ISSN:0031-7012    

DOI:10.1159/000137130

出版商:S. Karger AG    

年代:1968

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000137131

出版商:S. Karger AG    

年代:1968

数据来源: Karger

摘要:

A procedure to quantitatively assess diarrhea during morphine withdrawal in rats has been developed. Physical dependence on morphine was produced either by pellet implantation (75 mg morphine/rat) or by a single subcutaneous injection of morphine (150 mg/kg in oil). The gross morphine abstinence signs observed after naloxone administration included diarrhea, body weight loss, jumping, wet-dog shakes, hypothermia, teeth chattering, and irritability to handling. A dose-response relationship was observed for naloxone-precipitated withdrawal diarrhea, with an optimal naloxone dose of 0.4 mg/kg. The severity of diarrhea was dependent on the interval after morphine withdrawal prior to naloxone administration. The probably direct relationship between diarrhea (measured as total excrement) and body weight loss during narcotic withdrawal was documented. Morphine withdrawal diarrhea was found to be a useful index for the study of the effects of other drugs on morphine withdrawal. Ethanol (0.5–2.0 g/kg) was found to suppress diarrhea, wet-dog shakes and jumping, but enhance hypothermia during morphine withdrawal; these effects of ethanol were dose-dependent. The suppression of morphine withdrawal diarrhea by ethanol (2 g/kg) was prolonged, lasting up to 20 h. This suppression of withdrawal diarrhea by ethanol is nonspecific since ethanol also suppressed diarrhea induced by castor oil feeding and also gastrointestinal motility as measured by the movement of charcoal in the intestine after charcoal meal feeding. Suppression of some aspects of the morphine withdrawal syndrome by ethanol may account in part for the increase in ethanol consumption in that setting in rats and possibly also in ma

ISSN:0031-7012    

DOI:10.1159/000137224

出版商:S. Karger AG    

年代:1979

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000137132

出版商:S. Karger AG    

年代:1968

数据来源: Karger

摘要:

The opioid activities of peptide and non-peptide narcotics were studied in longitudinal muscle strip of guinea pig ileum (GPI) and in mouse vas deferens (MVD). The comparison of agonist activities of peptides found in GPI and MVD offered the opportunity to predict the presence but not the magnitude of potential analgesic activity. The kinetics of the antagonism between naltrexone and different types of agonists were also determined in these systems. Using C-6 epimers of naltrexone, it was found that the site of opiate receptors recognizing the information provided by the C-6 substituent of naltrexone are different in GPI and MVD.

ISSN:0031-7012    

DOI:10.1159/000137225

出版商:S. Karger AG    

年代:1979

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000137133

出版商:S. Karger AG    

年代:1968

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000137134

出版商:S. Karger AG    

年代:1968

数据来源: Karger

摘要:

The effect of isoniazid (INH) and procainamide (PA) on each other’s acetylation pathway was studied in 7 normal subjects (3 rapid acetylators, 3 slow acetylators, 1 of indeterminate phenotype). Oral PA (6 mg/kg) was administered every 4 h for a total of seven doses. Following the final dose subjects received a single 300-mg oral dose of INH. Analysis of the parent drugs and their acetylated metabolites in plasma and urine revealed no effect on the acetylation of either drug. In 2 subjects (1 rapid, 1 slow acetylator) increasing doses of PA were given and the effect on INH (300 mg) acetylation measured. High mean circulating levels of PA (7.1 µg/ml) appeared to inhibit acetylation of INH in the rapid acetylator whereas a mean PA plasma level of 8.6 µg/ml had no effect on INH acetylation in the slow acetylator. However, the results from this study suggest that alterations of INH acetylation by PA are unlikely to be of clinical significa

ISSN:0031-7012    

DOI:10.1159/000137227

出版商:S. Karger AG    

年代:1979

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000137135

出版商:S. Karger AG    

年代:1968

数据来源: Karger

摘要:

Chronic administration of epinephrine to adult male rats resulted in a significant increase in the rate of ethanol elimination, when given alone or together with the β-adrenergic blocker alprenolol1. This effect was observed concomitantly with an increased hepatic oxygen utilization and no changes in mitochondrial respiratory functions. Epinephrine given acutely did not modify the rate of ethanol metabolism. Blood glucose levels were enhanced in these conditions, but were unaffected in rats treated with epinephrine plus alprenolol. These results suggest that chronic epinephrine treatment induces an increased oxidative capacity in the liver characterized by enhanced rates of oxygen uptake and ethanol metabolism, which is not related to its β-adrenergic action

ISSN:0031-7012    

DOI:10.1159/000137228

出版商:S. Karger AG    

年代:1979

数据来源: Karger