Disease relevance of BURIMAMIDE

• The effects of burimamide, an H2-antihistamine, on the anaphylactic reaction in the skin of ovalbumin-sensitized guinea pigs were studied in vitro [1].
• Bronchospasm in guinea pigs given antigen challenge is enhanced by previous administration of metiamide or burimamide but not of cimetidine [2].
• Symptoms of toxicity to burimamide developed at doses in excess of 30 mumol/kg/hr; none occurred with doses of metiamide ranging from 1.8 to 7.5 mumol/kg/hr [3].
• Burimamide alone enhanced the growth of granuloma [4].
• 3 Although burimamide (i.c.v. or i.v.) afforded protection against histamine-induced emesis, there was no protection against intravenous apomorphine-or oral copper sulphate-induced emesis [5].

High impact information on BURIMAMIDE

• Starting from the structure of histamine, chemical modification led eventually to burimamide, the first described histamine H2-receptor antagonist [6].
• The effect of back diffusion of H+ PON THE POTENTIAL DIFFERence (PD), electrical resistance (R), and short circuit current (Isc) of spontaneously secreting and burimamide-inhibited amphibian gastric mucosae were studied in vitro [7].
• Electrophysiological effects of burimamide and 16,16-dimethyl prostaglandin E2 on the canine gastric mucosa [8].
• In the in vitro preparation, the unidirectional flux of sodium from mucosa to serosa increased after dm-PGE2 but not after burimamide [8].
• H2 antihistamines, including cimetidine, burimamide, metiamide, and tiotidine, consistently augmented antigen-induced histamine release from human basophils in vitro when control histamine release was less than 20% of total [9].

Chemical compound and disease context of BURIMAMIDE

• In certain models for inflammation, particularly rat paw edema induced by compound 48/80, burimamide in combination with the H1-receptor antagonist mepyramine shows anti-inflammatory activity [10].
• Tripelennamine and methysergide reduced anaphylaxis minimally and burimamide not at all [11].

Biological context of BURIMAMIDE

• Burimamide, on the other hand, was shown to act as a neutral antagonist and did as expected not induce H2 receptor upregulation after long-term exposure [12].
• When control secretory rates were similar, 40 mumol of burimamide per kg and 4 mumol of metiamide per kg produced the same degree of inhibition [3].
• Burimamide had no effect on the baroreflex [13].
• 2 At low doses all the compounds were inactive except for burimamide which delayed and ranitidine which accelerated gastric emptying [14].
• 4 Burimamide (2.5 x 10(-5) to 1.2 x 10(-4) M) inhibited sodium arachidonate-induced human platelet aggregation; the degree of inhibition was dependent upon the concentration of arachidonic acid used to aggregate the platelets [15].

Anatomical context of BURIMAMIDE

• 1 Burimamide selectively inhibited the formation of thromboxane A2 from prostaglandin endoperoxides by human platelet microsomes in a dose-dependent manner (IC50 = 2.5 x 10(-5) M) [15].
• 1 Burimamide injected intravenously in the anaesthetized or conscious cat produced significant increases in gastric acid secretion: in the anaesthetized cat it produced increased gastric mucosal blood flow [16].
• Only injections of burimamide into the third ventricle blocked the hypothermic response to systemic injection of histidine [17].
• 5 H2-receptor antagonists reversed the inhibitory effect of histamine in a dose-related manner, but both metiamide and burimamide, in high concentrations, augmented lymphocyte activation in their own right [18].
• 3 Burimamide (5 x 10(-4) to 2.3 x 10(-3) M) did not inhibit either the cyclo-oxygenase or the prostacyclin synthetase of sheep seminal vesicles or the prostacyclin synthetase of dog aortic microsomes [15].

Associations of BURIMAMIDE with other chemical compounds

• At physiological pH, cimetidine (1a) and its analogues burimamide (1b) and metiamide (1c) exist mainly as an equilibrium mixture of tautomers [19].
• Furthermore, the lack of potency of burimamide as a histamine antagonist and its lack of specificity compared to mepyramine, at the subcellular level, indicate that histamine-responsive adenylate cyclase from heart may not be a satisfactory molecular model for the H2 receptor pharmacology of histamine in cardiac tissue [20].
• 2 Mepyramine (H1-receptor antagonist) blocked the histamine-induced increase in capillary permeability whereas burimamide (H2-receptor antagonist) produced no significant blockade of the histamine-response [21].
• 5. [125I]-iodophenpropit was biphasically displaced by the histamine H3-receptor antagonists, burimamide and dimaprit, which may indicate the existence of histamine H3-receptor subtypes [22].
• Thioperamide (3 mg/kg) and impromidine (3 mg/kg), but not burimamide (10 mg/kg) blocked the reduction in blood pressure due to (R)-alpha-methylhistamine [23].

Gene context of BURIMAMIDE

• Certain chemical properties, which may determine the biological actions of the recently discovered histamine H2-receptor antagonists burimamide and metiamide, are identified, partly by considering the derivation of these antagonists [24].
• Effect of mepyramine, a histamine H1-, and burimamide, a histamine H2-receptor antagonist, on ovum implantation in the rat [25].
• 5. Burimamide (H2-receptor antagonist) produced a biphasic and dose-dependent stimulation and non-competitive inhibition of ADH and it non-competitively inhibited ALDH in both cytoplasmic and mitochondrial fractions [26].
• Following removal of burimamide, 3 X 10(-6) M tetrodotoxin did not block gastrin stimulation of H+ secretion indicating that neural mechanisms are not required [27].
• However, a distinct inhibition of human intestinal and pea seedling diamine oxidase was observed in presence of beta-aminopropionitrile (weak inhibition of the human enzyme, strong inhibition of pea seedling diamine oxidase) and burimamide (strong inhibition of human intestinal enzyme, nearly no influence on pea seedling diamine oxidase) [28].

Analytical, diagnostic and therapeutic context of BURIMAMIDE

• When the H2-receptor antagonists burimamide, metiamide and cimetidine were labelled with 35S, 14C or 3H and dosed to rats, whole body autoradiography showed that the stomach was predominantly labelled in the glandular mucosa from 5 to 120 min after administration [29].

References