{"title":"Effect of oral antidiabetics on the anaphylactoid reaction.","authors":"K Wellinger, M Koltai","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The dextran-induced anaphylactoid reaction in the rat is susceptible to changes in carbohydrate metabolism. Paw oedema evoked by dextran was studied in norma and streptozotocin diabetic rats whose blood sugar level was determined by the glucose oxidase method. Insulin and tolbutamide increased dextran oedema in normal animals, while butylbiguanide (BBG) did not. The marked inhibition observed in the diabetic state was reversed by insulin and BBG, but not by tolbutamide. The dextran response correlated with the blood sugar level. These results suggest that the weak response to dextran in diabetic rats is due to an impaired peripheral glucose utilization rather than insulin deficiency per se.</p>","PeriodicalId":7049,"journal":{"name":"Acta physiologica Academiae Scientiarum Hungaricae","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta physiologica Academiae Scientiarum Hungaricae","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
The dextran-induced anaphylactoid reaction in the rat is susceptible to changes in carbohydrate metabolism. Paw oedema evoked by dextran was studied in norma and streptozotocin diabetic rats whose blood sugar level was determined by the glucose oxidase method. Insulin and tolbutamide increased dextran oedema in normal animals, while butylbiguanide (BBG) did not. The marked inhibition observed in the diabetic state was reversed by insulin and BBG, but not by tolbutamide. The dextran response correlated with the blood sugar level. These results suggest that the weak response to dextran in diabetic rats is due to an impaired peripheral glucose utilization rather than insulin deficiency per se.