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PubMed1975

Effects of atropine on natural deflation flows and P-V curves of the isolated lung lobe.

Static pressure-volume (P-V) curves and natural deflation flows (NDF) in isolated dog's lung lobes were obtained before and after atropine. Since elastic pressure was the driving force for the expiratory flow this preparation was devoid of the influence of compressive forces. A significant shift to the left of the P-V curve was observed after atropine. Mean increase in volume in the range from 30 to 2 cmH2O transpulmonary pressure (Ptp) was 0.6 ml/g (about 4% increase in percent of maximal lung volume MLV). NDF at the same Ptp (referred to as airway conductance) were significantly higher after atropine (mean increase 3 ml/s per g, about 0.15 l/s). Increase in lung volume after atropine was interpreted as evidence of relaxation of residual bronchomotor tone which in turn, by increasing airway diameters, may produce higher flows. When NDF were plotted against volume, differences between control and atropine were reduced. This was attributed to the observed leftward displacement of the P-V curve. The linear relationship found between NDF and volume in the range 2-8 cmH2O of Ptp (about 35-75% MLV) suggests a proportionate change in airway conductance with lung size. This could indicate that the lobes behaved homogeneously during passive deflation. This pattern was not modified by atropine.

Airway Resistance↗
PubMed1982

Dose-dependent inhibition of cold air-induced bronchoconstriction by atropine.

We undertook a study to demonstrate whether inhalation of atropine could inhibit cold air-induced bronchoconstriction in a dose-dependent fashion. In seven subjects with asthma we assessed the effects of placebo and of various doses of inhaled atropine (0.13-2.08 mg) on a base-line specific airway resistance (sRaw) and on the increase in sRaw produced by 5 min of voluntary eucapnic hyperventilation with subfreezing air at -17 degrees C. We also assessed the effect of the lowest doses of atropine on the increase in sRaw produced by five breaths of 1.0% metacholine. Atropine in doses of 0.13 or 0.26 mg caused a maximal reduction in base-line sRaw and completely inhibited the effect of 1.0% methacholine on sRaw, but it did not inhibit the bronchomotor response to cold air. Higher doses of atropine did inhibit the effect of cold air on sRaw in a dose-dependent fashion. The dose of atropine required to inhibit this effect of cold air varied with the increase in sRaw produced by cold air after placebo. These results suggest that cold air causes bronchoconstriction through vagal pathways and that higher doses of antimuscarinic agents are required to inhibit vagally mediated bronchoconstriction than those required to reduce base-line airway tone or to inhibit the effects of a large dose of an inhaled muscarinic agonist.

Adult↗
PubMed1983

Intravenous versus inhaled atropine for inhibiting bronchoconstrictor responses in dogs.

We studied whether the muscarinic antagonist, atropine, given intravenously or by inhalation, inhibits the bronchoconstrictor responses to inhaled acetylcholine and to acetylcholine released by electrical stimulation of the vagus nerves to the same degree. We assessed bronchoconstrictor responses in anesthetized dogs by determining the increase in total pulmonary resistance before and after increasing doses of atropine and then constructing inhibition dose-response curves. Before atropine the responses to the two stimuli were equal in magnitude. After intravenous atropine (initial dose 0.12 micrograms/kg, total dose 16 micrograms/kg) both responses were progressively inhibited to a similar degree. By contrast, after inhaled atropine (initial dose 0.02 micrograms/kg, total dose 2.4 micrograms/kg) the response to acetylcholine inhalation was inhibited to a much greater degree than the response to vagal stimulation. Thus, in studies designed to inhibit bronchoconstriction due to an inhaled muscarinic agonist to the same degree as bronchoconstriction due to a vagal reflex, atropine might better be given intravenously than by inhalation.

Aerosols↗
PubMed1988

Effect of atropine on intestinal phase of pancreatic secretion in man.

The effect of atropine on prestimulatory and Lundh-meal-stimulated pancreatic secretion and on plasma cholecystokinin (CCK) levels has been studied in 20 human volunteers. Prestimulatory secretion was lowered by infusion of atropine. From 10 to 30 min after ingestion of the Lundh meal, atropine had no effect on secretion. From 30 to 120 min, the stimulated enzyme secretion was reduced by 90% during infusion of atropine. Plasma CCK levels were not altered by atropine. Similar results were obtained when the test meal was instilled into the duodenum to exclude a delay of gastric emptying caused by atropine. These data show that cholinergic blockade does not interfere with CCK-mediated stimulation of pancreatic secretion during the first 30 min after ingestion of a meal, and that afterwards the intestinal phase is mainly under cholinergic control.

Adult↗
PubMed1975

Use of atropine in patients with acute myocardial infarction and sinus bradycardia.

Fifty-six patients with acute myocardial infarction complicated by sinus bradycardia (SB) were treated with intravenous atropine and monitored in a coronary care unit. Atropine decreased or completely abolished premature ventricular contractions (PVCs) and/or bouts of accelerated idioventricular rhythm in 27 of 31 patients (87%) and brought systemic blood pressure up to normal in 15 of 17 patients (88%) with hypotension. In addition, atropine administration was associated with improved atrioventricular conduction in 11 of 13 patients (85%) with acute inferior myocardial infarction associated with 2 degrees or 3 degrees atrioventricular block. Seven patients developed ten significant adverse effects: ventricular tachycardia or fibrillation in three, sustainedsinus tachycardia in three, increased PVCs in three, and toxic psychosis in one. These major adverse effects correlated with either a higher initial dose of atropine (i.e., 1.0 mg aa compared with the usual 0.5 or 0.6 mg) or a total cumulative dose exceeding 2.5 mg over 21/2 hours. Atropine is the drug of choice for management of patients with SB and hypotension and is effective in the treatment of ventricular arrhythmias as well as conduction disturbances in patients with inferior myocardial infarction. Serious adverse effects, however, preclude use of atropine without careful medical supervision.

Acute Disease↗
PubMed1991

Influence of inhaled atropine on lung mucociliary function in humans.

The influence of aerosolized atropine sulfate on lung airway mucus clearance was investigated in healthy human subjects who were nonsmokers. Mucus transport was measured with radiolabeled insoluble particles inhaled by mouth and deposited onto mucosal surfaces; subsequent retention of radiolabel was quantitated over a 4- to 5-h period by a noninvasive, posteriorly aligned, gamma camera. Placebo and atropine clearance tests were matched in a given subject for initial and for final (24-h postinhalation) deposition pattern of labeled aerosol at the onset and conclusion, respectively, of tracheobronchial particle clearance. In seven subjects mucociliary function was delayed after inhalation of 0.025 mg/kg body weight atropine sulfate as compared with placebo (0.9% NaCl). On the basis of the area under the activity versus time curves, retention times during atropine exceeded placebo times by more than 30% (p less than 0.01). At 90 min postatropine inhalation, the Vmax50 exceeded baseline values by 21% (p less than 0.01). Urine retention was present in one subject and xerostomia was present in all subjects after atropine. These data suggest that a single dose of atropine sulfate delivered topically to the airway surfaces delays the continuous flow of airway mucus in healthy subjects and that basal autonomic tone is an inherent factor for optimal secretion and/or removal of tracheobronchial secretions.

Administration, Inhalation↗
PubMed1989

The effect of chronic atropine treatment on salivary composition and caries in rats.

Many instances of salivary dysfunction in humans can be traced to the use of medications that have hyposalivary side-effects. In this study, atropine, a cholinergic antagonist, was administered chronically to rats by use of osmotic mini-pumps. Steady-state blood levels, similar to levels obtained in human multiple oral dosing, were thus maintained. Atropine delivered in this manner for 24 days was found to decrease protein concentration of parotid saliva (p less than 0.05) elicited by pilocarpine, and to increase smooth-surface caries scores (p less than 0.05) in rats fed a cariogenic diet. Parotid saliva collected via ductal cannulation from rats subjected to chronic atropine administration (and stimulated to secrete by pilocarpine) exhibited increased levels of two basic proline-rich proteins (Peak A and SP-3), as evaluated by SDS-PAGE, compared with those observed in saliva from controls. Cannulation of sublingual glands in animals receiving high doses of atropine produced no measurable secretion upon pilocarpine stimulation. Carbachol stimulation of dispersed cell aggregates of sublingual glands from sham-operated and high-dose atropine groups indicated that the glands responded similarly once the antagonist was washed from the system, implying that the lack of secretion in vivo was caused by antagonism of the cholinergic receptor by atropine. Our observations suggest that this model system can be exploited for determination of the effects of chronic administration of hyposalivary drugs on salivary composition and caries rates.

Analysis of Variance↗
PubMed2004

Cardiovascular autonomic regulation in preterm infants: the effect of atropine.

To study cardiovascular autonomic control, we assessed the effect of atropine on heart rate (HR) and blood pressure (BP) variability in 12 preterm infants (range 26-32 wk) before intubation for respiratory insufficiency. Spectral power analysis of R-R interval and systolic BP (SBP) series were estimated in a low-frequency (LF; 0.04-0.15 Hz) and high-frequency (HF; 0.4-1.5 Hz) band and evaluated for a 10-min period before and a 10-min period after atropine sulfate (0.01 mg/kg). Baroreceptor reflex (BR) functioning was estimated using transfer function analysis at LF (coherence, gain, and phase). Atropine resulted in a significant 12% increase in steady-state HR (p < 0.01) and unchanged SBP. For R-R interval series, the total spectral power decreased 6-fold (p < 0.01), which was predominantly due to a reduction in the LF band (16-fold; p < 0.01). In contrast, we observed a significant increase (25%; p < 0.05) in total spectral power of SBP series partly as a result of an increase in HF power. The LF power of SBP series was not altered. The median LF transfer gain (BR sensitivity) between SBP and R-R interval decreased from 4.2 to 1.4 ms/mm Hg (p < 0.01) after atropine. The LF phase relationship (BP leads R-R interval fluctuations by approximately 4 s) was not changed after atropine. In conclusion, even in preterm infants in distress, atropine modulates HR and BP variability, suggesting that BR-mediated parasympathetic control of heart rate is of significance for cardiovascular control at that age.

Atropine↗
PubMed1982

Effect of atropine on escape mechanism of the subsidiary pacemakers in patients with dysfunction of the sinus node.

Effects of intravenous atropine on postpacing impulse recovery time of the subsidiary pacemakers were studied by incremental atrial pacing in 9 patients with sinus nodal (SN) dysfunction. Patients having either or both of the following anomalies are used: 1) persistent sinus bradycardia (sinus cycle length greater than 1000 msec), or documented episodes of sinoatrial block or arrest and/or 2) maximum corrected SN recovery time of longer than 525 msec before and after atropine. Seven patients had a history of cerebral ischemic symptoms. The mean +/- SEM of the maximum A-V junctional recovery times (MJRTs) before and after atropine, measured in 5 patients, were 2,485 +/- 825 msec and 1,164 +/- 281 msec, respectively (p less than 0.01). The average percent reduction of the junctional escape times in these 5 patients was 53.2%. In all 9 patients MJRT shortened to less than 1,610 msec after atropine. Moreover, a low atrial pacemaker also was the escape mechanism following pacing in 2 patients after atropine; the maximum atrial recovery times were 2,500 msec and 1,220 msec, respectively. We conclude that atropine can markedly enhance escape mechanism of the subsidiary pacemakers in patients with SN dysfunction.

Adult↗
PubMed1978

Muscarinic cholinergic receptors in mammalian brain: differences between bindings of acetylcholine and atropine.

Studies were made on the bindings of [3H]-acetylcholine and [3H]-atropine to synaptic plasma membranes from rat brain. Synaptic plasma membranes have reversible, high affinity binding sites for both ligands, the KD values for ACh and atropine being about 20 nM and 1 nM, respectively. The maximal binding capacities for ACh and atropine, respectively, are 0.8-1.2 pmoles and about 1.5 pmoles/mg protein of synaptic membranes. The specific binding of ACh is almost completely inhibited by oxotremorine and atropine. 5,5'-Dithiobis (2-nitrobenzoic acid) (DTNB) increased the ACh-binding to about 1.5 pmole/mg protein. It also increased the inhibition of atropine-binding by ACh about 10-fold. Marked discrepancies were found in the inhibitions of atropine- and ACh-bindings by muscarinic agonists, but not in the inhibitions by antagonists. These findings support the hypothesis that muscarinic receptors have different sites for agonists and antagonists. The possibility that one receptor can be simultaneously occupied by both an agonist and an antagonist is also discussed.

Acetylcholine↗
PubMed1981

Atropine and terbutaline aerosols in chronic bronchitis: efficacy and sites of action.

To examine the additive properties and the sites of action of inhaled atropine sulfate (0.05 mg/kg of body weight) and terbutaline sulfate (0.005 mg/kg) in patients with chronic airflow obstruction, we tested these aerosols separately and together in a double-blind random sequence. Twelve patients with chronic bronchitis and perennial obstruction of airflow were studied by measuring three indices of efficacy (specific airway conductance [Gaw/VL], the forced expiratory volume in one second [FEV1] and the forced vital capacity [FVC]) and three indices of the site of action within the airway (delta [(Gaw/VL)/FEV1], the difference between the change in forced expiratory flow at 75 percent of vital capacity and the change in forced expiratory flow at 25 percent of vital capacity, and the change in density dependence of maximal airflow at 50 percent of vital capacity). Both atropine and the combination of atropine and terbutaline improved all indices of efficacy significantly more than did terbutaline. With individual exceptions, the addition of terbutaline to atropine improved Gaw/VL but not forced airflow. All measures of site of action suggested an advantage for atropine in relatively proximal airways. These results indicate that combined therapy with beta-adrenergic and anticholinergic bronchodilator drugs is marginally more effective than therapy with atropine alone in these patients and suggest that anticholinergic aerosols dilate larger airways more effectively than the beta-agonists.

Aerosols↗
PubMed2001

The use of carbamates, atropine, and 2-pyridine aldoxime methoiodide in the protection of Artemia salina against poisoning by carbophenothion.

The acute toxicity of carbophenothion to three age classes of Artemia salina was evaluated. An increase in toxicity of carbophenothion was found following longer development of A. salina. The effect of pretreatment with the nonselective muscarinic antagonist atropine, the two reversible acetylcholinesterase-inhibitors physostigmine and pyridostigmine, and the cholinesterase-reactivating oxime 2-pyridine aldoxime methochloride (2-PAM) on carbophenothion-induced lethality in 24-h-old A. salina was also investigated. The lethal action of carbophenothion was completely prevented by pretreatment of A. salina with 2-PAM. Atropine and pyridostigmine afforded a maximal protection of approximately 87% and 72%, respectively, compared to control values. In contrast, physostigmine was ineffective. The inhibitory effects of combinations of 10(-5) M atropine with physostigmine, pyridostigmine, or 2-PAM were greater than those elicited by either drug alone, with the maximum protection afforded being 92.58%, 100%, and 100%, respectively. In the presence of 10(-7) M atropine, neither pyridostigmine nor 2-PAM provided additional inhibition of the lethality compared to that with either drug alone, whereas the protection afforded by 10(-7) M atropine plus physostigmine increased as the concentration of carbamate increased (up to 10(-3) M). Pretreatment with pyridostigmine or physostigmine plus 2-PAM (10(-6) M) slightly enhanced the maximal inhibition of carbophenothion lethality compared to that with either drug alone. It is suggested that the most active combined pretreatment studied here was physostigmine plus atropine.

Animals↗
PubMed1980

The effect of atropine on secretin release and aspirated bicarbonate secretion after duodenal acidification in man.

The effect of duodenal instillation of hydrochloric acid on peripheral plasma immunoreactive secretin (IRS) concentration--without or with a constant intravenous infusion of atropine--was studied in eight healthy volunteers. Without atropine infusion, IRS increased from 1.2 +/- 0.3 pmol/l to a peak value of 17.1 +/- 4.4 pmol/l. The volume of duodenal aspirates increased from 0.74 +/- 0.12 ml/min to 5.03 +/- 0.46 ml/min, and the bicarbonate output from 7.6 +/- 1.7 mumol/min to 349 +/- 39 mumol/min. With atropine infusion (bolus of 500 micrograms + 750 micrograms/h of atropine sulphate), IRS increased from 1.4 +/- 0.3 pmol/l to 14.8 +/- 3.6 pmol/l. The volume of the duodenal aspirates increased from 0.71 +/- 0.08 ml/min to 2.76 +/- 0.37 ml/min and the bicarbonate output from 4.0 +/- 1.6 mumol/min to 142 +/- 33 mumol/min. The integrated IRS response to acidification was 18% lower during atropine infusion (p < 0.05). Both the aspirated flow rate from the duodenum and the bicarbonate output were markedly reduced by atropine infusion, 45% and 59%, respectively (p < 0.005).

Adult↗
PubMed1982

Effect of thyrotropin-releasing hormone and atropine on the gastric motility stimulated by insulin-induced hypoglycemia.

The effects of thyrotropin-releasing hormone (TRH) and atropine on the gastric motility after stimulation by insulin-induced hypoglycemia were studied by the intragastric balloon technique. Four healthy young men were examined in two different ways on different days. In one experiment the effect of 50 micrograms TRH, 500 micrograms atropine, and 10 micrograms TRH, all intravenously injected, and in the other 500 micrograms atropine and 50 micrograms TRH were analyzed in this specific sequence. In two subjects the effect of intravenously injected TRH, 200 micrograms, and atropine, 500 micrograms, on the carbacholine-stimulated gastric motility was tested. The hypoglycemic stimulation of the gastric motility was immediately and completely blocked for a period of 9.3 +/- 0.7 min after 50 micrograms TRH and for 3.4 +/- 0.1 min after 10 micrograms TRH. The intragastric basal pressure was immediately reduced in all after TRH injection (-2.5 +/- 0.48 cm H2O pressure). Atropine had no significant effect on the gastric motility after hypoglycemic stimulation. The inhibiting effect of TRH on the carbacholine-stimulated gastric motility was similar to the effect of TRH on the hypoglycemia-stimulated gastric motility. These results demonstrate that TRH effectively inhibits the atropine-resistant stimulation of the gastric motility after insulin-induced hypoglycemia and also has potent relaxing effects on the muscular tonus of the gastric wall.

Adult↗
PubMed1994

Sulphotransferase-dependent dehydration of atropine and scopolamine in guinea pig.

1. Enzymatic dehydration of atropine and scopolamine was studied in guinea pig. 2. The incubation of these alkaloids with guinea pig liver cytosol in the absence of cofactors gave no dehydrated metabolite. However, when atropine and scopolamine were incubated with cytosol supplemented with ATP and sodium sulphate, dehydrated metabolites, apoatropine and aposcopolamine were formed. The formation of these metabolites was confirmed by gas chromatography-mass spectrometry. 3. The reaction required ATP as well as cytosol as the obligatory factors. Deletion of sodium sulphate from the reaction mixture also resulted in a decrease of the activities, although this treatment showed limited effect when the low concentration of atropine was used. Furthermore, dehydroepiandrosterone, an excellent substrate for hydroxysteroid-sulphotransferase, effectively inhibited the in vitro activity of atropine dehydration. 4. Administration of dehydroepiandrosterone to guinea pig followed by atropine treatment caused decreased urinary excretion of apoatropine. 5. These results strongly suggested that the dehydration of atropine and scopolamine takes place via the sulphate conjugate intermediates produced from the sulphotransferase-catalysed reaction. The present finding is the first example of the sulphotransferase-dependent dehydration of a drug, and its generality in drug metabolism is discussed.

Animals↗
PubMedDate not supplied

Dose-response effects of atropine and HI-6 treatment of organophosphorus poisoning in guinea pigs.

HI-6 (1-2-hydroxyiminomethyl-1-pyridino-3-(4-carbamoyl-1-pyridino -2- oxapropane dichloride) has been evaluated as an oxime alternative to pralidoxime, and toxogonin in the treatment of organophosphorus (OP) poisoning. The dose response effects of atropine (ATR) and HI-6 were investigated to more fully explore the interaction of these compounds in the treatment of OP poisoning. ATR, HI-6 and various combinations of the two drugs were evaluated against lethal poisoning by soman (GD) and tabun (GA) in guinea pigs. The effect of adjunctive diazepam treatment on the efficacy of atropine and HI-6 against soman was also investigated. Animals of either sex were challenged s.c. with OP and treated i.m. 1 min later with ATR and/or HI-6. When used, diazepam was injected immediately after ATR+HI6. LD50s of each treatment were calculated from probit models based on 24-hour survival against 5 levels of nerve agent and 6 animals per challenge level. A protective index (PI) was calculated by dividing the nerve agent LD50 in the presence of treatment by the LD50 in the absence of treatment. Treatment with HI6 alone had little effect on the toxicity of either OP. Treatment with ATR alone was more effective than HI-6 alone and was significantly more effective against soman than against tabun. When used in combination atropine and HI-6 had a strong synergistic effect against both agents. The dose of atropine used with HI-6 was critical in determining the efficacy of HI-6 against either agent. The slopes of the dose-lethality curves were minimally affected by the dose of ATR or HI-6. Adjunctive treatment with diazepam enhanced the efficacy of HI-6 and atropine against soman. It is concluded that 1) ATR has a large effect on the efficacy of HI-6 against OP poisoning, 2) the dose of ATR must be carefully selected in studies investigating the efficacy of HI-6 against OP poisoning, 3) the effective dose of ATR in the guinea pig is approximately 16 mg/kg, and 4) diazepam is a useful adjunct to atropine and HI-6.

Animals↗
PubMed1989

Effects of atropine on adrenergic responsiveness and reflex vasoconstriction in humans.

To determine whether cholinergic mechanisms contribute to blood pressure regulation, we examined the effects of atropine on pressor responses to phenylephrine and vasoconstrictor responses to the cold pressor test (CPT) and lower body negative pressure (LBNP) in 16 healthy subjects. Heart rate, blood pressure and cardiac index were significantly increased, and central venous pressure (CVP) was significantly decreased after atropine (0.04mg/kg). After atropine, pressor responses to phenylephrine at doses of 20, 40 and 80 micrograms were significantly increased by 101, 112 and 93% (p less than 0.001); however, atropine attenuated pressor responses to CPT (p less than 0.001) and forearm vasoconstrictor responses to LBNP. In 6 propranolol-treated subjects, atropine also augmented pressor responses to phenylephrine but attenuated pressor responses to CPT. These results suggest that atropine augments the pressor response to an alpha-agonist, which may be partly explained by inhibition of compensatory vascular responses mediated by cholinergic mechanisms.

Adult↗
PubMed1976

The effect of atropine on calculated sinoatrial conduction time in man.

This study investigates the effect of atropine on the length of the return cycles after premature atrial stimulation in man. On the assumption that sinus node automaticity is not changed by premature depolarization of the sinus node, sinoatrial conduction time (SACT) was calculated from the differences between the length of the return cycles and the spontaneous cycle length. 11 patients were studied before and after the injection of atropine. In all cases atropine caused an increase in heart rate. In 8 patients the return cycles exhibited a typical behavior. In 6 patients without signs of sinus node dysfunction, the mean calculated SACT was 109 msec, whereas 2 patients with a sick sinus syndrome (SSS) had a mean calculated SACT of 190 and 225 msec, respectively. 3 patients with SSS demonstrated an atypical pattern of the postextrasystolic pauses. In 6 patients without sinus node dysfunction, atropine caused a reduction of calculated SACT about 35%. In 2 patients with SSS the reduction was 38 and 49% of the control value, respectively, whereas in the remaining 3 patients with SSS who had an atypical return cycle pattern, a normalization occurred after the administration of atropine. We conclude that, besides its effects on sinus node automaticity, atropine has also a marked effect on sinoatrial conduction, even in patients with the sick sinus syndrome.

Arrhythmia, Sinus↗