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PubMed1984

Prostaglandin E2 in basal gastric secretion and during stimulation of muscarinic receptors in man. Measurements with gas chromatography--mass spectrometry.

The physiological importance of prostaglandin E2 (PGE2) biosynthesis in the gastric mucosa is unknown. A role of endogenous prostaglandins in protecting the gastrointestinal epithelia has been suggested, but the evidence is insufficient and rarely supported by concomitant measurement of PG production. Amounts of PGE2 in luminal gastric contents which can be sampled atraumatically may reflect PGE2 synthesis in the gastric mucosa in vivo. To confirm earlier reported measurements made with radioimmunoassay we have measured by gas chromatography - mass spectrometry (GC-MS) PGE2 in gastric juice of five healthy men under basal conditions and during stimulation of muscarinic receptors with iv. bethanechol which in dog is reported to enhance PGE2 output. PGE2 was detected in all basal samples. The output was in median 32.1 pmol/15 min (range 17.0-105.4, 1 pmol = 0.352 ng), which is similar to results from earlier studies. Bethanechol infusion (60 micrograms . kg-1 . h-1) did not affect PGE2 outputs systematically in spite of a significant increase in outputs of acid and chlorides. Stimulation of muscarinic receptors does not seem to influence PGE2 synthesis in gastric mucosa in vivo. Alternatively changes in PGE2 synthesis may be masked by rapid chemical or enzymatical degradation or reabsorption of PGE2. Studies are under way to explore those phenomena.

Adult↗
PubMed1987

Mechanisms involved in colonic vasoconstriction and inhibition of motility induced by neuropeptide Y.

Neuropeptide Y (NPY) and noradrenaline are suggested to coexist as neurotransmitters in sympathetic neurons. The present study investigated the mechanisms involved in the colonic vasoconstriction and inhibition of motility induced by infusion of NPY and noradrenaline close i.a. Colonic blood flow was monitored using a drop recorder, and motility was registered by a volume recording device, both operating an ordinate writer. Colonic motility was stimulated either by electrical stimulation of the pelvic nerves (PNS; 4 Hz, 5 ms, 8 V) acting via enteric ganglia or by i.v. infusion of bethanechol (10 nmol kg-1 min-1) acting directly on muscarinic receptors on smooth muscle. With both types of motility stimulation, an immediate colonic vasodilatation was registered. Electrical stimulation of the lumbar colonic nerves (4 Hz, 5 ms, 8 V) induced colonic smooth muscle relaxation and vasoconstriction during continuous PNS (P less than 0.05). Colonic contraction induced by PNS (P less than 0.01) was dose-dependently reduced by NPY (50-400 pmol min-1; P less than 0.05-0.01) and noradrenaline (1000-6000 pmol min-1; P less than 0.05-0.01). Simultaneously, vasoconstriction was induced by both NPY and noradrenaline (P less than 0.01). Colonic contraction induced by infusion of bethanechol (P less than 0.01) was not inhibited by NPY (50-200 pmol min-1). However, at the highest dose (400 pmol min-1) the motility response was reduced (P less than 0.05). Similarly, noradrenaline only at the highest dose (6000 pmol min-1) reduced the contractile response (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Substance P and vasoactive intestinal peptide influence polyamine metabolism in salivary glands of the rat.

In parotid, sublingual and submaxillary glands stimulated by continuous intravenous infusion of the neuropeptides substance P or vasoactive intestinal peptide at various doses for 3 h, the concentrations of the polyamines putrescine, spermidine, spermine and N1-acetylspermidine as well as the activity of ornithine decarboxylase were determined. This enzyme catalyses the synthesis of putrescine and is the key enzyme in polyamine formation. Vasoactive intestinal peptide induced the most marked effects, and the most conspicuous findings were made in the sublingual glands, where the ornithine decarboxylase activity was found to have increased more than 100-fold, accompanied by an increased level of putrescine in those glands which were removed immediately after the end of the infusion. When, instead, the glands were removed 5 h after the end of the infusion there was no longer any increase in the activity of ornithine decarboxylase or in putrescine concentration, but now spermidine and spermine were found to be increased. Interestingly, the parasympathetic non-adrenergic, non-cholinergic regulation of polyamine metabolism in the major salivary glands of the rat is most predominant in the sublingual glands.

Animals↗
PubMed1994

Depletion of secretory granules from the feline parotid gland: action of NANC transmitters per se.

A parotid acinar degranulation of approximately 60 and 40% was observed in cats under pentobarbitone anaesthesia after a 90-min period of continuous stimulation of the parasympathetic auriculo-temporal nerve at 10 Hz in the absence and presence of atropine, respectively. Atropine completely abolished the large fluid response of the gland to the nerve stimulation. In the non-atropinized cats, bethanechol, infused into the carotid artery at a dose rate evoking a salivary flow similar to that in response to parasympathetic nerve stimulation, caused an acinar degranulation of approximately 25% and acinar vacuolation. Vasoactive intestinal peptide (VIP; 0.5 microgram kg-1 min-1 also infused into the carotid artery for 90 min) caused an acinar degranulation of the same magnitude as the parasympathomimetic drug but the peptide did not give rise to any fluid secretion or vacuole formation. The experiments were performed in the presence of alpha- and beta-adrenoceptor blockers. Thus, in parotid glands of the cat, producing no overt secretion of fluid, non-adrenergic, non-cholinergic (NANC) mechanisms may be at work causing exocytosis of the acinar granules. These mechanisms are also likely to contribute to the secretion of granules in response to parasympathetic nerve activity in the absence of blockade of the classical autonomic receptors.

Adrenergic alpha-Antagonists↗
PubMed1988

Intracerebroventricular bethanechol chloride administration in Alzheimer's disease.

In June 1983 we began evaluating intracerebroventricular (ICV) cholinergic drug infusion in patients with biopsy-documented Alzheimer's disease (AD). An initial trial in four patients showed this treatment approach to be feasible, but objective improvement in cognitive or social function was not documented. A double-blind, placebo-controlled crossover study involving a larger number of patients has since been done. The results of this study, presented here, document a statistically significant improvement in some neuropsychological test results during periods of drug infusion. However, the degree of improvement is not sufficient to justify further treatment with the presently available drug, bethanechol chloride.

Aged↗
PubMed1988

New intrathecal drugs in Alzheimer's disease and psychometric testing.

Bethanechol chloride, a muscarinic agonist, was administered intrathecally to a sample of AD patients in double-blind crossover and open escalating-dose trials. There was a modest amelioration of disturbed behavior at a moderately high dose level, but no improvement in memory or cognition was seen at any dose. At the highest dose, cognition deteriorated. These findings, in conjunction with the results of the multicenter trial described by Harbaugh, suggest that the clinical efficacy of bethanechol in AD is limited. The disappointing results of trials with varied cholinomimetic therapies suggest that more than one biochemical abnormality is responsible for the AD dementia. The neuropeptide, somatostatin, is also reduced in AD, and the level of reduction is correlated with the degree of dementia. Manipulation of this transmitter, alone or in conjunction with acetylcholine, would appear to be a next logical step in the development of an effective neurotransmitter replacement therapy for AD. Implanted drug pumps will be needed for such clinical trials. The naturally occurring somatostatin-14 is not suitable because of its short half life. Sandostatin, an analog, is chemically stable and not metabolized by brain tissue. It does not cross the blood-brain barrier so that intrathecal administration is necessary. Pharmacological research in AD is complicated by a variety of psychometric problems including the criterion-related and construct validity of the outcome measures. Patients differ in their tolerance of various therapeutic agents and in the extent of the neurochemical pathology. It is critically important, therefore, to evaluate individual, as well as group, responses to treatment. The telephone log method may provide a useful way of generating enough observations for single subject analyses without overburdening the patient with repeated testing.

Activities of Daily Living↗
PubMed1986

Pathophysiology of equine postoperative ileus: effect of adrenergic blockade, parasympathetic stimulation and metoclopramide in an experimental model.

An experimental model of postoperative ileus was developed in ponies using trauma to, and exposure of, a length of small intestine which gave rise to a reproducible and reversible set of changes in gut activity. This was assessed by recordings of electrical and mechanical activity and by propulsion of spheres from stomach to anus. Activity was depressed, especially in the stomach and colon, and transit was slowed. All drugs given increased electromechanical activity but propranolol was the least effective and did not alter the delayed transit of spheres. Yohimbine was more effective and the addition of bethanechol produced a little extra propulsive action. Metoclopramide had the best effect, virtually returning transit to normal and was the only drug fully restoring coordination of gastric and small intestinal activity which was disrupted by the ileus procedure. Loss of gastroduodenal coordination is probably the central lesion in equine ileus and may be mediated by dopamine.

Animals↗
PubMed1984

Effect of secoverine and atropine on intestinal secretion and motor activity in the rat small intestine in-vivo.

The actions of secoverine and atropine on bethanechol-induced intestinal secretion, hypermotility and transintestinal potential difference were investigated in the rat jejunum in-vivo. Both secoverine (10(-7) mol kg-1) and atropine (1.2 X 10(-9) mol kg-1) inhibited motility at doses that did not affect secretion or transintestinal potential difference. However, secoverine was a less potent antagonist of all the bethanechol-induced changes than atropine. Increases in transintestinal potential difference were more closely related to production of fluid secretion than to increases in motility.

Animals↗
PubMed1986

Luminal acid in stress ulceration and the antiulcer action of verapamil in rat stomachs.

The role of luminal acid and the influence of the antisecretory action of verapamil in stress ulcer prevention in rat stomachs have been studied. Intraperitoneally injected verapamil, 4 mg kg-1, inhibited gastric acid secretion and ulcer formation, however, a 2 mg kg-1 dose, which did not significantly influence acid output, also had an antiulcer effect. Intraperitoneal injection of bethanechol, 1.2 or 3.6 mg kg-1, increased gastric acid output, but did not influence stress-induced ulcer formation. Oral administration of HCl, 25 or 50 mu equiv, aggravated stress ulceration in a dose-dependent manner; this lesion-worsening effect was prevented by pretreatment with verapamil or bethanechol. The gastric luminal acid content in 2 h pylorus-ligated rats was similar in the groups given either bethanechol or HCl. These findings indicate that the antisecretory action of verapamil may not account for its antiulcer effect. It is suggested that endogenous and exogenous luminal acid may have different influences on stress ulcer formation.

Animals↗
PubMed1987

Central muscarinic activation elicits compulsive drinking behaviour in the rat.

Injection of bethanechol into the lateral cerebral ventricle of the rat induces a marked increase in drinking, within 30 min from administration. The response is dose-related, maximal water intake (6.1 +/- 0.55 mL; mean +/- s.e.) occurring at 10 micrograms of bethanechol. Peripheral administration of the agonist (up to 3 mg kg-1 i.p.) fails to elicit drinking. Among several specific antagonists only antimuscarinic drugs produced a significant inhibition of the response, suggesting that the compulsive drinking behaviour in the rat is caused by activation of central muscarinic receptors. The drinking behaviour emerges as a reliable test to assess central muscarinic activity of both agonists and antagonists.

Animals↗
PubMed1989

The rat distal ileum has a reduced absorptive and secretory capacity compared with proximal ileum--is it to facilitate its chemosensing function?

Compared with the proximal ileum, the distal ileum in rat has a greatly reduced capacity for electrogenic ion secretion induced by secretagogues and for electrogenic, sodium-linked glucose transfer assessed in vitro. Similarly, in vivo, there is a great reduction in distal ileal basal fluid absorption and secretagogue-activated fluid secretion compared with proximal ileal values. This reduced absorptive and secretory capacity of the distal ileum would allow minimal changes in the concentrations of the luminal contents, facilitating its putative role as final chemosensor of the luminal contents of the small intestine.

Acetylcholine↗
PubMed1990

The effects of K+ channel blockers on ovine parotid secretion depend on the mode of stimulation.

The vascularly isolated parotid glands of sheep were submaximally stimulated for 4 min by nerve stimulation, or by infusion of acetylcholine (ACh) or bethanechol directly into the artery supplying the gland. The three modes of stimulation caused almost equal increases in the rate of salivary flow, initial losses of K+ and phosphate from the gland and total glandular deficits of K+ and phosphate. Concurrent arterial infusion of the K+ channel blocker tetraethylammonium (TEA), at 1.5-3.3 mM in blood, almost abolished these responses to bethanechol but did not alter the responses to nerve stimulation or ACh. The responses to bethanechol were restored by increasing the concentration fourfold. Concurrent arterial infusion of 4-aminopyridine (4-AP), at 0.1-2.3 mM in blood, partially inhibited the increase in salivary flow due to bethanechol but not the response to nerve stimulation or ACh. The specificity and competitive nature of the action of TEA and 4-AP on responses to direct muscarinic stimulation by bethanechol are consistent with blockade of K+ channels in secretory end-piece cells. The failure of TEA and 4-AP to inhibit responses to nerve stimulation and ACh may be due to the blocking agents potentiating the release of neurotransmitter ACh. It is also possible that nerve stimulation and ACh may cause the release of a co-transmitter which bethanechol does not.

4-Aminopyridine↗
PubMed1990

Rectal electrogenic secretion--is it a putative indicator of intestinal secretory status induced by nutritional deprivation in the rat?

Intestinal secretion is enhanced by starvation in rats. The rectum from fed and 3-day-starved rats generates a basal electrogenic ion transfer (short-circuit current) in vitro which is mainly electrogenic Na+ absorption (amiloride-sensitive, 66-71%) with a small component of electrogenic chloride secretion (furosemide-sensitive, 14-22%). Bethanechol, a muscarinic agonist, caused an increase in the short-circuit current (mainly furosemide-sensitive chloride secretion) and potential difference in rectums from both fed and starved rats but the respective values for the starved animals were 100% and 64% greater. In starvation, the rat rectum is an indicator of intestinal secretory status. The result warrants investigation of human rectal electrogenic secretion in nutritional deprivation.

Absorption↗