摘要:

Serum bromine levels in psoriatic Danes increased 2- to 3-fold during a 4-week bathing course in the Dead Sea. This increase correlated well with the improvement in their clinical and psychic condition. Serum bromine levels in psoriatic Danes were somewhat lower than those in healthy subjects residing in Denmark, but the difference was not significant. Israelis working in the open air in the Dead Sea area (air bromine 20-fold higher than in Jerusalem) had higher bromine levels than psoriatic or healthy Israelis residing in Jerusalem or healthy Israelis working in air-conditioned rooms in the Dead Sea area (p < 0.05), but those levels were still within the normal range. As our animal experimentation indicates that the skin is a major target organ for 82Br, applied either by bathing or as an aerosol, we conclude that the higher bromine levels noticed in the psoriatic Danes after their 4-week stay at the Dead Sea may be equally due to their contact with the bromine-containing aerosol and the high bromine level of the Dead Sea waters.

ISSN:0031-7012    

DOI:10.1159/000137756

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

Since cocaine or diazepam are used clinically and/or abused concomitantly with narcotics, this study was designed to determine if morphine-dependent, morphine-withdrawn, or acute morphine rats exhibit an altered core body temperature at 24 or 4 °C to either cocaine (10, 20, or 30 mg/kg i.p.) or diazepam (2 or 4 mg/kg i.p.). At 24 °C, each dose of cocaine manifested hyperthermia in all groups of rats except morphine-dependent whereas at 4 °C cocaine produced hypothermia in all groups except morphine-dependent. At both 24 and 4°C, diazepam, 2 or 4 mg/kg, caused a hypothermic response in control, dependent, and withdrawn animals. At 24 °C, administration of acute morphine alone induced a hyperthermia which was antagonized by both doses of diazepam. At 4°C, acute morphine alone induced an initial hypothermia followed by a hyperthermia; both doses of diazepam potentiated the hypothermic response to acute morphine. Thus, significant alterations in core body temperature may be induced following the administration of cocaine or diazepam to morphine-treated

ISSN:0031-7012    

DOI:10.1159/000137757

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

Stimulants (histamine, acetylcholine and substance P) and relaxants (isoprenaline and bradykinin) of the guinea pig trachea were tested in the absence and presence of mepacrine, eicosatetraynoic acid, BW 755C and indomethacin in order to evaluate the involvement of prostaglandins and congeners in the effects of amines and peptides. While histamine appeared to stimulate tracheal smooth muscle directly, acetylcholine acted in part by promoting the release of contractile leukotrienes. Substance P was unable to express its full stimulating effect because of a likely release of an inhibitory prostaglandin. Isoprenaline inhibited tracheal smooth muscles by a direct action, while the relaxation of the trachea in response to bradykinin appeared to depend on the release of prostaglandins, since it was reduced in the presence of inhibitors of cyclo- and lipooxygenase. It is concluded that enzymes involved in the metabolism of arachidonic acid are present in the guinea pig trachea and are activated both by relaxant and stimulant agents.

ISSN:0031-7012    

DOI:10.1159/000137758

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

The present experiments were designed to elucidate the pharmacological mechanism of the relaxing action of the ovarian hormone, relaxin, upon KCl-contracted rat uteri in vitro. Rat uterine segments were made to contract by superfusion with a physiological solution, in which 15 % of the normal NaCl content had been replaced by an equimolar amount of KC1. The effect of relaxin, in reversing this contraction, was achieved in part by a direct action upon the tissue and in part (about 45% at the concentration of relaxin used) by the liberation of endogenous catecholamines which relax the uterus via β-adrenergic activity. The effect of relaxin was reduced by propranolol, and it was not blocked by indomethacin, cimetidine or diphenhydramine. The effect of the ovarian peptide on uterine segments was potentiated in the presence of theophylline and indomethacin in the supervising fluid. This effect of theophylline was shown to be insensitive to β-adrenergic blockade. The results suggest that relaxin relaxes the KCl-contracted rat uterus in part by a direct inhibitory action upon the uterine muscle and in part by facilitating the release of intramural catecholamines. It is also suggested that relaxin may act via the production of cyclic AM

ISSN:0031-7012    

DOI:10.1159/000137759

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

Insulin secretion and blood glucose homeostasis were studied in mice following administration of cholinergic agonists, antagonists and other possible modifiers of cholinergic insulin secretory mechanisms. It was observed that administration to mice of the cholinergic agonists acetylcholine, carbachol and pilocarpine resulted in an increase in plasma immunoreactive insulin levels accompanied by a significant fall in blood glucose levels. Nicotine had no effect. Carbachol was found to enhance insulin release in a dose-dependent manner. Muscarinic blockade by atropine or methylatropine totally suppressed carbachol-induced insulin secretion. No blocking effect was accomplished by β-adrenoceptor blockade. Glucose-induced insulin secretion was not affected by atropine in normal non-fasted mice. In mice fasted for 24 h, however, the insulin response to glucose was impaired by atropine suggesting that the nutritional state is important for cholinergic modulation of glucose-induced insulin response. Pretreatment of animals with the glycogenolytic hydrolase, acid amyloglucosidase, enhanced tolbutamide-induced insulin release but did not influence insulin secretion stimulated by carbachol. Pretreatment with the monoamine oxidase inhibitor, pargyline, plus L-dopa, leading to an intracellular accumulation of dopamine in the insulin cells, totally suppressed carbachol-induced insulin release. It is suggested that, in mice, cholinergic stimulation promotes insulin secretion through activation of muscarinic receptors on the insulin cell. Blockade of these receptors does not influence glucose-stimulated insulin release in the non-fasting state, but may impair the insulin response to glucose after fasting. Cholinergic stimulation of insulin release is inhibited after L-dopa-induced accumulation of dopamine in the insulin cells. In contrast to tolbutamide-induced insulin release cholinergic insulin release is not dependent on acid amyloglucosidase activity

ISSN:0031-7012    

DOI:10.1159/000137760

出版商:S. Karger AG    

年代:1982

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000137761

出版商:S. Karger AG    

年代:1982

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000137762

出版商:S. Karger AG    

年代:1982

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000137755

出版商:S. Karger AG    

年代:1982

数据来源: Karger