ライフサイエンスコーパス: neostigmine

1 ection of the acetylcholinesterase inhibitor neostigmine.

2 showing a higher affinity of the sensor for neostigmine.

3 reased by the acetylcholinesterase inhibitor neostigmine.

4 with acetylcholinesterase inhibitors such as neostigmine.

5 down with the acetylcholinesterase inhibitor neostigmine.

6 he breakdown of acetylcholine was blocked by neostigmine.

7 he decay phase of current was accelerated by neostigmine.

8 ection of the acetylcholinesterase inhibitor neostigmine.

9 ellular electrodes, often in the presence of neostigmine.

10 the MEPP was not reversed by 1 microgram/mL neostigmine.

11 antagonist scopolamine (40 mM) together with neostigmine (20 mM) attenuated the neostigmine-dependent

12 B by addition of the anticholinesterase drug neostigmine (20 mM) sharpened the ORF responses of mitra

13 usion) or the acetylcholinesterase inhibitor neostigmine (7.5-75 pmol per infusion) into the posterio

14 ivity in an atropine-sensitive manner, while neostigmine (a peripherally restricted cholinesterase in

15 Bath application of 10 microM neostigmine, a potent acetylcholinesterase inhibitor, pr

16 hout an initial response received open-label neostigmine; all had colonic decompression.

17 ing, samples were collected every 60 s while neostigmine, an acetylcholine esterase inhibitor, was in

18 ynamic changes elicited by microinjection of neostigmine, an inhibitor of acetylcholinesterase, that

19 ined from the fits were 3.8 x 10(3)M(-1) for neostigmine and 1.7 x 10(3)M(-1) for eserine, showing a

20 These results indicate that neostigmine and carbaryl directly block the nicotinic AC

21 Neostigmine and carbaryl showed a biphasic effect; enhan

22 t duration were decreased in the presence of neostigmine and carbaryl.

23 nvolved in the analgesic effects of epidural neostigmine and could be more specifically targeted for

24 Both neostigmine and DFP applied after AChE inhibition by DFP

25 quent anesthetics during which they received neostigmine and glycopyrrolate for NMB reversal.

26 Neuromuscular blockade (NMB) reversal with neostigmine and glycopyrrolate has been reported to caus

27 , our experience would support the safety of neostigmine and glycopyrrolate in cardiac transplantatio

28 ore, the antiallodynic effect of intrathecal neostigmine and muscarine was largely eliminated by CGP5

29 Neostigmine and/or N-acetyl-cysteine (NAC) were applied

30 e first co-application with 10 or 100 microM neostigmine, and the current was eventually suppressed b

31 mice) the EPSCs resembled those observed in neostigmine but the steady inward current was much small

32 The pharmacological inactivation of AChE by neostigmine caused the appearance of an ultra-slow (seco

33 iously we showed that Ani (anisodamine)/Neo (neostigmine) combination produced anti-shock effect via

34 ther with neostigmine (20 mM) attenuated the neostigmine-dependent sharpening of ORFs.

35 cologic acetylcholinesterase inhibition with neostigmine diminishes liver damage in acute liver failu

36 In the presence of neostigmine, EFS increased pT38, pT853 and pS19.

37 the presence of the cholinesterase inhibitor neostigmine, EFS led to an additional increase in phosph

38 the placebo group and the one patient in the neostigmine group without an initial response received o

39 Ten of the 11 patients who received neostigmine had prompt colonic decompression, as compare

40 llodynic actions of intrathecal muscarine or neostigmine in normal rats and in a rat model of diabeti

41 y attenuated the effect of both muscarine or neostigmine in normal rats.

42 Side effects of neostigmine included abdominal pain, excess salivation,

43 VTA ACh levels (resulting from 10 microM VTA neostigmine infusion) increased VTA dopamine levels and

44 Injection of NLA into the mPRF before neostigmine injection also blocked the ability of neosti

45 lution of the acetylcholinesterase inhibitor neostigmine into the L7 level of the dorsal horn of anes

46 ke state (REM(Neo)) caused by microinjecting neostigmine into the PRF.

47 We randomly assigned 11 to receive 2.0 mg of neostigmine intravenously and 10 to receive intravenous

48 Neostigmine is an acetylcholinesterase inhibitor that am

49 used: as little as 0.015-0.025 mg kg(-1) of neostigmine is required at a train-of-four count of four

50 Uncontrolled studies have suggested that neostigmine, may be an effective treatment.

51 Measured motility with neostigmine (mean, 0.39 au) was significantly higher tha

52 lation was manipulated by direct infusion of neostigmine, MLA, and scopolamine into the OB during olf

53 When the solution contained 10 microM neostigmine (NEO) 3000 stimuli reduced [integral]MEPCs b

54 otremorine, or the cholinesterase inhibitor, neostigmine (NEOS), in the rRPa of anaesthetized rats de

55 nd sensitive method for the determination of neostigmine (Ns) ion in its bulk powder, different pharm

56 ensors were applied for the determination of neostigmine (Ns) ion in its bulk powder, different pharm

57 ted by manipulation (using either drugs like neostigmine or genetic tools to inactivate neurotransmit

58 -controlled crossover study of either 0.5 mg neostigmine or saline (n = 11) or 20 mg intravenous buty

59 n a low-Mg(2+)-Ca2+ solution, sometimes with neostigmine present.

60 onse to conservative therapy, treatment with neostigmine rapidly decompresses the colon.

61 Two patients who had an initial response to neostigmine required colonoscopic decompression for recu

62 with the peripheral cholinesterase inhibitor neostigmine showed prolonged survival and improved outco

63 Intrathecal injection of muscarine or neostigmine significantly increased the withdrawal laten

64 njection were eligible to receive open-label neostigmine three hours later.

65 igmine injection also blocked the ability of neostigmine to decrease respiratory rate during the REM

66 nts such as opioids, clonidine, ketamine and neostigmine to potentiate the effects of local anestheti

67 g, IHG exercise increased sweat rate at both neostigmine-treated and untreated sites.

68 0.0086), APAP-alone-treated mice vs. APAP + neostigmine-treated mice) and histopathological signs of

69 0.0013), APAP-alone-treated mice vs. APAP + neostigmine-treated mice), inflammatory cytokine levels

70 ia, IHG exercise increased sweat rate at the neostigmine-treated site but not at the control site.

71 Neostigmine treatment led to significant reduction of se

72 The effect of intrathecal muscarine or neostigmine was examined through pretreatment with the s

73 y times (t1/2), regardless of whether or not neostigmine was present.

74 detection limits of 26 pM eserine and 0.3 nM neostigmine were achieved.

75 used with the acetylcholinesterase inhibitor neostigmine, while the other was perfused with the vehic