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In diabetic patients it has been shown that tolbutamide and carbutamide enhanced and glibenclamide did not influence the incidence of digitalis intoxication, or that of multifocal ectopic beats or coupling due to premature ectopic ventricular beats during digitalis therapy. In rabbits glibenclamide decreased and tolbutamide and carbutamide increased strophanthidin toxicity in a dose dependent manner. It was concluded that glibenclamide should be preferred to tolbutamide or carbutamide in digitalis-treated diabetics, when satisfactorily metabolic control is not achieved with a dietary regime alone.

The aim of this study was to clarify the role of altered diabetic vascular reactivity in ischaemic heart disease. In diabetic condition, the necrotic area of myocardial infarction was significantly extended and myocardial oedema failed to develop after administration of norepinephrine 2 or 48 hours after ligation of the left anterior descending coronary artery. In metabolically healthy dogs the necrotic area of myocardial infarction was considerably smaller and an increase in myocardial water content, in myocardial thiocyanate space, in microscopically demonstrable permeability and in diastolic stiffness of left ventricular wall occurred when norepinephrine was administered 2 or 48 hours after coronary infarction. A close correlation was demonstrable between enhanced water content, thiocyanate space and diastolic stiffness in metabolically healthy animals, whereas in diabetic condition diastolic stiffness was primarily increased, and decreased when norepinephrine was infused after coronary ligation. Therefore, the altered vascular reactivity in diabetes is supposed to be responsible for the lack of oedema in the nonischaemic part of myocardium after norepinephrine infusion as well as for the size and severity of myocardial infarction.

Rats were sensitized with a single intraperitoneal dose of bovine serum albumin in alhydrogel plus Bordetella pertussis vaccine, and local anaphylaxis was elicited in the paw by soluble antigen 2 weeks later. The response was mainly due to IgE-type antibodies and proved to be highly sensitive to beta-adrenoceptor agonists. Dexamethasone inhibited the response after a lag phase. Methysergide, disodium chromoglycate, diethylcarbamazine, BW 775/c, nordihydroguajaretic acid, and FPL 55712 were also suppressive, while mepyramine was without effect. A synergism between methysergide and FPL 55712 was shown. Active local paw anaphylaxis appears to be adequate and easily applicable for large-scale screening of anti-allergic drugs.