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PubMed2002

Atropine-induced gastric dysrhythmia is not normalized by electroacupuncture.

Acupuncture has been shown to improve the regularity of gastric myoelectric activity. The aim of this study was to evaluate whether atropine-induced gastric dysrhythmia can be normalized by electroacupuncture. Fifteen healthy male volunteers were enrolled for this study. Each subject was studied for three sessions in a randomized sequence which included electroacupuncture on the Zusanli (St 36) points with or without premedication with atropine and a placebo stimulation on a nonacupoint. Cutaneous EGG was performed for 30 min at the baseline, 30 min during acupuncture, and for an additional 30 min after acupuncture. Serum gastrin, motilin, and human pancreatic polypeptide (hPP) levels were also measured. When applying 2 Hz of electrical stimulation on the Zusnali point, there was a significant increase in the percentage of normal frequency (2-4 cpm) during acupuncture (baseline versus acupuncture, 82.09 +/- 12.37% versus 93.08 +/- 8.17%, P < 0.01). There was a significant decrease in the percentage of bradygastria as well as tachygastria during 2 Hz of electrical stimulation on the Zusnali point. Using intravenous atropine immediately before electroacupuncture, the percentage of normal frequency during acupuncture and postacupuncture periods decreased significantly (baselines versus acupuncture and postacupuncture, 83.86 +/- 13.79% versus 55.07 +/- 29.44% and 56.76 +/- 33.44%, P < 0.01). There was a significant decrease in serum PP after intravenous atropine. This observation indicated that atropine-induced gastric dysrhythmia might be mediated partly via the vagal pathway. However, atropine-induced gastric dysrhythmia is not normalized by electroacupuncture.

Adult↗
PubMed1988

Long-term atropine treatment lowers the efficacy of carbachol to stimulate phosphatidylinositol breakdown in the cerebral cortex and hippocampus of rats.

The effect of long-term treatment with atropine, a muscarinic antagonist, known to cause up-regulation of receptor numbers, was examined on the muscarinic-receptor-mediated stimulation of phosphoinositide breakdown in the rat cerebral cortex and hippocampus. Although the numbers of both M1 muscarinic receptors, as measured by [3H]pirenzepine binding, and M1 and M2 receptors increased in both brain regions, the maximal breakdown of myo-[3H]inositol-labelled phosphoinositides was unaltered in the presence of carbachol at a saturating concentration (10(-2) M). In fact the efficacy of carbachol was decreased in slices from atropine-treated cerebral cortex [EC50 (concentration producing half-maximal effect) = 93 microM] as compared with the saline-treated control (EC50 = 23 microM)(P less than 0.005). Similarly the EC50 value (23 microM) in hippocampal slices from saline-treated rats increased in atropine-treated rats to 126 microM (P less than 0.005). This lowered efficacy of muscarinic stimulation could not be explained in terms of residual atropine in the tissue from treated rats. The noradrenaline- or serotonin (5-hydroxytryptamine)-stimulated breakdown or the K+ potentiation of the muscarinic-receptor-stimulated breakdown of [3H]phosphoinositides was not affected by the atropine treatment. Chromatography of the released [3H]inositol phosphates shows that atropine treatment did not cause any qualitative change in the pattern of [3H]inositol phosphates released by carbachol stimulation.

Animals↗
PubMed1982

Effect of atropine on alveolar gas mixing in man.

1. Atropine is known to diminish bronchomotor tone. In order to investigate the acute effect of atropine on respiration and alveolar gas mixing, a dose of 2.4 mg was given intravenously. 2. Ten normal male volunteers were each studied three times with a nitrogen washout method, once before administration of atropine and then 20 min and 60 min thereafter. 3. After the administration of atropine there was a reduction in tidal volume, a slight increase in frequency of respiration and an increase in series dead space. The tidal mixing volume showed a fall of 25%. In spite of the reduced alveolar dead space the effective mixing volume fell by 29%. Multi-breath alveolar mixing efficiency fell by 3.5%. 4. Multi-breath alveolar mixing efficiency was found to be less with smaller tidal mixing volumes, a fall of 518 ml in the latter causing a reduction of 17.2% in mixing efficiency. 5. A reduction of 100 ml in tidal volume in normal subjects was associated with a decrease of 6.9% in alveolar mixing efficiency. In the subjects receiving atropine tidal volume reduced by 96 ml, but the observed fall in alveolar mixing efficiency was only 3.5%, This suggests an improvement in alveolar mixing of 3.4% due to the administration of atropine. Despite this small improvement, the mixing efficiency is still only 66%. The residual inefficiency of 34% cannot therefore be explained on the basis of bronchomotor tone.

Adult↗
PubMed2002

Vecuronium bromide, phenylephrine and atropine combinations as mydriatics in juvenile double-crested cormorants (Phalacrocorax auritus).

Topical vecuronium bromide (Norcuron) and combinations with atropine and phenylephrine, were evaluated as mydriatics in juvenile double-crested cormorants (Phalacrocorax auritus). Nine cormorants were treated with each of four protocols: 1% atropine; 4 mg/mL vecuronium bromide (total 0.16 mg/eye); atropine with vecuronium; and atropine, 2.5% phenylephrine, followed by vecuronium. Drugs were applied topically at 15-min intervals (0.01 mL/drop). Pupil diameter was measured manually every 15 min with a pupil gauge calibrated to the nearest 0.5 mm. No effect was observed with atropine alone. Average +/- SD peak pupil diameter for vecuronium, atropine/vecuronium, and atropine/phenylephrine/vecuronium were 5.4 +/- 1.1 mm, 5.7 +/- 0.8 mm and 6.2 +/- 0.4 mm, respectively; and duration of peak diameters were 38 +/- 28 min, 79 +/- 71 min and 103 +/- 58 min, respectively. The combined atropine, phenylephrine and vecuronium provided the most consistent dilation with larger average pupil size and longer average duration. No side-effects from vecuronium were observed in these birds.

Animals↗
PubMed1998

Inhibitory effects of propiverine, atropine and oxybutynin on bladder instability in rats with infravesical outlet obstruction.

OBJECTIVE: To compare the inhibitory effects of propiverine HCl(BUP-4) with those of atropine and oxybutynin on the detrusor instability induced by partial obstruction of the bladder neck of female rats. MATERIALS AND METHODS: Partial obstruction was created using partial ligation of the proximal urethra in 20 female Sprague-Dawley rats. Both the obstructed rats and a control group of 15 rats were evaluated cystometrically about 6 weeks later and the values compared both baseline and after injection with BUP-4, atropine or oxybutynin. During cystometry, the bladder capacity (BC), residual volume (RV), compliance and frequency of spontaneous activity (SA) were determined. RESULTS: The BC, RV and frequency of SA were significantly increased, and compliance markedly decreased, in obstructed compared with normal rats. The micturition pressure was significantly decreased only after injection with BUP-4 in both normal and obstructed rats. For both, the BC was increased significantly after injection with atropine or BUP-4 (P < 0.05), with the increase greater after BUP-4 than after atropine in both groups (P < 0.01). After injecting BUP-4, the RV was significantly increased in both groups (P < 0.05); atropine increased the RV only in normal rats (P < 0.01) and oxybutynin had no significant effect on RV. Increases in compliance after the administration of each drug were significant only in obstructed rats (P < 0.01) and were markedly higher after oxybutynin (780%) than after the other drugs (180-250%). The frequencies and amplitude of SA after injection with each drug were significantly lower only in obstructed rats, but in these rats, there were no significant differences in this reduction after injecting oxybutynin or BUP-4, whereas they were significantly greater after injecting oxybutynin than after atropine. CONCLUSION: Partial bladder outlet obstruction successfully created a hyperactive (unstable) bladder, typified by increased BC, RV, frequency of SA and a marked decrease in compliance. The greater BC, lower MP and frequency and amplitude of SA were prominent after the administration of BUP-4. Thus it is suggested that BUP-4 effectively inhibited bladder instability in rats induced by infravesical outlet obstruction and was more effective than oxybutynin in increasing BC.

Animals↗
PubMed2003

The influence of diazepam on atropine reversal of behavioural impairment in dichlorvos-treated rats.

Acute effects on the behaviour of the organophosphate insecticide dichlorvos and its standard antidotes possessing behavioural activity, atropine and diazepam, were studied separately and in combinations in male Wistar rats. In the spontaneous locomotor activity test, dichlorvos and diazepam decreased, whereas atropine increased performance. The effect of dichlorvos was obtained at a dose (5 mg/kg) that induced overt intoxication, and could not be reversed during first half hour-period after administration of any combination of drugs. In the other two tests, active avoidance learning and rotarod performance, the effective dose of dichlorvos (2 mg/kg) was devoid of somatic signs of intoxication. In these more sensitive tests, the effective atropine dose (40 mg/kg) completely reversed dichlorvos-induced incapacitation. In the rotarod test, diazepam (0.5 mg/kg) contributed to the incapacitating effect of dichlorvos, and impeded desirable influence of atropine as well. In the active avoidance test, diazepam (2.5 mg/kg) contributed to failure to escape; it did not influence the dichlorvos-induced decrease of avoidance performance, nor did it impair the completely reversing effects of atropine. The results point to the possible summation of acute incapacitating effects of organophosphates and diazepam on motor performance, which seems to be, at least partly, antagonized by sufficiently high doses of atropine. However, taking into account the long-term neuroprotective role of the anticonvulsant diazepam, and hence its delayed beneficial influences on behaviour, the immediate testing of atropine/diazepam treatment of organophosphate intoxication in active avoidance paradigm could possess beside sensitivity the predictive value as well.

Animals↗
PubMed2002

[Bronchoscopy and rhythmic disorders. Premedication with atropine-sulfate, as a rule?].

Ikeda has introduced flexible bronchoscopy in the seventies of the last century. Since then the over one hundred year old procedure of direct airways inspection has widely spread and enhanced the diagnostic and therapeutic means. Thus the flexible bronchoscopy has become an important part of modern medicine. The close combination of atropine as premedication with bronchoscopy is justified with the terms "cardioprotection" and reduction of mucus secretion. As there is to this date no controlled study to prove this assumption, with the start of bronchoscopy we controlled every patient with a holter-ecg for 24-hours and estimated semiquantitatively the mucus secretion during procedure by a four point scale. Consecutively 55 patients could be randomised, 25 (7 females, 18 males) in the group with and 30 (7 females, 18 males) without atropine. In the records there were no detectable significant differences between the groups with atropine (A) and without atropine (P), as well as for registered bradycardias (A: 0 vs. P: 0, minimum of heart beats A: 63.8 vs. P: 74.1 min -1) as well as for alterations of heart rhythms, e. g. SVES (A: 7.3 % vs. P: 5.5 %), VES (A: 9.0 % vs. P: 9.0 %) or a combination of SVES with VES (A: 12.7 % vs. P: 10.9 %). The same results could be seen for each single of the first twenty minutes, additionally the first and the second recorded hour and the whole registered 24 hours. Moreover the times needed to complete the bronchoscopy showed no significant difference (mean of t A: 16.8 vs. P: 15.6 min, t-minimum 10 vs. 10 min, t-maximum A: 30 vs. P: 35 min). The same absence of differences was seen in estimated endobronchial mucus secretion (mean A: 1.88 vs. P: 2.0). According to these results of our studied group, there are no reasons, why a premedication with atropine in flexible bronchoscopy in local anaesthesia should be used. Even without the administration of atropine, flexible bronchoscopy could be performed as a safe and sophisticated method in direction of not inducing relevant arrhythmia, with low impact on patients.

Arrhythmias, Cardiac↗
PubMedDate not supplied

Use of atropine in patients with submaximal heart rate during exercise myocardial perfusion SPECT.

BACKGROUND: Failure to reach 85% of maximal predicted heart rate (MPHR) during exercise may render a myocardial perfusion single photon emission computed tomography (MPS) study nondiagnostic for ischemia detection. Although commonly used to increase heart rate (HR) during dobutamine stress, the administration of atropine for patients failing to achieve 85% of MPHR during exercise performed for MPS is still infrequent. METHODS AND RESULTS: Patients undergoing dual-isotope MPS were considered candidates for the study when, during exercise treadmill testing, they had less than 85% of MPHR and were unable to continue because of fatigue, without an ischemic response. Forty-seven patients (aged 65.3 +/- 12.5 years, 78.7% men) received atropine (0.6-1.2 mg). Maximal HR achieved before and after atropine was 118.0 +/- 14.8 beats/min (76.3% +/- 6.2% of MPHR) and 146.4 +/- 12.6 beats/min (94.4% +/- 8.1% of MPHR), respectively (P < .001). Of patients, 44 (93.6%) reached at least 85% of MPHR after atropine and had diagnostic MPS studies. After atropine, arrhythmias occurred in 14 patients (29.8%) and other minor side effects in 1 (2.1%). CONCLUSIONS: Atropine allows patients initially failing to achieve 85% of MPHR during exercise to increase HR and have a diagnostic MPS study, without major complications. It may provide an alternative to pharmacologic stress for patients with a blunted HR response to exercise.

Aged↗
PubMed2006

Prevention of myopia progression with 0.05% atropine solution.

AIM: The aim of this study was to evaluate the efficacy of 0.05% atropine solution for controlling myopia progression in school-aged children. RESULTS: This retrospective, case-control study enrolled myopic school-aged children who had presented at Kaohsiung Chang Gung Memorial Hospital (Kaohsiung, Taiwan) from 2001 to 2004. A group of 57 children (30 boys, 27 girls; 6-12 years of age) with regular follow-up was divided into a subgroup of 21 children (12 boys, 9 girls) who received atropine eyedrops (0.05%) every evening, and a subgroup of 36 children (18 boys, 18 girls), who remained untreated, served as controls. The changes in refractive status of 114 eyes in 57 children were collected and compared for patients treated with 0.05% atropine eyedrop and those without medical control. The initial spherical equivalent of refractive status range was between -0.5 and -5.5 D. Mean myopia progression for the group of patients treated with 0.05% atropine eyedrop (n = 21) was -0.28 +/- 0.26 D/year, significantly lower than that of the control group of -0.75 +/- 0.35 D/year (36 patients; P < 0.001). The 0.05% atropine group had a significant lower ratio of uncontrolled myopia, that progressed greater than -0.50 D in 1 year, relative to the controls (16.7% versus 77.8%; P < 0.001). CONCLUSIONS: The results of this study demonstrate that, with regular instillation, topical 0.05% atropine is an effective agent for controlling myopia progression in a majority of school-aged children for at least a period of 1 year.

Atropine↗
PubMed2004

Haemodynamic effects of remifentanil in children with and without intravenous atropine. An echocardiographic study.

BACKGROUND: Remifentanil is known to cause bradycardia and hypotension. We aimed to characterize the haemodynamic profile of remifentanil during sevoflurane anaesthesia in children with or without atropine. METHODS: Forty children who required elective surgery received inhalational induction of anaesthesia using 8% sevoflurane. They were allocated randomly to receive either atropine, 20 microg kg(-1) (atropine group) or Ringer's lactate (control group) after 10 min of steady-state 1 MAC sevoflurane anaesthesia (baseline). Three minutes later (T0), all children received remifentanil 1 microg kg(-1) injected over a 60 s period, followed by an infusion of 0.25 microg kg(-1) min(-1) for 10 min then 0.5 microg kg(-1) min(-1) for 10 min. Haemodynamic variables and echocardiographic data were determined at baseline, T0, T5, T10, T15 and T20 min. RESULTS: Remifentanil caused a significant decrease in heart rate compared with the T0 value, which was greater at T20 than T10 in the two groups: however, the values at T10 and T20 were not significantly different from baseline in the atropine group. In comparison with T0, there was a significant fall in blood pressure in the two groups. Remifentanil caused a significant decrease in the cardiac index with or without atropine. Remifentanil did not cause variation in stroke volume (SV). In both groups, a significant increase in systemic vascular resistance occurred after administration of remifentanil. Contractility decreased significantly in the two groups, but this decrease remained moderate (between -2 and +2 sd). CONCLUSION: Remifentanil produced a fall in blood pressure and cardiac index, mainly as a result of a fall in heart rate. Although atropine was able to reduce the fall in heart rate, it did not completely prevent the reduction in cardiac index.

Adjuvants, Anesthesia↗
PubMed1975

Electrophysiology of atropine.

The effect of atropine on the refractory periods of the human atrium, A-V node, and His-Purkinje system was studied. The A-V node in man appears more sensitive to atropine than the atria as evidenced by a reduction in the effective and functional refractory periods of the A-V node without alteration of atrial conduction. Although atropine does not directly alter the refractory periods of the His-Purkinje system, atropine-induced facilitation of A-V nodal conduction results in block of premature atrial impulses in the His-Purkinje system, demonstrating an indirect effect of atropine on His-Purkinje conduction. Rarely, atropine may precipitate re-entrant atrial tachycardia (one patient) through facilitation of A-V nodal conduction.

Adult↗
PubMed1997

Intramuscular atropine sulfate in children: comparison of injection sites.

In children undergoing inhaled induction of anesthesia with halothane who suffer bradycardia, submental glossal injection of atropine may result in more rapid onset of vagolysis than traditional intramuscular sites. We compared the intervals between injection and onset of heart rate acceleration (tHR increases) after intramuscular injection of atropine into the deltoid, vastus lateralis, and glossa in children between 1 mo and 10 yr of age scheduled for elective surgery. The tHR increases was determined by measuring the interval between atropine injection and the time point at which the slope of the heart rate curve initially became positive. To ensure that the drug had taken effect before surgical stimulation, heart rate observation was continued until it increased at least 5% above baseline with evidence of continuing acceleration. Anesthesia was induced in all subjects by mask with nitrous oxide and halothane. After tracheal intubation, constant inspired concentrations of the anesthetics were administered for 3 min. While heart rate was monitored, atropine (0.02 mg/kg) was injected into one of the three sites. Each patient's end-tidal anesthetic concentrations were recorded, and minimum alveolar anesthetic concentrations (MAC) were subsequently calculated and adjusted for age. The tHR increases was recorded and averaged for each group. The study groups did not differ by age, weight, end-tidal anesthetic concentrations, age-adjusted MAC, or heart rate at the time atropine was administered. After submental glossal injection (n = 11), tHR increases increase was fastest (3.0 +/- 1.1 min) and was significantly faster than that found with deltoid injection (n = 16; 4.4 +/- 1.1 min) or vastus lateralis injection (n = 8; 6.4 +/- 2.4 min) (P < 0.05 compared with both). The tHR increases also differed significantly between the deltoid and the vastus lateralis (P < 0.05). We conclude that submental glossal injection of atropine results in a more rapid onset of vagolysis than injection at traditional intramuscular sites.

Anesthesia, Inhalation↗
PubMed1995

Modulation of the relationship between amylase and chymotrypsinogen secretion in atropine- and MK329-infused rats.

We demonstrated previously in ad libitum fed and fasted rats that chymotrypsinogen and amylase secretions were weakly or not at all correlated (1). However, the mechanisms controlling these correlations remain undetermined. We investigated the influences of cholinergic and cholecystokinin-related systems on the relationship between amylase and chymotrypsinogen in rats. Animals provided with pancreatic, biliary, duodenal, and jugular vein cannulas were kept in restraint cages under controlled temperature and humidity, with a regular 12-h light cycle, and divided into five groups. The first group of fed rats was constantly infused with 200 micrograms kg-1 h-1 atropine, the second with 0.5 mg kg-1 h-1 MK329, and the third with both. In the group in which both drugs were simultaneously infused, 500 micrograms kg-1 h-1 atropine was intraperitoneally administered, whereas MK329 was infused by intravenous cannula. Two groups consisted of fasted rats, of which one was also atropinized (100 micrograms kg-1 h-1). Three-day experiments were performed separately with fed rats, and 2-day experiments with fasted rats; atropine and/or MK329 infusion was constant over 48 h, in both fed and fasted rats. Atropine alone did not alter the correlation between enzymes even though the total protein and amylase outputs decreased, whereas the chymotrypsinogen output increased; MK329, slowly but significantly, increased the correlation between enzymes, whereas it decreased the outputs for all secretory parameters. When both antagonists were simultaneously infused in fed rats, correlation coefficients between amylase and chymotrypsinogen rapidly and markedly increased. In fasted rats, atropine infusion induced a tremendous decrease in total protein and amylase mean outputs but a significant increase in chymotrypsinogen output, without any significant change in the correlation between both enzymes. These results indicate that the nonparallel secretion of amylase and chymotrypsinogen is strongly modulated by a cholecystokinin-dependent mechanism and that this modulatory process is potentiated by the parasympathetic system.

Amylases↗
PubMed1997

Atrioventricular block after administration of atropine in patients following cardiac transplantation.

BACKGROUND: Atropine is widely used as a parasympatholytic agent during diagnostic and therapeutic procedures. We observed an unexpected paradoxical response to atropine after cardiac transplantation. METHODS: In a study investigating the occurrence of autonomic reinnervation after cardiac transplantation, atropine, at 0.015 mg/kg body weight, was given intravenously to 23 patients (mean age, 56+/-8 years) 98 days to 6.4 years after transplantation. RESULTS: Two patients experienced a witnessed syncope 40 and 150 min after administration of atropine. Second-degree atrioventricular (AV) block was documented in the first patient immediately afterward, and third-degree AV block was seen on 24-hr electrocardiogram monitoring in the second patient. A third patient developed documented AV block 15 min after atropine but experienced no sequelae because of a previously implanted pacemaker. CONCLUSIONS: Although the underlying mechanism is not clear, these findings suggest that atropine may paradoxically cause high-degree AV block in patients after transplantation. Accordingly, it should be used with caution and appropriate monitoring in these patients.

Adult↗
PubMed1984

Comparison of atropine and glycopyrronium in patients with pre-existing cardiac disease.

The effects of atropine and glycopyrronium, when given intravenously with neostigmine during the reversal of neuromuscular blockade in patients with cardiovascular disease, were compared in a double blind trial. Atropine was associated with a significantly greater elevation of heart rate and rate-pressure product than glycopyrronium. This elevation was also more sustained with atropine. The entire atropine population also showed a significantly greater incidence of ST-segment depression on the electrocardiogram than that observed in those who had received glycopyrronium. Furthermore, patients with ischaemic heart disease and previous myocardial infarction who received atropine showed a significantly greater incidence of dysrhythmias than those given glycopyrronium. It is suggested that at the time of reversal of neuromuscular blockade in patients with cardiovascular disease, glycopyrronium is a more suitable agent than atropine.

Aged↗
PubMed1988

Evaluation of the antimuscarinic activity of atropine, terfenadine and mequitazine in healthy volunteers.

1 The anticholinergic effects of atropine and two antihistamines (terfenadine and mequitazine) were investigated vs placebo in a double-blind study. 2 Salivary secretion, basal pupil diameter, pilocarpine (0.25%) induced miosis and heart rate were determined in eight healthy volunteers, seven male and one female, aged between 23 and 35 years. Each volunteer received all four separate courses of treatment: i.e. terfenadine 60 mg or mequitazine 5 mg twice daily for 3 days, and one single dose on the day of the trial; for the placebo or atropine courses they received the placebo twice daily during 3 days and, on the morning of test day, either the placebo again or atropine 1 mg. Pupillary diameter was measured under standardized conditions using a pupil gauge (Smith and Nephew Pharmaceuticals Ltd). 3 Atropine significantly reduced salivary output (-2.25 +/- 0.36 ml from control values of 4.17 +/- 0.42 ml, P less than 0.001) and heart rate (-9.7 +/- 3.7 beats min-1 from 77.5 +/- 2.7, P less than 0.05). These maximal effects were observed 3 h after atropine dosing for salivary secretion and 1 h for heart rate. Atropine did not affect basal pupil diameter or pilocarpine-induced miosis. 4 Mequitazine and terfenadine did not affect salivary flow, heart rate or pilocarpine-induced miosis. 5 Terfenadine and mequitazine had no anticholinergic effect in these tests involving a limited number of subjects.

Adult↗
PubMed1971

Stimulating action of atropine on the release of acetylcholine by rat cerebral cortex in vitro.

1. In cortical slices from rat brain incubated in a medium containing the irreversible cholinesterase inhibitor, soman (0.005 mM) and a high concentration of KCl (25 mM), atropine exerts a stimulating action on the release of acetylcholine (ACh).2. Two possible explanations for this action were examined. Atropine might expel ACh from the nerve endings by occupying its storage sites or it might prevent an inhibitory action of the released ACh on its further release by occupying muscarinic receptors at the presynaptic endings; its action would then be a kind of ;disinhibition.'3. The stimulating action of atropine on ACh release persisted during prolonged incubation (up to 3.5 h) provided choline was added to the medium. This finding would be difficult to explain if atropine acted by expelling ACh from its storage sites.4. The stimulating action of atropine on ACh release was inhibited by oxotremorine and by methacholine, added to the medium in high concentrations. This finding is readily explained if atropine acts by ;disinhibition.'

Acetylcholine↗
PubMed1994

Tachykinin NK1 and NK2 receptor antagonists and atropine-resistant ascending excitatory reflex to the circular muscle of the guinea-pig ileum.

1. The aim of this study was to investigate the effect of various antagonists, selective for the tachykinin NK1 or NK2 receptor, on the atropine-resistant ascending excitatory reflex (AER) to the circular muscle of the guinea-pig ileum elicited by radial stretch (balloon distension) or electrical field stimulation. 2. Submaximal and maximal atropine- (1 microM) resistant AER elicited by balloon distension averaged about 40-50% and 70-90% of maximal circular spasm to 80 mM KCl, respectively. The NK1 receptor antagonist, (+/)-CP 96,345 (1 microM) inhibited both maximal and submaximal AER. FK 888 (1-3 microM) inhibited submaximal AER only. RP 67,580 (1 microM) was ineffective. The NK2 receptor antagonist, GR 94,800, inhibited both maximal and submaximal AER at all concentrations tested (0.1-3.0 microM), while SR 48,968 was effective only at 1.0 microM. The NK2 receptor antagonists, MEN 10,376 and MEN 10,573 inhibited both submaximal and maximal AER at 10 and 1.0 microM, respectively. 3. In other experiments, an NK1 receptor antagonist, (+/-)-CP 96,345 or FK 888 (1.0 microM in each case) was administered first and the effect of GR 94,800 (1.0 microM) on the residual AER response was determined; or GR 94,800 was administered first and the effect of (+/-)-CP 96,345 or FK 888 was determined. The results of these experiments indicated an additive effect produced by the combined treatment with NK1 and NK2 receptor antagonists. 4. Electrical field stimulation (10 Hz for 0.5 s, 10-20 V, 0.15-0.3 ms pulse width) with electrodes placed at 1.4-1.8 cm anal to the recording site, produced ascending contractions which were almost abolished by 10 MicroM hexamethonium (electrically-evoked AER). In the presence of apamin (0.1 MicroM) and N0-nitro-L-arginine (30 MicroM) these contractions were reproducible over 10 consecutive stimulation cycles.GR 94,800 (1 MicroM) and FK 888 (1 MicroM) both produced a partial inhibition of the electrically-evoked AER and their combined administration produced an inhibitory effect which was larger than that induced by each antagonist alone.5. FK 888 (1-3 MicroM), GR 94,800 (1-3 MicroM), MEN 10,573 (1 MicroM) and MEN 10,376 (10 MicroM) did not significantly affect the atropine-sensitive twitch contractions produced by electrical field stimulation of the guinea-pig ileum longitudinal muscle-myenteric plexus preparation, which were abolished by 10-30 MicroM procaine, 1 MicroM tetrodotoxin or 1 MicroM atropine. (+/-)-CP 96,345 (1 MicroM) and SR 48,968 (1 ILM)produced 12% and 27% inhibition of cholinergic twitches in the longitudinal muscle of the ileum,respectively.6. We conclude that both NK1 and NK2 receptors mediate the atropine-resistant AER to the circular muscle of the ileum. NK2 receptor activation plays a more important role than NK1 receptor activation in the AER evoked by radial stretch. Since a consistent fraction of the distension- and electrically evoked atropine-resistant AER persists in the presence of combined NK1 and NK2 receptor blockade,the existence of a third excitatory transmitter to the circular muscle of the ileum, in addition to acetylcholine and tachykinins, is suggested.

Animals↗