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STUDY OBJECTIVES: Sulfonylurea agents are widely used as therapy for hyperglycemia in type 2 diabetes mellitus. In overdose, these agents can produce sustained and profound hypoglycemia that is refractory to treatment with dextrose alone. Our objective was to determine whether treatment with octreotide decreases glucose requirements and the number of hypoglycemic episodes in patients with sulfonylurea-induced hypoglycemia. METHODS: We retrospectively reviewed the charts of patients treated with octreotide for sulfonylurea-induced hypoglycemia from 1995 through 1998. The study took place in a large urban teaching hospital in the United States. We measured the number of episodes of hypoglycemia reported and the amount of dextrose used before and after treatment with octreotide. Using a failure time analysis, we compared the risk of hypoglycemia before and after octreotide administration. RESULTS: The age range of the 9 patients was 20 to 65 years. Six patients ingested glyburide and 3 ingested glipizide. The number of hypoglycemic events recorded per patient before octreotide (mean 3.2) was greater than the number of hypoglycemic events recorded per patient after octreotide (mean 0.2, P =.008). Similarly, the number of ampules of 50% dextrose administered per patient before octreotide (mean 2.9) was greater than the number of ampules administered per patient after octreotide (0.2, P =.004). The risk of recurrent hypoglycemia before octreotide treatment was 27 times the risk of the group after octreotide treatment (P <.001). Stabilization of blood glucose concentration and cessation of rebound hypoglycemia occurred immediately after the administration of octreotide in all 9 patients. CONCLUSION: Octreotide appears to be safe and effective in preventing rebound hypoglycemia after sulfonylurea ingestion. Octreotide in combination with dextrose should be considered for first-line therapy in the treatment of sulfonylurea-induced hypoglycemia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10918104&dopt=Abstract
Pharmacol Res. 1994 Dec;30(4):317-24.
Supramaximal decrease of sulphonylurea-induced accumulation of sodium in pancreatic islets.
Saha S, Hellman B.
Department of Medical Cell Biology, University of Uppsala, Sweden.
Sodium was measured in beta-cell-rich pancreatic islets of mice under steady state conditions or after 6 min of exposure to 1 mM ouabain. The islet content of sodium increased when 100 microM tolbutamide or 1 microM glipizide were added to an albumin-containing (1 mg ml-1) medium, but remained unaffected at 10-fold higher concentrations. Both sulphonylurea compounds promoted the uptake of Na+ in the presence of ouabain. Whereas tolbutamide was stimulatory at 10 microM or above in a medium containing 10 mg ml-1 albumin, only 0.1 microM was required in the absence of albumin. In the latter situation there was a reduction of the stimulatory action with increase of the tolbutamide concentration from 100 to 1000 microM. The inhibitory component in the sulphonylurea action on the Na+ uptake was particularly impressive with glipizide, maximal stimulation being reached at 10 microM in the presence of 1 mg ml-1 albumin. Diazoxide (400 microM) modified the glipizide action on Na+ uptake, making 1000 microM stimulatory instead of 1 microM. The latter concentration of glipizide became inhibitory after removal of K+. Glipizide stimulated the Na+ uptake both at low and high concentrations in a medium deficient in Ca2+ or when the cotransport of Na+, K+ and Cl- was blocked by 20 microM bumetanide. The observation that the sulphonylurea-induced islet accumulation of sodium is diminished at supramaximal concentrations reinforces existing arguments for additional effects of high concentrations of hypoglycemic sulphonylureas.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7716105&dopt=Abstract
J Clin Invest. 1995 May;95(5):2403-8.
Glucose modulates rat substantia nigra GABA release in vivo via ATP-sensitive potassium channels.
During MJ, Leone P, Davis KE, Kerr D, Sherwin RS.
Molecular Pharmacology and Neurogenetics Laboratory, Yale University School of Medicine, New Haven, Connecticut 06520-8039, USA.
Glucose modulates beta cell insulin secretion via effects on ATP-sensitive potassium (KATP) channels. To test the hypothesis that glucose exerts a similar effect on neuronal function, local glucose availability was varied in awake rats using microdialysis in the substantia nigra, the brain region with the highest density of KATP channels. 10 mM glucose perfusion increased GABA release by 111 +/- 42%, whereas the sulfonylurea, glipizide, increased GABA release by 84 +/- 20%. In contrast, perfusion of the KATP channel activator, lemakalim, or depletion of ATP by perfusion of 2-deoxyglucose with oligomycin inhibited GABA release by 44 +/- 8 and 45 +/- 11%, respectively. Moreover, the inhibition of GABA release by 2-deoxyglucose and oligomycin was blocked by glipizide. During systemic insulin-induced hypoglycemia (1.8 +/- 0.3 mM), nigral dialysate GABA concentrations decreased by 49 +/- 4% whereas levels of dopamine in striatal dialysates increased by 119 +/- 18%. We conclude that both local and systemic glucose availability influences nigral GABA release via an effect on KATP channels and that inhibition of GABA release may in part mediate the hyperexcitability associated with hypoglycemia. These data support the hypothesis that glucose acts as a signaling molecule, and not simply as an energy-yielding fuel, for neurons.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7738204&dopt=Abstract
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