Administration Of Cholinergic Agents Research Articles

Pharmacological analysis of changes in the contentof diene conjugation, methyl esters of fatty acids of liver lipid fractions by cholinotropic agents during the overcooling of rats

The analysis of changes in the content of diene conjugation, fatty acid methyl esters (FAME) C20 of total lipids, fractions of free fatty acids (FFA) in the liver of animals exposed to overcooling for 3 hours and for 5 days after administration of cholinergic agents has been made. The obtained results indicate changing in the content of methyl esters of fatty acids and diene conjugation of FFA fractions after administration of pharmacological agents as neostigmine, pilocarpine, and atropine to animals on the background of cooling. Changes in the content of diene conjugation coincide with changes in the content of fatty acids (FA) C20 : 4 Δ-5,8,11,14 eicosatetraenoic acids (FA Arakhia) when pilocarpine or atropine was used. The presence of reciprocity was revealed. Basing the reciprocity factor, it was suggested that there was a possible effect of muscarine-sensitive structures of the plasmic membrane hepatocytes on the link between the content of FAME C20 Arakhia, phospholipase A2 activity and the change in the content of diene conjugation in fraction of liver FFA. A possible effect of cholinotropic agents on phospholipase A2 activity in the period of animal cooling was suggested.

Determination of Bicarbonate Output Using pH Deflection in the Rat Duodenum: Influences of Prostaglandins and Cholinergic Agents

AbstractWe set up a system to measure the luminal ρH, potential difference (PD) and bicarbonate output in the anesthetized rat duodenum, and investigated these responses caused by prostaglandins (PGs) and cholinergic agents. When the proximal duodenum (1.7 cm) was perfused at a flow rate of 0.7 ml/min with saline adjusted to pH 4.5, the duodenal pH. PD and HCO3− output were 5.5 to 6.0. −4 to −6 mV and 1.2 to 1.6 μEq/10 min, respectively; they were markedly reduced by i.v. injection of saturated KCl. Both natural (PGE1, PGE2) and synthetic (PGE2, PGI2) PGs, given either s.c. or i.v.. significantly elevated all these parameters, while indomethacin (s.c.) decreased the pH as well as the PD. Small but significant increases of the pH were observed after i.v. administration of cholinergic agents (carbachol, bethanechol), a GABAergic agent (baclofen) and an analogue of thyrotropin releasing hormone (YM-14673), with a temporal elevation of the PD; the degree of net HCO3− output caused by these agents was 20–50% of the values obtained with PGE2 (100 μg/kg, i.v.). and they were significantly reduced in the presence of atropine. These results suggest that (a) the system using pH deflections can be used to sensitively detect HCO3− output in the rat duodenum, and (b) duodenal acid neutralizing capacity may be regulated by central and peripheral cholinergic systems as well as endogenous PGs.

Determination of bicarbonate output using pH deflection in the rat duodenum: Influences of prostaglandins and cholinergic agents.

We set up a system to measure the luminal pH, potential difference (PD) and bicarbonate output in the anesthetized rat duodenum, and investigated these responses caused by prostaglandins (PGs) and cholinergic agents. When the proximal duodenum (1.7 cm) was perfused at a flow rate of 0.7 ml/min with saline adjusted to pH 4.5, the duodenal pH, PD and HCO3- output were 5.5 to 6.0, -4 to -6 mV and 1.2 to 1.6 muEq/10 min, respectively; they were markedly reduced by i.v. injection of saturated KCl. Both natural (PGE1, PGE2) and synthetic (PGE2, PGl2) PGs, given either s.c. or i.v., significantly elevated all these parameters, while indomethacin (s.c.) decreased the pH as well as the PD. Small but significant increases of the pH were observed after i.v. administration of cholinergic agents (carbachol, bethanechol), a GABAergic agent (baclofen) and an analogue of thyrotropin releasing hormone (YM-14673), with a temporal elevation of the PD; the degree of net HCO3- output caused by these agents was 20-50% of the values obtained with PGE2 (100 micrograms/kg, i.v.), and they were significantly reduced in the presence of atropine. These results suggest that (a) the system using pH deflections can be used to sensitively detect HCO3- output in the rat duodenum, and (b) duodenal acid neutralizing capacity may be regulated by central and peripheral cholinergic systems as well as endogenous PGs.

Neurochemical changes in the cholinergic system of the rat lateral vestibular nucleus following hemilabyrinthectomy

The neurochemistry of the cholinergic system in the lateral vestibular nucleus (LVN) of the hemilabyrinthectomized rat was studied in view of the previous findings of other research showing that the process of vestibular compensation (VC) following hemilabyrinthectomy can be influenced by the administration of cholinergic agents. At 15 min, 2 h, and 7 days after right hemilabyrinthectomy, animals were killed and the LVNs were removed from sections of the brain stem for various neurochemical measurements. The content of acetylcholine (ACh) and the activity of acetylcholinesterase in the LVN showed no significant changes at any time interval. In contrast, choline acetyltransferase activity decreased slightly in the nucleus on the unoperated side 15 min after the operation. These findings possibly implicate alterations in ACh synthesis in the LVN at an early stage of VC. However, there was no significant alteration in either high-affinity choline transport into the LVN or ACh release from the LVN 15 min after the operation. Furthermore, muscarinic ACh-receptor binding also showed no significant changes. These results suggest that the possible alterations in the function of cholinergic synapses in the course of VC indicated by previous pharmacological studies may take place in regions of the brain other than the LVN.

Oesophageal peristalsis in the cat: the role of central innervation assessed by transient vagal blockade.

Studies were performed on five cats to assess the role of extrinsic vagal innervation in the control of peristalsis in the smooth muscle oesophagus. Transient vagal nerve blockade was accomplished by cooling the cervical vagosympathetic nerve trunks previously isolated in skin loops on each side of the neck. Peristalsis throughout the body of the oesophagus was monitored using a continuously perfused multilumen manometry tube. Striated and smooth muscle portions of the esophagus were delineated by abolishing smooth muscle activity with atropine. Secondary peristalsis was assessed by intra-oesophageal balloon distension studies. The threshold volume for balloon-induced secondary peristalsis was lower in the smooth muscle oesophagus. Unilateral vagal blockade reduced the incidence of primary and secondary peristalsis in the striated muscle oesophagus but not in the smooth muscle oesophagus. Bilateral vagal nerve blockade abolished primary swallow-induced peristalsis and secondary peristalsis in both the smooth and striated muscle cat oesophagus. Administration of cholinergic agents or adrenergic blocking agents failed to restore secondary peristalsis in the smooth muscle oesophagus during vagal cooling. We conclude that connections to the central nervous system via the vagal nerve trunks are required for normal secondary as well as primary peristalsis in both the smooth and striated muscle portions of the cat oesophagus.

Effects of intraseptal administration of cholinergic agents on morphine-induced behavior of cats.

Behavioral effects of intraseptal administration of cholinergic agents were analysed in cats pretreated with morphine 15–20 min or 40 min earlier. Drug-induced changes were measured both quantitatively (onset, duration, and frequency of behavioral items) and qualitatively (presence or absence of stereotyped and ritualized behavior patterns). Carbachol and scopolamine given 15–20 min after morphine accelerated and retarded, respectively, the normal development of the morphine syndrome: Carbachol resulted in the display of stereotyped and ritualized patterns, i.e., symptoms characteristic of cats pretreated 30–40 min earlier with morphine, whereas scopolamine reduced the frequency of the behavioral items in comparison with controls, and retarded the onset of stereotyped and ritualized patterns. Carbachol given 40 min after morphine also affected the fully developed morphine syndrome: It increased the frequency of stereotyped and ritualized patterns displayed at that time. This dose-dependent effect, mimicked by arecoline and the combination of acetylcholine and physostigmine, could be antagonized by atropine and scopolamine, which per se had no influence on the stereotyped and ritualized patterns. It is concluded that the degree of cholinergic muscarinic activity within the septal nuclei at least partly determines the genesis of the morphine syndrome in cats. The data are discussed in view of the hypothesis that systemically administered morphine and intraseptally applied cholinergic agents affect the cholinergic septo-hippocampal system in a common way via distinct sites of action at the level of the septal nuclei.