Detail of "59-99-4"

Reference

Motility of the distal portion of the jejunum and pelvic flexure in ponies: effects of six drugs

Motility of the distal portion of the jejunum and pelvic flexure in ponies: effects of six drugs. Adams, Stephen B.; Lamar, Carlton H.; Masty, Jerome (Sch. Vet. Med., Purdue Univ., West Lafayette, IN 47907, USA). Am. J. Vet. Res., 45(4), 795-9 (English) 1984. CODEN: AJVRAH. ISSN: 0002-9645. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Bipolar stainless steel electrodes were surgically implanted in 4 ponies to record myoelec. and mech. activity of the distal portion of the jejunum and pelvic flexure. After detg. normal activity, the effects of neostigmine [59-99-4], xylazine [7361-61-7], flunixin meglumine [42461-84-7], dipyrone [68-89-3], panthenol [81-13-0], and atropine [51-55-8] were detd. Flunixin meglumine, dipyrone, and panthenol had no effect on the motility of the jejunum or pelvic flexure.In this experiment, several chemicals are used like 81-13-0 and 7361-61-7 Xylazine and atropine sulfate decreased motility of the distal portion of the jejunum and pelvic flexure, with atropine having a greater effect and lasting longer. Neostigmine stimulated propulsive motility in the pelvic flexure only. .

Adverse interaction between acetazolamide and anticholinesterase drugs at the normal and myasthenic neuromuscular junction level

Adverse interaction between acetazolamide and anticholinesterase drugs at the normal and myasthenic neuromuscular junction level. Carmignani, M.; Scoppetta, C.; Ranelletti, F. O.; Tonali, P. (Sch.Chemicals with cas numbers 9001-03-0 and 9001-08-5 also play role. Med., Catholic Univ. Rome, Rome 00168, Italy). Int. J. Clin. Pharmacol., Ther. Toxicol., 22(3), 140-4 (English) 1984. CODEN: IJCPB5. ISSN: 0300-9718. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Adverse interactions between acetazolamide [59-66-5] and cholinesterase [9001-08-5]-inhibiting drugs were studied at skeletal neuromuscular junction level in in vivo and in vitro expts. Acetazolamide (500 mg, i.v.) prevented the increase in amplitude induced by edrophonium chloride [116-38-1] (5 mg, i.v.) on the action potentials derived by surface electrodes from the opponens pollicis muscle of patients affected by myasthenia gravis, when the median nerve was stimulated at the wrist by low frequency repetitive pulses (5/s). Similarly, acetazolamide significantly reduced the contractile force potentiation induced by neostigmine [59-99-4] on the rat phrenic-diaphragm prepn., indirectly stimulated by means of low frequency repetitive pulses on the motor nerve. Under such exptl. conditions acetazolamide did not show any significant action of its own, but it counteracted the effects of anticholinesterase drugs only when tested before them. The effect of acetazolamide on the skeletal neuromuscular junction may occur at presynaptic and/or postsynaptic sites by a mechanism only partly ascribable tothe well-known carbonic anhydrase [9001-03-0] inhibitory activity of this drug. .