketone production from exogenous oleate did not change. The effect of chlorpropamide on hepatic triglyceride metabolism was further studied in the isolated perfused liver of normal rats in the presence of a continuous [3H]oleate infusion and in isolated liver cells incubated in the presence of [3H]oleate. In liver perfusion experiments, 1 mM chlorpropamide enhanced the incorporation of tritium into triglycerides (but not other lipid classes) and increased both liver triglyceride content and triglyceride secretion. Using isolated cells similar effects could be demonstrated at 0.5 mM chlorpropamide. Chlorpropamide, tolbutamide, and carbutamide, all of which inhibited endogenous ketogenesis in isolated liver cells, also inhibited lysosomal triglyceride lipase activity in rat liver homogenates. The drugs were not inhibitory towards alkaline lipase activity. Demethylglycodiazin (2-benzolsulfonamid--5-(beta-hydroxyethoxy)-pyrimidin), which did not inhibit endogenous ketogenesis in isolated liver cells, did not affect lysosomal lipase activity. The lysosomotropic drug chloroquine was markedly antiketogenic when tested in liver cells. The reduction in endogenous ketogenesis, the enhanced accumulation of liver triglycerides, and the stimulation of hepatic triglyceride output by chlorpropamide are ascribed to an interference of the drug with hepatic triglyceride breakdown. The present results also suggest that the lysosomes play a significant role in hepatic lipolysis.  (+info)

A drug-specific leuco-agglutinin in a fatal case of agranulocytosis due to chlorpromazine. (8/73)

A fatal case of agranulocytosis due to chlorpromazine is reported. Mechanisms other than immunological are generally believed to be responsible for chlorpromazine-induced agranulocytosis. However, the demonstration of a drug-specific leuco-agglutinin in the serum of this patient suggests that an immunological mechanism was responsible for the agranulocytosis.  (+info)

  • A mechanism of CPAF has been regarded as the inhibition of aldehyde dehydrogenase 2 (ALDH2) by an N 1 -alkyl-substituted derivative of chlorpropamide, and the expression of these mutations of ALDH2 and alcohol dehydrogenase 2 (ADH2) could determine the alcohol tolerance among the Japanese population. (
  • Chlorpropamide is a first line option for treating type 2 diabetes in people who are not overweight, or who cannot take metformin. (
  • High performance affinity chromatography and affinity microcolumns containing immobilized HSA were used to investigate binding by the sulfonylurea drug chlorpropamide to normal HSA and glycated HSA, which is a modified form of HSA that has an increased serum concentration in diabetes. (
  • Experiments employing frontal analysis indicated that the binding by chlorpropamide gave a good fit to a two-site model for both normal HSA and glycated HSA samples that were representative of controlled or advanced diabetes. (
  • These results suggest that chlorpropamide inhibition of repair processes may potentiate the effects of known mutagenic hazards and may also be responsible for the increased incidence of chromosome aberrations in patients treated with the drug. (
  • Chlorpropamide gave a larger 1.4- to over 1.5-fold increase at Sudlow site II when the affinity of this drug was compared between normal HSA and the same samples of glycated HSA. (
  • Chlorpropamide, an oral hypoglycemic agent, was tested for effects on excision repair and postreplication repair of ultraviolet (UV) damage of DNA in CHO-K1 cells. (
  • Chlorpropamide is not recommended for the treatment of NIDDM as it increases blood pressure and the risk of retinopathy (UKPDS-33). (
  • Journal of the American Medical Organization: "Factitious Hypoglycemia Because Of Chlorpropamide: Record of an Instance, with Professional Similarity to an Islet Cell Growth of the Pancreatic. (
  • pfizer inc. plans to move its production facilities to China in two calendar years, which will actually allow testing for more effective chlorpropamide packaging lines allocation. (
  • The affinity of chlorpropamide at Sudlow site I had a small increase of up to 1.2-fold when comparing the normal HSA and glycated HSA samples. (
  • Diabinese (chlorpropamide) is a less commonly used medicine for lowering blood sugar, but it can cause low blood sugar levels so always carry some form of sugar with you that can be readily used. (
  • Diabinese (chlorpropamide) is effective at controlling blood sugar and A1c levels.It is an oral medicine and a good alternative for those who don't like injections. (
  • Diabinese (chlorpropamide) is available as a cheaper, generic form. (
  • Diabinese (chlorpropamide) can cause blood sugar levels to be low. (
  • While taking Diabinese (chlorpropamide), your blood sugars should be checked regularly. (
  • Diabinese (chlorpropamide) can lose its effectiveness over time. (
  • Diabinese (chlorpropamide) stimulates your body to release more insulin, which lowers the amount of sugar in your blood and reduces damage to vital organs. (
  • Medicines that lower blood sugar similarly to Diabinese (chlorpropamide) can increase your risk of death from heart problems when compared to other methods of controlling blood sugar, specifically with diet alone or diet and insulin. (
  • Talk to your doctor about the risk and benefits of taking Diabinese (chlorpropamide) to decide if it is the right medicine for you. (
  • There is evidence to indicate that exposure to Chlorpropamide (an antidiabetic drug) during pregnancy may have a teratogenic effect on the fetus. (
  • The present results support the view that CPAF is associated with elevated blood acetaldehyde levels due to inhibition of aldehyde dehydrogenase by chlorpropamide. (
  • These results suggest that chlorpropamide inhibition of repair processes may potentiate the effects of known mutagenic hazards and may also be responsible for the increased incidence of chromosome aberrations in patients treated with the drug. (
  • One patient died and another developed serious symptoms after receiving 750 mg of chlorpropamide instead of 75 mg of chlorpromazine daily. (
  • Previously untreated DI patients may be given intranasal or subcutaneous desmopressin or oral chlorpropamide (adults only) for 2 or 3 days. (
  • citation needed] Chlorpropamide is a white crystalline powder with no characteristic taste or smell. (
  • Pseudoephedrine may interfere with blood glucose control and reduce the effectiveness of chlorproPAMIDE and other diabetic medications. (
  • Knowing that hyperglycemia is a hallmark of vascular dysfunction in diabetes and that neonatal streptozotocin-induced diabetic rats (n-STZ) present reduced inflammatory response, we decided to evaluate the effect of chlorpropamide-lowered blood glucose levels on carrageenan-induced rat paw edema and pleural exudate in n-STZ. (
  • n-STZ diabetic rats were treated with chlorpropamide (200mg/kg, 15d, by gavage) 8 weeks after STZ injection. (
  • Chlorpropamide treatment by restoring β-cell function, reducing blood sugar levels, and improving glucose tolerance might be contributing to the correction of the reduced inflammatory response tested as paw edema and pleural exudate in n-STZ diabetic rats. (
  • Its blood-glucose-lowering potential in both normoglycemic and alloxan-induced diabetic male Sprague-Dawley rats compared favourably to that of chlorpropamide. (
  • Chlorpropamide Fitzgerald, M.G. (1962). (
  • Chlorpropamide has appreciably more side-effects, mainly because of its very prolonged duration of action and the consequent hazard of hypoglycemia and it should no longer be used. (
  • Less common side effects of chlorpropamide include gastrointestinal symptoms such as nausea, vomiting, and diarrhea. (
  • Roles of chlorpropamide, alcohol and acetaldehyde in determining the chlorpropamide-alcohol flush. (
  • After smaller alcohol challenges (with chlorpropamide pretreatment) there were positive intercorrelations between flush-score, rise in facial skin temperature, and plasma concentrations of chlorpropamide and blood acetaldehyde. (
  • Chlorpropamide-alcohol flushing: a dominantly inherited trait associated with diabetes. (
  • Chlorpropamide-alcohol flushing, malar thermal circulation ind. (
  • Chlorpropamide-alcohol flushing, malar thermal circulation index, and baseline malar temperature. (
  • Mechanism of chlorpropamide-induced antidiuresis in man: Evidence for release of ADH and enhancement of peripheral action. (
  • There time was, however, no significant linguistic difference between the responses observed mechanism for chlorpropamide versus fenofibrate at discouraging any time. (