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At least 181 records · Page 10Linked to original sources
PubMed1993

Beta-receptor responsiveness after desipramine treatment.

To examine whether a tricyclic antidepressant affects the functional response to a beta-receptor agonist in man, the response of heart rate, blood pressure, and plasma cAMP to isoproterenol was measured in 14 normal controls taking 75 mg desipramine daily. Desipramine significantly increased the bolus dose of isoproterenol needed to increase heart rate by 25 bpm at 14-30 days but not at 3-8 days. During infusions of isoproterenol, the increase in systolic blood pressure was blunted at both 3-8 days and 14-30 days, while the decrease in diastolic blood pressure was unaffected. Blood pressure findings were not affected by preadministration of bethanechol. In ten controls, isoproterenol infusions increased plasma cAMP, but this was unaffected by desipramine treatment. These findings suggest a decrease in the functional response of beta 1, but not beta 2, receptors after treatment with desipramine.

Adult↗
PubMed1989

The use of anxiolytic and parasympathomimetic agents in the treatment of postoperative urinary retention following anorectal surgery. A prospective, randomized, double-blind study.

Approximately 30 percent of patients undergoing anorectal surgery will develop acute urinary retention. The cause of this complication is poorly understood. Anxiety, anal distention, bladder distention as a result of vigorous hydration during surgery, and reflex inhibition of the urinary bladder detrusor muscle secondary to pain have been postulated as contributing factors. A four-armed prospective, double-blind, randomized trial was carried out to determine whether an anxiolytic agent (midazolam, 5 mg intramuscularly) and/or a parasympathomimetic agent (bethanechol, 10 mg subcutaneously) reduce the incidence of postoperative urinary retention following anorectal surgery. One hundred thirty-two patients (ages, 18 to 50 years), in acute urinary retention 6 to 12 hours following anorectal surgery, were enrolled. Sixty-nine percent of patients responded to bethanechol. Side effects were minimal. Midazolam alone had no effect on retention. Bethanechol and midazolam in combination resulted in less retention than midazolam and a placebo (P less than 0.05). Bethanechol alone was better than a placebo (P less than 0.002). Mean intraoperative intravenous fluid volume for the entire study group was 900 cc. Initial postoperative urinary volumes of patients who failed the treatment protocol were significantly higher than in those responding to bethanechol (mean of 527 cc vs. 241 cc, P less than 0.001). The use of an anxiolytic agent was not effective in the treatment of postoperative urinary retention. Bladder distention may increase the incidence of urinary retention. Bethanechol, in a dose of 10 mg subcutaneously, significantly lowered the incidence of postoperative urinary catheterization and should be considered as initial treatment of postoperative urinary retention following anorectal surgery.

Acute Disease↗
PubMed1987

Urecholine prophylaxis for urinary retention in anorectal surgery.

A randomized prospective trial with 108 patients undergoing anorectal surgery was conducted comparing the use of Urecholine orally or subcutaneously to no treatment controls. There was no difference in postoperative urinary retention rates and caudal or general anesthesia, nor was there an earlier postoperative bowel movement with Urecholine. The volume of intravenous fluids significantly affected retention rates.

Anal Canal↗
PubMed1981

Cyclic nucleotide response to acid-secreting stimuli in guinea pig gastric mucosa in vitro.

To investigate the mechanism of intracellular transmission of three representative stimuli for gastric acid secretion, the dose-response relations of cyclic nucleotides accompanied by acid secretion stimulated by histamine, pentagastrin and bethanechol were comparatively studied using an in vitro preparation of guinea pig gastric mucosa surviving with a constant potential difference and acid secretion sensitive to amytal. The following results were obtained. (1) Both histamine- and pentagastrin-stimulated acid secretion accompanied a significant increase in cyclic AMP contents in the gastric mucosa and in the serosal solution without any increase in cyclic GMP. However, the ratio of the increase in acid secretion to that in cAMP content was significantly greater with pentagastrin than with histamine, indicating that pentagastrin exerts its acid-secreting stimulus with less increase in cyclic AMP. (2) Stimulation with bethanechol resulted in a significant increase in the mucosal cyclic GMP content without any change in cyclic AMP. From these findings, it has been concluded that the above three stimuli were transmitted differently in the target cells, presenting evidence against the common final mediator theory of histamine for gastric acid secretion.

Animals↗
PubMed1993

The role of thyrotropin-releasing hormone (TRH) in the pathogenesis of water-immersion stress in rats--inhibition of TRH release from the stomach by atropine, ranitidine or omeprazole.

The role of thyrotropin-releasing hormone (TRH) in the development of gastric erosions and ulcers induced by water-immersion stress was studied. Intraperitoneally administered bethanechol induced a decrease in the gastric wall immunoreactive TRH (ir-TRH) concentrations and an increase in gastric juice ir-TRH concentrations in a dose-related manner, while atropine induced an increase in gastric wall ir-TRH concentrations and a decrease in gastric juice ir-TRH concentrations under non-stress condition. Intraperitoneally administered omeprazole did not influence gastric wall ir-TRH concentrations but elevated gastric pH. Water-immersion stress induced a decrease in gastric wall ir-TRH concentrations and an increase in gastric juice ir-TRH concentrations with a decrease in gastric pH prior to ulcer formation. Pretreatment with atropine or ranitidine inhibited the development of stress ulcers, reduced changes in ir-TRH concentrations in the gastric wall and gastric juice, and induced an increase in gastric pH. Omeprazole inhibited stress ulcer formation and changes in gastric wall and gastric juice ir-TRH concentrations. These results suggest that TRH release from the stomach wall into gastric juice is of importance in the pathogenesis of stress ulcer and that its release is mediated by both muscarinergic and histaminergic (H2) systems. Furthermore, omeprazole has an inhibitory effect on TRH release under stress ulcer.

Animals↗
PubMed1997

The role of CGRP and afferent nerves in the modulation of pancreatic enzyme secretion in the rat.

CONCLUSION: Stimulation of pancreatic sensory nerves by capsaicin produced secretory effects probably caused, at least in part, by the release of CGRP. BACKGROUND: In the pancreas calcitonin gene-related peptide (CGRP) has been localized in the sensory nerves, but its physiological role is unknown. This study was undertaken to compare the changes of pancreatic enzyme secretion produced by CGRP and by stimulation or destruction of sensory nerves. METHODS: To stimulate sensory nerves, low doses of capsaicin (0.25-0.5 mg/kg) were given intraduodenally to the conscious rats with chronic pancreatic fistula. To inactivate sensory nerves high doses of capsaicin (100 mg/kg) were given subcutaneously 10 d before tests. For the in vitro experiments pancreatic slices and isolated pancreatic acini were prepared from intact and capsaicin-denervated rats. RESULTS: In conscious rats, CGRP given subcutaneously (5-10 micrograms/kg) and low doses of capsaicin given intraduodenally reduced basal pancreatic secretion. In isolated pancreatic acini, CGRP (10(-10)-10(-6) M), but not capsaicin, increased basal or secretagog-stimulated amylase release. In pancreatic slices (containing nerve fibers) capsaicin (10(-10)-10(-6) M) increased enzyme secretion, and this secretion was abolished by previous inactivation of sensory nerves by this neurotoxin. Capsaicin deactivation did not affect the secretory response of pancreatic acini to CGRP, cerulein, or urecholine. Sensory denervation by capsaicin did not change basal protein secretion, but reduced that produced by feeding or diversion of pancreatic juice to the exterior during first 2 h of the tests.

Amylases↗
PubMed1987

Subtypes of muscarinic receptors in canine pancreatic secretion in vivo and in vitro.

In conscious dogs with esophageal, gastric and pancreatic fistulae, sham-feeding and meat feeding increased the pancreatic protein secretion to a peak, reaching about 39% and 69% of CCK8 maximum, and raised plasma pancreatic polypeptide (PP) levels. Pirenzepine given intravenously (i.v.) (30 nmol.kg-1 or 3 mumol.kg-1) reduced dose-dependently the pancreatic protein and plasma PP responses to sham-feeding and meat feeding, being about 100 times less potent as an inhibitor than atropine. Neither pirenzepine nor atropine affected near-maximal pancreatic bicarbonate and protein responses to secretin (164 pmol.kg-1.h-1) and CCK8 (170 pmol.kg-1.h-1), but both antimuscarinic agents significantly inhibited pancreatic responses to lower doses of these secretagogues. When added to the incubation medium of dispersed canine pancreatic acini, pirenzepine reduced dose-dependently the amylase responses only to urecholine, and not to CCK or gastrin, being about 1000 times less potent as an inhibitor than atropine. This report provides an evidence that pirenzepine inhibits pancreatic secretion in a similar manner to atropine, but that pirenzepine, in both in vivo and in vitro studies, is 2-3 orders of magnitude less potent as an inhibitor than atropine, indicating that the muscarinic pathway of the exocrine pancreas has a low affinity for pirenzepine and may thus involve M2-receptors.

Amylases↗
PubMed1988

Effects of peptide YY on dog and rat pancreatic secretion in vivo and in vitro.

The action of peptide YY (PYY) on exocrine pancreatic secretion in dogs and rats was compared in in vivo and in vitro studies. PYY infused i.v. in the physiological dose range (125-1000 pmol/kg.h) reduced in a dose-dependent manner the pancreatic protein response to caerulein and suppressed basal and meat feeding or duodenal oleate-induced pancreatic secretion in conscious dogs. Both meat feeding and duodenal oleate caused significant elevation of plasma PYY levels and these showed several-fold increase during infusion of exogenous PYY (500 pmol/kg.h) inducing significant inhibition of the postprandial or oleate-stimulated pancreatic secretion. PYY in a dose range of 2.5-40 nmol/kg.h also inhibited the response to caerulein in conscious rats but failed to prevent the increment in the postprandial protein secretion in this species. PYY added in various concentrations (10(-11)-10(-6) M) to the incubation medium of the isolated dog and rat pancreatic acini failed to affect basal or caerulein- and urecholine-stimulated amylase release. This study shows that PYY is an effective inhibitor of the pancreatic secretion in vivo but not in vitro suggesting that the inhibition is mediated by an indirect mechanism.

Amylases↗
PubMed1995

The involvement of endogenous nitric oxide in vagal-cholinergic stimulation of exocrine and endocrine pancreas in dogs.

Previous studies showed that nitric oxide (NO), synthesized from L-arginine (L-arg) by NO synthase (NOS) in vascular epithelium and nerve terminals, affects exocrine pancreatic secretion, but its role in control of endocrine pancreas has not been studied. In this study, the role of NO in the control of pancreatic secretion in response to vagal-cholinergic stimulation and duodenal infusion of nutrients was determined in conscious dogs with chronic pancreatic fistulas. Sham feeding (SF), urecholine iv infusion, and duodenal perfusion with nutrients were used to stimulate the pancreatic protein secretion, and insulin and glucagon release in tests without and with iv infusion of NG-nitro-L-arginine (L-NNA), an inhibitor of NO synthase, L-arg, a substrate of NOS, or their combination was used. SF, urecholine, and duodenal nutrient resulted in the stimulation of pancreatic protein secretion reaching, respectively, 50, 20, and 42% of cerulein maximum. Infusion of L-arg almost doubled the basal protein secretion and tended to increase the secretory response to SF and duodenal nutrient. After infusion of L-NNA, the pancreatic secretory responses to SF, urecholine, and duodenal nutrient were inhibited by about 70, 30, and 75%, respectively. When L-arg was combined with L-NNA, the reduction in pancreatic secretion by L-NNA was significantly attenuated. SF resulted in a significant rise in plasma insulin and glucagon, and this response was completely abolished by L-NNA infusion. Urecholine and duodenal nutrient also resulted in a marked increment in plasma insulin and glucagon, the insulin (but not glucagon) increment being abolished by the pretreatment with L-NNA and reversed by the addition of L-arg.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1980

Comparison of two agents in prevention of urinary retention after benign anorectal surgery.

In an attempt to substantiate the efficacy of Urecholine and Dibenzyline in prevention of urinary retention, 263 patients who had rectal surgery for benign anorectal abnormalities were divided into three comparable groups; one group was given Urecholine, another group was given Dibenzyline in 10-mg doses orally, four and eight hours after surgery and the third group was given nothing as a control. The control group had a higher incidence of urinary retention 28.2 per cent; but Dibenzyline did not prevent urinary retention in 20 per cent of the patients and was no more effective than Urecholine at 22.4 per cent.

Anal Canal↗
PubMed1987

The effects of the antimuscarinic drugs pirenzepine and atropine on plasma portal levels of somatostatin and gastrin in the dog.

The effects of the antimuscarinic drugs pirenzepine and atropine on somatostatin and gastrin portal levels under basal conditions and during bethanechol infusion have been investigated in anesthetized dogs. Iv bolus administration of pirenzepine (1 mg/kg) or atropine (0.1 mg/kg), decreased gastrin concentrations, but did not affect basal somatostatin levels. During 120 min of bethanechol infusion (160 micrograms/kg/h) gastrin levels increased but somatostatin levels were unchanged. Pirenzepine (1 mg/kg iv bolus), administered at the 60th min of bethanechol infusion, decreased the gastrin concentrations, and markedly enhanced somatostatin levels. Under the same conditions atropine (0.1 mg/kg iv bolus) decreased gastrin levels, but had little or no effect on somatostatin levels. These results indicate that muscarinic receptors with similar affinity for pirenzepine and atropine mediate excitatory cholinergic influences on gastrin release. By contrast, muscarinic receptors with higher affinity for pirenzepine seem to be involved in the cholinergic inhibition of somatostatin release: by selectively blocking these receptors, pirenzepine may increase portal somatostatin levels.

Animals↗