Articles: histamine.
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Physiol. Chem. Phys. · Jan 1980
Carbon dioxide balance in rat stomach and peripheral tissue: effects of histamine.
Total carbon dioxide content of arterial, gastric venous, and peripheral venous blood of the rat has been measured by a gas extraction-gas solid chromatographic technique. In control animals total contents were 24 to 29 mmol/l and the venous/arterial ratio 1.148 +/- 0.020 (xav +/- SEM). Net change of carbon dioxide content (delta CO2) was 1.17 +/- 0.56 and 1.11 +/- 0.45 mmol/l in gastric and peripheral circulations and these were not significantly different from each other or zero. ⋯ Similar oscillations occurred in the venous/arterial ratio with values up to 1.35. The results confirm previous reports of oscillations of carbon dioxide venous/arterial ratios induced by histamine as revealed by pulse radiolabeling experiments. The positive, if oscillatory, carbon dioxide balance in the presence of histamine supports the concept of sequestration of carbon dioxide in tissue with subsequent release on histamine stimulation.
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Acta Obstet Gynecol Scand · Jan 1977
Histamine metabolism in normal pregnancy and in toxaemia of pregnancy.
The urinary excretion of histamine and its metabolites, methylhistamine, methylimidazoleacetic acid and imidazoleacetic acid, was measured under standardized dietary conditions in 24 women with normal pregnancies and in eleven patients with toxaemia of pregnancy. In addition, histamine metabolism was studied in five healthy women at delivery and in four other healthy pregnant women during treatment with aminoguanidine, which is an inhibitor of diamino oxidase (histaminase). A slight increase in the urinary excretion of methylimidazoleacetic acid was observed in normal pregnancy as well as in toxaemia of pregnancy compared to non-pregnant women. ⋯ Despite the very high diamino oxidase activity in the plasma and in the uterus during pregnancy, there were no signs of altered catabolism of endogenous histamine in the pregnant women. Smoking increased the urinary excretion of the quantitatively dominant histamine metabolite, methylimidazolacetic acid, in pregnant subjects as it also does in nonpregnant subjects. The necessity of standardized dietary conditions in the study of histamine metabolism in man was again emphasized.
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Arch Int Pharmacodyn Ther · Nov 1975
The influence of temperature increase, elevation of extracellular h+-concentration, and of triiodothyronine on the actions of phenylephrine, histamine, and beta-sympathomimetic drugs on rabbit aortic strips.
In the isolated preparation from the rabbit thoracic aorta, the affinities of the vasoconstrictor agents phenylephrine and histamine, as well as of the vasodilator beta-sympathomimetic drugs isoprenaline, fenoterol (TH 1165a), terbutaline, and salbutamol under the conditions of temperature increase, triiodothyronine and decrease of extracellular pH were investigated. It was observed that (1) a temperature increase from 25 degrees to 42 degrees C significantly indreased the maximal tension evoked by histamine, whereas that induced by the alpha-sympathomimetic drug phenylephrine was not altered significantly; the maximal relaxation caused by beta-sympathomimetic drugs either at 25 degrees or at 42 degrees C did not differ from one another; (2) the affinities of histamine, phenylephrine and of the beta-sympathomimetic drugs isoprenaline, fenoterol, terbutaline, and salbutamol each were comparable at either 25 degrees or 42 degrees C; the rank order of efficacy of the beta-sympathomimetic drugs is isoprenaline greater than fenoterol greater than salbutamol greater than terbutaline; (3) a decrease of the pH from 7.37 to 7.15 diminished the affinities of histamine and of the beta sympathomimetic drugs whereas that of the alpha-adrenergic drug phenylephrine was not altered. A further decrease of the pH to 6.8 diminished additionally the affinity of histamine and of isoprenaline, and especially that of the other beta-sympathomimetic drugs to such an extent that in the latter case complete dose-response curves could not be determined any more; (4) pretreatment of the animals with 0.4 mg/kg of triiodothyronine (T3) for two days, which strongly depressed the tension induced by either histamine or phenylephrine, did not alter the affinity of both drugs; T3 in vitro (10(-6) M) only diminished the affinity of histamine but left that of phenylephrine unaltered; pretreatment for two days with 0.2 mg/kg of T3 yielded a significant diminution of the pD2-values for two beta-sympathomimetic drugs investigated, namely isoprenaline and fenoterol; also the administration of T3 in vitro in a final concentration of 10(-6) M resulted in a diminution of the affinity of both beta-sympathomimetic drugs; (5) the results obtained show that also on the aorta beta-adrenoceptor stimulants are dependent on the metabolic state while alpha-adrenoceptor stimulants are not.
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The release of histamine and mortality was studied in mice after various types of experimental shock. In burn shock, serum histamine rose significantly after injury, but there was no correlation between increased serum histamine and high mortality as a consequence of several therapy regimens. For example, after treatment with histamine or Compound 48/80 before burning, there was a rise of serum histamine, yet shock mortality fell significantly. ⋯ In tourniquet shock, serum histamine rose significantly, and treatment with both antagonists before trauma produced a significant elevation of shock mortality. In endotoxin shock, prior treatment with one or both drugs did not change mortality. These results suggest that endogenous histamine is not a lethal factor in burn and tourniquet trauma, but rather it appears to have a compensatory, beneficial effect.