Use of corticosteroids in the prevention of post-ERCP pancreatitis.

BACKGROUND: Pancreatitis frequently complicates diagnostic and therapeutic ERCP. A variety of causes have been implicated. A number of different agents have been used, without success, in an attempt to prevent pancreatitis. METHODS: In the current study, 824 patients with a history of iodine sensitivity were given preprocedure corticosteroid therapy (651 oral steroids and 173 intravenous steroids) in an attempt to prevent allergic reactions. These patients were retrospectively studied in an attempt to determine if corticosteroid administration prevents ERCP-related pancreatitis. Two control groups were used for comparison, including 1000 patients during the same study period (Control Group I) and 1954 patients from the Midwest Pancreaticobiliary Group (Control Group II). RESULTS: There was a significant difference in the overall incidence of post-ERCP pancreatitis in the corticosteroid treated group (4.6%) compared with either control group (Control Group I = 7.4% and Control Group II = 9.1%). Of those patients undergoing therapeutic ERCP, results were even more significant in favor of the steroid-treated group (5.2%) compared with Control Group I (9.7%) and Control Group II (11.2%). CONCLUSIONS: These results demonstrate that the administration of corticosteroids prior to ERCP results in a decreased incidence of post-ERCP pancreatitis. A prospective, randomized, controlled trial is warranted.

DSP4-induced noradrenergic lesions increase beta-adrenergic receptors and hippocampal electrophysiological responsiveness.

Following profound (greater than 90%) depletions of norepinephrine (NE) by the noradrenergic neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4), the numbers of beta-adrenergic receptors were significantly increased (20-25%) in rat hippocampal and somatosensory cortical membranes; however, the numbers of alpha 1-adrenergic receptors and the affinities of both types of receptors were unaffected. This selective up-regulation of beta-adrenergic receptors was evident 1 week after DSP4 administration and was maintained for at least 2 more weeks. In electrophysiological experiments in the hippocampal slice preparation, responses to threshold as well as maximal concentrations of isoproterenol were enhanced 150% and 33%, respectively, in the DSP4-lesioned animals. The results demonstrate that nearly complete depletion of brain NE produced by administration of DSP4, like that produced by 6-hydroxydopamine, results in increased numbers of beta- but not alpha-adrenergic receptors, and suggest that the density of the former are regulated by afferent noradrenergic fibers. Furthermore, the functional significance of the increased number of hippocampal beta-adrenergic receptors is directly manifested in a greater electrophysiological responsiveness to an exogenously administered beta-adrenergic receptor agonist.

Behavioural sensitivity to PIA in selectively bred mice is related to a number of A1 adenosine receptors but not to cyclic AMP accumulation in brain slices.

In a dose of 0.1 mg/kg, PIA had marked behavioural effects in long-sleep mice (which show a high sensitivity to ethanol, while no significant effect was observed in short sleep mice (low sensitivity to ethanol). The number of [3H]PIA binding sites in cortex and subcortical brain regions was significantly higher in long-sleep than in short-sleep mice. The KD value was higher in cortex and cerebellum in the short-sleep mice, but there were no differences in the number of hippocampal beta-adrenoceptors or in the adenosine analogue-induced increase in cyclic AMP accumulation in slices of mouse hippocampus.