Abstract:Strips of longitudinal muscle from guinea‐pig ileum, retaining Auerbach's plexus, were superfused with oxygenated Krebs solution. Addition of 50 mm KCl led to a pronounced Ca2+‐dependent increase in the activities of both acetylcholinesterase and non‐specific cholinesterase (butyrylcholinesterase) in the perfusate but with no change in lactate dehydrogenase activity.
No release of acetylcholinesterase, either spontaneous or K+‐evoked was observed in tissue freed of the nerve plexus, although release of butyryl… Show more
“…They claim that neurotransmitter hydrolysis may be controlled via two enzymatic pathways: the primary system is acetylcholinesterase for the acetylcholine, which is held in the synaptic cleft and the secondary system, using plasma cholinesterase, for the extraneuronal acetylcholine which has diffused into the smooth muscle regions. This physiological finding agrees with the anatomical findings of Appleyard & Smith [13] who found that the acetylcholinesterase was present in Auerbach's plexus of a guinea-pig's ileum whereas the plasma cholinesterase was detected mainly in the smooth muscle.…”
Section: Physiology Of the Cholinesterasessupporting
SummaryPlasma cholinesterase is an enzyme which has importance to the anaesthetist primarily for its rôle in the metabolism of suxamethonium, although other anaesthetic related drugs that this enzyme metabolises are also increasingly important. In this article we review current thoughts on the function, profile and chemistry of plasma cholinesterase. Causes of variations in the activity of the enzyme are described and the basis of genetic variations is explained.
“…They claim that neurotransmitter hydrolysis may be controlled via two enzymatic pathways: the primary system is acetylcholinesterase for the acetylcholine, which is held in the synaptic cleft and the secondary system, using plasma cholinesterase, for the extraneuronal acetylcholine which has diffused into the smooth muscle regions. This physiological finding agrees with the anatomical findings of Appleyard & Smith [13] who found that the acetylcholinesterase was present in Auerbach's plexus of a guinea-pig's ileum whereas the plasma cholinesterase was detected mainly in the smooth muscle.…”
Section: Physiology Of the Cholinesterasessupporting
SummaryPlasma cholinesterase is an enzyme which has importance to the anaesthetist primarily for its rôle in the metabolism of suxamethonium, although other anaesthetic related drugs that this enzyme metabolises are also increasingly important. In this article we review current thoughts on the function, profile and chemistry of plasma cholinesterase. Causes of variations in the activity of the enzyme are described and the basis of genetic variations is explained.
“…AChE inhibitors decrease metabolism of ACh released from enteric neurons. 26 Blocking metabolism of ACh increases the availability of ACh and probably the effective distance over which ACh can diffuse from excitatory nerve terminals to affect postjunctional receptors. A result of preserving ACh in the tunica muscularis should be enhanced binding of muscarinic receptors that exert ionotropic and chronotropic effects in gastric muscles.…”
Background/AimsGastric peristalsis begins in the orad corpus and propagates to the pylorus. Directionality of peristalsis depends upon orderly generation and propagation of electrical slow waves and a frequency gradient between proximal and distal pacemakers. We sought to understand how chronotropic agonists affect coupling between corpus and antrum. Methods Electrophysiological and imaging techniques were used to investigate regulation of gastric slow wave frequency by muscarinic agonists in mice. We also investigated the expression and role of cholinesterases in regulating slow wave frequency and motor patterns in the stomach. Results Both acetycholinesterase (Ache) and butyrylcholine esterase (Bche) are expressed in gastric muscles and AChE is localized to varicose processes of motor neurons. Inhibition of AChE in the absence of stimulation increased slow wave frequency in corpus and throughout muscle strips containing corpus and antrum. CCh caused depolarization and increased slow wave frequency. Stimulation of cholinergic neurons increased slow wave frequency but did not cause depolarization. Neostigmine (1 M) increased slow wave frequency, but uncoupling between corpus and antrum was not detected. Motility mapping of contractile activity in gastric muscles showed similar effects of enteric nerve stimulation on the frequency and propagation of slow waves, but neostigmine (> 1 M) caused aberrant contractile frequency and propagation and ectopic pacemaking. Conclusions Our data show that slow wave uncoupling is difficult to assess with electrical recording from a single or double sites and suggest that efficient metabolism of ACh released from motor neurons is an extremely important regulator of slow wave frequency and propagation and gastric motility patterns.
“…Apical fluids were sampled at regular intervals after tissue mounting and extracellular LDH levels were measured using an enzyme assay kit (Sigma, Poole, Dorset, UK) adapted for isolated intestinal tissue enzyme release (32). The percent cytotoxicity was determined by comparing the amount of extracellular LDH observed in the apical chamber to the maximum releasable LDH induced by exposure to 0.01% Triton-X-100.…”
Section: Viability Of Ileal Mucosal Sheetsmentioning
C(10) does not promote the permeation of a common bacterium across isolated intestinal tissue upon acute co-exposure. It prevents S. typhimurium attachment to epithelia and impedes growth of a range of different bacterial strains.
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