Action de l'acide acétylsalicylique sur le système nerveux végétatif

Delbarre, B; Aron, E; Dumas, G.; Chatelus, A.

doi:10.1007/bf02135745

Cited by 8 publications

(4 citation statements)

References 2 publications

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“…Delabarre and co-workers [a] showed, histochemically, that (pseudo-)cholinesterases in the cerebral blood vessels of rats were inhibited after the tissue had been incubated with aspirin. Also, this drug had parasympatheticomimetic actions in several organs [41]. These actions may be related to, or dependent upon the hydrolysis of aspirin by cholinesterases such that aspirin because of its interaction with these enzymes.…”

Section: Discussionmentioning

confidence: 99%

“…For instance, on a molar basis aspirin (a) is more potent as an analgesic/anti-inflammatory agent, (b) has greater gastric ulcerogenic activity, and (c) is much more effective as an inhibitor of prostaglandin biosynthesis and platelet aggregation than salicylate [8-121. Since activity of aspirin esterase in plasma has been correlated with the half-time and rate ofelimination of salicylate [I31 this enzymic activity could determine the non-spontaneous conversion of aspirin to salicylate in vivo. 41 have suggested that the depression in plasma aspirin esterase which they observed in women and patients with alcoholic liver disease may be related to the increased propensity of these two groups to gastric ulceration and haemorrhage. However, it appears that there are no reports of the optimal conditions for the assay (pH, substrate concentration) or even the isolation and characterization of aspirin esterase activity in plasma.…”

Section: Introductionmentioning

confidence: 99%

“…Hence, in the present work optimum conditions for enzymic activity have been determined and the components of plasma responsible for aspirin esterase activity isolated and characterized. The reported differences [I, 41 in plasma aspirin esterase between the sexes and in patients with 413 alcoholic liver disease were re-investigated and also patients with rheumatoid arthritis have been studied. The latter group comprise an appreciable proportion of the population, require high doses of aspirin and are known to have defects in liver metabolism (14,IS] which could reflect the capacity of this organ to produce enzymes involved in hydrolysing aspirin [4.…”

Section: Introductionmentioning

confidence: 99%

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Plasma aspirin esterases in normal individuals, patients with alcoholic liver disease and rheumatoid arthritis: characterization and the importance of the enzymic components

Rainsford

Ford

Brooks

et al. 1980

Eur J Clin Investigation

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Abstract. Two enzymes in human plasma capable of hydrolysing aspirin (‘aspirin esterases’) were isolated (by ion exchange and gel chromatography) and characterized, since their activity has been reported to be important in certain disease/therapeutic situations. The optimum pH and calcium concentration for plasma aspirin esterases were 80 and 5 mmol/1 respectively. The main enzymic activity (enzyme ‘C’) was associated with plasma cholinesterases. This component had a Km of 6‐5 mmol/1 for aspirin and a Kmax of 0–27 /imol salicylate/mg protein/min at pH 80 (Ca2+ present). It was not acetylated by aspirin but was inhibited by anti‐cholinesterase agents (eserine, echothiophate) and the neuromuscular blocking agent, decameth‐onium. The other enzymic component in plasma was albumin esterase. The sex difference in aspirin esterase activity in normal individuals previously reported by Menguy and co‐workers [1] was re‐investigated since it appeared that they had employed non‐optimal assay conditions. No significant differences were observed between the sexes in either normal individuals or patients with rheumatoid arthritis when the enzyme was assayed at either pH 7‐4 or the optimal pH of 80 (with Ca2+ added). The plasma albumin esterase activity was, however, markedly depressed in patients with alcoholic liver cirrhosis when assayed at pH 7‐4 and 80. Plasma aspirin esterases were elevated in nine rheumatoid arthritic patients receiving gold salt or D(‐)penicil‐lamine. Aspirin esterase 'C activity was negatively correlated with pain score in the plasma of female but not male rheumatoid arthritics. Also the percentage activation by calcium of aspirin esterase was correlated with the concentration of plasma calcium indicating that small changes in plasma calcium concentration may markedly affect enzymic activity. These results suggest that certain drugs (anti‐cholinesterase agents), disease states (e.g. alcoholic liver cirrhosis) or genetic deficiences (e.g. inactive pseudo‐cholinesterase) may be potentially important in the pharmacological and iatrogenic activities of aspirin.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Plasma aspirin esterases in normal individuals, patients with alcoholic liver disease and rheumatoid arthritis: characterization and the importance of the enzymic components

Rainsford

Ford

Brooks

et al. 1980

Eur J Clin Investigation

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“…A second possibility lies in the demonstration that PGE can inhibit cholinergic transmission 22 and that sodium salicylate augments cholinergic responses, 23 suggesting a potentiation by sodium salicylate of hypoglycemia-induced cholinergic discharge, with consequent enhanced counterregulatory hormone secretion. Finally, a third possibility must be considered: inhibition of the cyclooxygenase pathway by salicylates may shunt arachidonic acid metabolism in the lipoxygenase pathway.…”

Section: Discussionmentioning

confidence: 99%

Normalization by Sodium Salicylate of the Impaired Counterregulatory Glucagon Response to Hypoglycemia in Insulin-dependent Diabetes: A Possible Role for Endogenous Prostaglandins

et al. 1985

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The present study was undertaken to evaluate the influence of sodium salicylate on the counterregulatory glucagon response to insulin-induced hypoglycemia in both insulin-dependent diabetic subjects (IDDM) and normal controls. The IDDM group consisted of 5 patients with recent onset of disease (less than 45 days), a normal glucagon response to hypoglycemia, and no detectable insulin antibodies (group 1); and 7 patients with duration of disease between 1 and 5 yr, a reduced glucagon response to hypoglycemia, and no insulin antibodies (group 2). Ten healthy subjects served as a control group. The infusion of sodium salicylate (40 mg/min) during insulin-induced hypoglycemia (1 mU/kg-min for 60 min) in normal subjects caused a significant increase of the counterregulatory glucagon response both in terms of glucagon peak and integrated areas. Sodium salicylate itself significantly increased basal insulin and decreased glucose, but did not change basal glucagon. In the diabetic subjects of group 1, sodium salicylate amplified the glucagon response to the same degree of hypoglycemia without affecting the rates of glucose fall and recovery. Compared with normals and diabetic subjects of group 1, diabetic subjects of group 2 presented, in basal conditions, a reduced glucagon response to hypoglycemia and a slower rate of glucose recovery. Sodium salicylate normalized both defects. These results indicate that sodium salicylate may augment glucagon responses by improving the recognition of hypoglycemia in both normals and IDDM. Moreover, the restoration by sodium salicylate of a normal glucagon response to hypoglycemia in diabetic subjects of group 2 suggests a role for endogenous prostaglandins in this selective deficiency of the counterregulatory response.

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