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PubMed1980

Plasma atropine concentrations determined by radioimmunoassay after single-dose i.v. and i.m. administration.

The plasma concentrations of atropine following i.v. or i.m. administration to surgical patients were determined by radioimmunoassay. When atropine sulphate 1 mg was given i.v. there was a rapid initial removal of the drug from the circulation in the first 10 min; thereafter the plasma concentration decreased more slowly. Atropine i.m. was rapidly absorbed with peak concentrations occurring at 30 min following injection. The plasma atropine concentration then decreased slowly, probably because of uptake of atropine by muscarinic cholinergic receptors. The chronotropic effect of atropine appeared to correspond to the concentration in plasma following i.m. administration. We conclude that i.m. atropine, as a premedication, should be given not later than 30 min before induction of anaesthesia.

Adolescent↗

PubMed1991

Heart rate response to an i.v. test dose of adrenaline and lignocaine with and without atropine pretreatment.

In order to evaluate the sensitivity of an adrenaline test dose for detecting intravascular injection and the effect of atropine pretreatment, 90 ASA physical status I and II patients were allocated randomly to two groups, to receive i.v. saline 1 ml (n = 46) or i.v. atropine 0.5 mg (n = 44). Five minutes later, all patients received an i.v. test dose of 2% lignocaine 3 ml with adrenaline 15 micrograms at a rate of 1 ml s-1. The groups were similar with respect to basal heart rate (HR). HR remained unchanged after saline injection, but increased slightly 5 min after atropine injection (mean 78 (SD 15) beat min-1 vs 87 (20) beat min-1 (P less than 0.05). After the test dose of lignocaine with adrenaline, HR increased significantly in both groups at 30 s, 1 and 2 min, and remained increased at 3 min in the atropine group. The maximum increase in HR was greater in the atropine group than in the saline group (31 (4) beat min-1 vs 26 (11) beat min-1 (P less than 0.05). However, when individual maximum HR changes are considered, five patients in the saline group and four in the atropine group had an increase less than or equal to 10 beat min-1, and three patients in the saline group had no change or a decrease in HR. Defining a positive result to a test dose as an increase in HR of greater than 10 beat min-1, the sensitivity of the adrenaline test dose was 83 (5.5)% in the saline group and 91 (3.5)% in the atropine group (ns).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1998

Atropine premedication and the cardiovascular response to electroconvulsive therapy.

A report by the Royal College of Psychiatrists recommended avoiding atropine premedication during electroconvulsive therapy (ECT). We have examined the cardiovascular effects of ECT with or without atropine premedication. Consenting patients (n = 30) were allocated randomly before their third ECT session to receive atropine or no premedication. The rate pressure product (RPP) was recorded before anaesthesia, before ECT stimulus and at 1-min intervals thereafter for 5 min. Patients who did not receive atropine had significantly lower RPP values after all stimulus recordings. Administration of atropine or not explained 32% of the variance of summated RPP after the stimulus. There was no clinically significant bradyarrhythmia in those who did not receive atropine. Our findings support the recommendation of the Royal College of Psychiatrists. The study suggests that when threshold determination is not needed, avoiding atropine effectively contains potentially harmful cardiovascular responses.

Adjuvants, Anesthesia↗

PubMed2006

Testing for atropine and scopolamine in hair by LC-MS-MS after Datura inoxia abuse.

Datura inoxia belongs to the family of Solanaceae. This is a very common plant in New Caledonia that contains two main toxic alkaloids, l-atropine and l-scopolamine. In this study, we report the case of a 20-year-old male admitted to an Emergency Unit after consumption of 6 dried flowers in hot water for hallucinations, mydriasis, and agitation associated with tachycardia and increase of systolic blood pressure to 180. Full recovery was observed after one week. Three weeks later, a lock of about 80 hairs (200 mg) was collected from the subject in vertex posterior with scissors to be tested for both atropine and scopolamine. After decontamination with dichloromethane, a strand of hair was segmented into three parts, cut into small segments (< 1 mm), incubated overnight in 1 mL pH 8.4 phosphate buffer in the presence of 2.5 ng atropine-d(3), the internal standard, then extracted with 5 mL dichloromethane/isopropanol/n-heptane (50:17:33). The residue was reconstituted in 100 microL of methanol, from which 10 microL was injected into an XTerra MS C18 column (100 x 2.1 mm, 3.5 microm) eluted with a gradient of acetonitrile and formate buffer delivered at a flow rate of 0.2 mL/min. A Quattro Micro triple-quadrupole mass spectrometer (MS) was used for analyses. Ionization was achieved using electrospray in the positive ionization mode. For each compound, detection was related to two daughter ions (atropine: m/z 290.2 to 124.0 and 92.9; atropine-d(3): m/z 293.1 to 127.0 and 92.9; scopolamine: m/z 304.1 to 138.0 and 156.0). Although atropine was never detected (limit of detection = 2 pg/mg), scopolamine was identified in the three segments, in the range 14 to 48 pg/mg. The absence of atropine in hair is consistent with its very low dosage in the flower of Datura inoxia. Hair segmentation indicated that the subject was previously exposed on several occasions to the plant. Liquid chromatography-tandem MS appears to be a necessity for testing tropane alkaloids of the Datura group, given the low concentrations to be measured.

Adult↗

PubMed1987

Atropine-nonsensitive feedback regulatory mechanism of rat pancreatic enzyme secretion in response to food protein intake.

The effect of atropine on pancreatic enzyme secretion in response to removal of intraluminal protease was investigated using rats with an indwelling bile-pancreatic cannula. Stimulation of pancreatic enzyme secretion by diversion of bile-pancreatic juice was blocked by intravenous atropine [100 micrograms/(kg X h)] injection. On the other hand, stimulation of pancreatic enzyme secretion by intraluminal infusion of soybean trypsin inhibitor (SBTI) was not blocked by atropine administration. These results suggest that the feedback response of pancreatic enzyme secretion after removal of the intraluminal protease is controlled by at least two different systems, an atropine-sensitive mechanism and an atropine-nonsensitive mechanism. We detected and purified a peptide from rat bile-pancreatic juice that enhanced pancreatic enzyme secretion when the peptide was infused into the proximal intestine. In the atropine-administered rat whose small intestine was deprived of protease after intraluminal washing with saline containing SBTI, intraluminal infusion of the purified peptide stimulated pancreatic enzyme secretion markedly. These findings suggest that the atropine-nonsensitive feedback response of pancreatic enzyme secretion is at least in part mediated by the peptide.

Animals↗

PubMed1994

Atropine increases the accuracy of dobutamine stress echocardiography in patients taking beta-blockers.

Dobutamine-atropine stress echocardiography is used for the non-invasive diagnosis of coronary artery disease, but stress test results may be influenced by beta-blockers. The aim of this study was to assess if the addition of atropine can compensate for the presence of beta-blockers in dobutamine stress echocardiography. Twenty-six patients referred for evaluation of chest pain were studied twice, on and off metoprolol 100 mg b.i.d. (in random order sequence) with a wash-out period of at least 48 h. Dobutamine stress echocardiography was performed using up to 40 micrograms.kg-1.min-1, followed, if necessary, by the addition of atropine to achieve 85% of the age-predicted maximal heart rate, unless symptoms or markers of ischaemia appeared. Atropine was given to patients on beta-blockers more often [(22/26) vs (6/26)] than to those off beta-blockers (P < 0.001). Heart rate at every stage of the test was lower on beta-blockers. Chest pain occurred in patients on beta-blockers significantly less than in those off beta-blockers (8% vs 46%), and the addition of atropine made no significant difference (31% vs 46%). During dobutamine stress, new wall motion abnormalities occurred in three patients on beta-blockers (12%); this number increased to 15 after the addition of atropine (57%). New or worsened wall motion abnormalities occurred in 12 patients (46%) off beta-blockers with dobutamine alone and in 14 patients after adding atropine (53%).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1989

Atropine pharmacokinetics are affected by moderate hemorrhage and hypothyroidism.

Atropine is used both to treat a variety of clinical disorders and as an antidote to cholinesterase poisoning. While various conditions affect the physiologic responses to atropine, little is known of the pharmacokinetics of this drug except under resting conditions. Pharmacokinetic studies were performed in mongrel dogs under two experimental conditions, moderate hemorrhage and hypothyroidism, to determine whether im absorption and elimination of atropine (0.05 mg/kg body weight) were affected by changes in hemodynamic or metabolic status. Using a randomized, crossover experimental design, it was found that during hypovolemia the mean volume of distribution was reduced by 22% (2.50 +/- 0.62 vs. 3.21 +/- 0.63 L/kg), with no changes in peak serum level, total atropine availability, elimination half-life, or whole-body clearance. Hypothyroidism was associated with a significant increase in peak serum atropine concentration (26.4 +/- 3.9 vs. 20.6 +/- 4.9 ng/ml) and drug bioavailability (48.5 +/- 8.8 vs. 30.0 +/- 10.7 ng/ml.h), while the clearance was reduced by 39% (426 +/- 34 vs. 696 +/- 187 ng/ml.min). These results suggest that atropine kinetics are not altered appreciably during moderate hemorrhage. In hypothyroidism, alterations in atropine pharmacokinetics may warrant modification of drug dose and frequency of administration.

Animals↗

PubMed1992

Central action of atropine on cardiovascular reflexes in humans.

Effects of exciting the central nervous system (CNS) with low doses of atropine on cardiovascular reflexes was investigated in 6 healthy volunteers. Cumulative doses of atropine sulfate (1.43-28.57 micrograms/kg intravenously, i.v.) were used. The ECG parameters used to quantify the nervous activities on the heart were ratios of the longest to the shortest R-R intervals recorded during forced expirations and deep inspirations (respiratory sinus arrhythmia), the ratio of the longest to the shortest R-R intervals which occur immediately after one rises from a low sitting position (30:15 ratio), and the SD of R-R intervals recorded in standing and supine positions. Very low doses of atropine (1-3 micrograms/kg) increased the 30:15 ratios from (means +/- SEM) 1.21 +/- 0.07 to 1.34 +/- 0.04 (60% increase, p less than 0.01) and SD recorded in standing positions from 32.4 +/- 3.5 to 56.0 +/- 11.0 ms (71% increase, p less than 0.01). Respiratory sinus arrhythmia was not affected in either the standing or supine position, nor was SD recorded in supine positions significantly affected by these low doses of atropine. The only indexes increased by low doses of atropine were those that measure cardiovascular responses to active standing, consistent with an increased excitability of the medullary cardiovascular (vasomotor) centre. There was no evidence of central vagal excitation caused by low doses of atropine in the conscious, spontaneously breathing volunteers. The increased excitability of the medullary cardiovascular centre in response to a low dose of atropine may suggest that normal responses of this centre to arterial baroreceptor stimulation is restrained by a cholinergic inhibitory pathway.

Atropine↗

PubMed2004

Effect of atropine on denervated rabbit ear blood vessels.

Surgical denervation of rabbit ear blood vessel beds was combined with the isolated perfused rabbit ear technique to investigate the mechanism of atropine's vasodilator action. Intramuscular injection of atropine 0.2 mg/kg dilated the denervated blood vessels in the rabbit ear like innervated ones in vivo. Atropine at the maximal concentration (Cmax) of 3 x 10(-6) to 3 x 10(-4) M did not increase effluent flow of the isolated perfused denervated rabbit ear under constant perfusion pressure, but chlorpromazine at a Cmax of 10(-6) M and acetylcholine (ACh) at 2.5 x 10(-7) M significantly increased it and noradrenaline (NA) at 10(-7) M significantly decreased it. Atropine at Cmax of 3 x 10(-7) M did not affect, but at 3 x 10(-6) M it abolished the increase of the effluent flow induced by ACh 2.5 x 10(-7) M. Atropine at 3 x 10(-7) M did not affect it, but at 10(-6), 3 x 10(-6), and 10(-5) it significantly alleviated the decrease of effluent flow induced by NA 10(-7) M. Because the increase of effluent flow of rabbit ear under constant perfusion pressure reflects vasodilation of the ear to some extent, the study suggests that atropine has no direct vasodilator action; its vasodilator action is not attributed to blockade of M-cholinoreceptors located on the vascular wall; however, the alpha1-adrenoceptor might be a target site mediating atropine's vasodilator action in vivo.

Animals↗

PubMed1990

Atropine enhances food-stimulated CCK secretion in the rat.

The effect of atropine on plasma cholecystokinin (CCK) and pancreatic secretion during intraintestinal infusion of a conventional defined formula liquid diet (Ensure HN, Ross Laboratories, 1.06 kcal/ml) was studied in conscious rats. Rats were prepared with cannulae draining bile and pancreatic juice, which were returned to the duodenum at all times. Pancreatic secretion was monitored during intraduodenal infusion of 0.15 M NaCl for 2 h followed by Ensure HN, both infused at 4.62 ml/h. Rats were infused i.p. with atropine (500 micrograms/kg/h) or vehicle throughout the experiment, beginning 1 h before monitoring of basal pancreatic secretion. Basal and 15 min postprandial plasma CCK concentrations were determined by bioassay. Atropine inhibited basal pancreatic protein secretion by approximately 60%. However, protein secretion during infusion of the diet was not decreased by atropine, due to a larger incremental pancreatic protein secretory response in atropine-treated rats. Plasma CCK 15 min after beginning the diet infusion was significantly increased by atropine (8.09 +/- 1.77 pM in atropine-treated rats versus 3.14 +/- 0.64 pM in controls). The results indicate that rats compensate for loss of cholinergic input to the pancreas by increasing CCK release in response to a meal. This is hypothesized to occur by virtue of reduced feedback inhibition of CCK release due to anticholinergic reduction of basal levels of intestinal protease activity.

Animals↗

PubMed2004

Atropine often results in complete atrioventricular block or sinus arrest after cardiac transplantation: an unpredictable and dose-independent phenomenon.

BACKGROUND: A paradoxic response to atropine with development of atrioventricular (AV) block has been described in patients after heart transplantation (HTx). We investigated further the incidence and dose-response relationship of this paradoxic atropine response and explored predictive factors. METHODS: We investigated 25 clinically stable patients (age 55 +/- 2 years) 18 to 126 months after HTx. After endomyocardial biopsy, a temporary pacemaker was introduced and patients were monitored. Atropine was given in ascending doses (0.004 mg/kg body weight initially, total cumulative dose 0.035 mg/kg body weight). Physiologic tests were performed to evaluate the presence of reinnervation. RESULTS: In 20% of the patients (5/25), a paradoxic response to atropine was observed. Four patients exhibited third degree AV block, one of whom also demonstrated sinus arrest. A fifth patient showed sinus arrest only. In all patients but one, there was no ventricular escape rhythm before ventricular pacing was commenced (10 sec after block). The observed adverse effect was not correlated with the applied atropine dosage, and predisposing factors could not be identified, apart from a slightly lower resting heart rate (80 +/- 5 vs. 90 +/- 2 beats/min, P = 0.07). CONCLUSION: A significant proportion of patients respond paradoxically to atropine after HTx, leading to asystole as the result of sinus arrest or AV block. Although a plausible explanation for this effect remains speculative, our data indicate that the use of atropine or other anticholinergic drugs in patients after HTx is contraindicated.

Arrhythmia, Sinus↗

PubMed1986

Atropine selectively blocks GHRH-induced GH secretion without altering LH, FSH, TSH, PRL and ACTH/cortisol secretion elicited by their specific hypothalamic releasing factors.

The role of acetylcholine in the regulation of the hypothalamo-pituitary system in man was assessed using atropine, which selectively blocks cholinergic muscarinic receptors. Paired tests were performed in 10 normal men using either GHRH (1 microgram/kg i.v.), or TRH (300 micrograms i.v.) plus LHRH (100 micrograms i.v.) plus corticotrophin releasing hormone (CRH) (1 microgram/kg i.v.) with or without atropine given 30 min previously (1 mg i.m.). The GHRH-induced GH secretory peak (17.8 +/- 3.0 ng/ml) was completely blocked by atropine administration (2.8 +/- 0.6 ng/ml) (P less than 0.05). Atropine did not, however, modify TRH-induced TSH and PRL secretion, nor FSH and LH release induced by the LHRH pulse. ACTH/cortisol secretion elicited by CRH was also unaffected by atropine. These results suggest that atropine blockade of GHRH-induced GH secretion is highly specific, and constitutes an indication of the importance of cholinergic control of GH function. Furthermore, atropine's lack of action on the other pituitary hormones rules out the possibility that it acts non-specifically, i.e. via blood flow changes or toxic effects.

Adrenocorticotropic Hormone↗

PubMed1988

Pharmacokinetic implications for the clinical use of atropine, scopolamine and glycopyrrolate.

Several specific and sensitive new methods for determining atropine and its metabolites in biological fluids have increased the possibility to characterise the pharmacokinetic properties of this antimuscarinic agent. Following i.v. injection, atropine disappears very quickly from the circulation, resembling its fast onset of action. Age, but not sex, appears to have a clear effect on its kinetics, explaining at least partly the higher sensitivity of very young and very old patients to this anticholinergic agent. Following i.m. or oral atropine administration, typical anticholinergic effects coincide quite well with the absorption rate of the drug, indicating that the premedication should be given about 1 and 2 h before induction of anaesthesia. A sufficient absorption after rectal administration offers an alternative treatment, especially in children. Differing from its placental transfer, atropine has a delayed and incomplete lumbar cerebrospinal fluid penetration, indicating a fundamental difference between these two biological membranes. Oropharyngeally administered atropine has a very variable absorption, but inhaled or intratracheally given drug has produced interesting new results, e.g. pulmonary atropine administration appears to have clinical significance in special situations, such as cardiac arrest and organophosphate poisoning (military personnel). Depending on the method used, different data on the metabolism and excretion for atropine have been reported and therefore further studies are needed in this respect. The pharmacokinetics of scopolamine and glycopyrrolate and their relation to clinical response are poorly understood.

Aging↗

PubMed1993

Echocardiographic evaluation of vagolytic effects of atropine sulfate during pediatric halothane anesthesia.

The aims of this study were to define the antagonistic effects of atropine sulfate to halothane-induced cardiovascular depression in children, and to clarify whether or not a larger dose of atropine is more effective in attenuating the cardiovascular depression. Thirty-four children aged 1-12 years who had undergone minor surgery, free from cardiac or pulmonary disease, were assigned at random to two groups. M-mode echocardiographic evaluation of left ventricular function in each patient was performed at three points (before induction, point A; after induction, point B; and following administration of atropine, point C). Results were compared between points A and B, B and C and C and A, and between the two study groups with different doses of atropine (0.01 mg/kg vs 0.02 mg/kg). Heart rate (HR), mean blood pressure (MBP) and left ventricular shortening fraction (LVSF) decreased, and left ventricular end-diastolic dimension (LVEDD) were increased significantly by halothane induction. Although HR and MBP recovered following atropine, LVSF and LVEDD remained unchanged. There were no differences found between the values after vagolysis in both study groups, except for HR and mean velocity of circumferential fiber shortening (mVcf). Heart rate increased above that of pre-induction, even following the smaller dose of atropine. The myocardial depression cannot be necessarily attenuated by vagolysis regardless of the dosage of atropine. The smaller dose (i.e. 0.01 mg/kg) seems to be sufficient only to antagonize the bradycardia and hypotension during halothane anesthesia in children.

Adolescent↗

PubMed2000

A prospective study of atropine premedication in flexible bronchoscopy.

AIM: This study aimed to assess the effect of atropine premedication prior to flexible bronchoscopy. The rationale for using atropine is that it will dry secretions and allow a better view of the bronchial tree. There is also the theoretical benefit of protection against vasovagal episodes and bronchospasm. METHODS: Twenty patients were randomised in a double-blind manner to receive either 500 mcg of atropine intramuscularly or 1 mL of 0.9% saline intramuscularly 30 minutes prior to bronchoscopy. Both groups received a standard dose of intramuscular pethidine. Variables studied included a pre-procedure electrocardiograph, a rhythm strip during the procedure, serial measurements of blood pressure, continuous pulse oximetry, and spirometry pre- and post-bronchoscopy. Subjective measures recorded were a secretion score, rated 0-3 by the bronchoscopist using a four point visual analogue scale. A patient questionnaire was designed to establish the presence or absence of symptoms, including those related to atropine. RESULTS: There were no significant differences recorded in the duration of procedure, percentage fall in FEV1, secretion scores, or other physiological measures. The only significant difference between the two groups was dry mouth in the atropine group (p<0.001). There was a fall in forced vital capacity from baseline which was significant in the saline group (p<0.005), and not the atropine group, but it was not significant when compared between groups. A beta2 adrenergic agonist would, however, be more appropriate to prevent such a fall in spirometry. CONCLUSIONS: These results fail to demonstrate a benefit of intramuscular atropine as premedication for fibreoptic bronchoscopy.

Aged↗

PubMed1977

The effect of atropine on acid secretion stimulated by acetylcholine, histamine and gastrin in the isolated whole stomach of the rat.

1 An isolated stomach preparation from immature rats has been used to study the effect of atropine on gastric acid secretion. 2 The acid secretory response to acetylcholine was not inhibited by atropine at a concentration of 0.3 micrometer. Concentrations of atropine of 1 to 3 micrometer produced a measurable inhibition of acid secretion, and a concentration of atropine of 10 micrometer caused a complete block of acid secretion which could not be surmounted by high concentrations of acetylcholine. 3 The acid secretory response to histamine was not inhibited by concentrations of atropine of up to 1 mM. 4 Concentrations of atropine of 1 micrometer and 10 micrometer did not inhibit gastrin-stimulated acid secretion, although a significant inhibition of acid output was observed with atropine at concentrations of 0.1 mM and 1 mM. 5 These findings are discussed in relation to the role of cholinergic mechanisms in the control of gastric acid secretion.

Acetylcholine↗

PubMed1992

The influence of atropine and atenolol on the cardiac haemodynamic effects of NG-nitro-L-arginine methyl ester in conscious, Long Evans rats.

1. In the present study, the extent to which baroreflexes contribute to the cardiac effects of NG-nitro-L-arginine methyl ester (L-NAME) was assessed in conscious, Long Evans rats chronically instrumented with thoracic electromagnetic flow probes for the measurement of cardiac haemodynamics. 2. L-NAME (10 mg kg-1, i.v.) was administered in the absence (n = 6) and in the presence (n = 7) of atropine (1 mg kg-1) and atenolol (1 mg kg-1). 3. L-NAME caused a marked increase in mean arterial pressure and marked reductions in total peripheral conductance, cardiac output, heart rate, stroke volume, peak thoracic flow and the maximum rate of rise of aortic flow. 4. Administration of atropine, after the maximal bradycardic effect of L-NAME was established, restored the heart rate to resting levels. Concurrently, there was a reduction in stroke volume, such that cardiac output, although transiently elevated, did not show a sustained increase. No other variables were significantly affected by atropine. Additional administration of atenolol had no effect other than to cause a slight bradycardia, such that in the presence of atropine and atenolol, heart rate was not different from that in animals receiving atropine and atenolol before L-NAME. 5. In the presence of atropine and atenolol, L-NAME had similar pressor, vasoconstrictor and cardiac haemodynamic effects to those in untreated animals, although the bradycardia was significantly attenuated. However, there was still a significant reduction in heart rate following L-NAME in the presence of atropine and atenolol.6. These results indicate that the major component of the bradycardia following L-NAME is indirect and mediated through an increase in vagal efferent activity. However, the substantial reduction in cardiac function caused by L-NAME is not dependent on the autonomic control of the heart but rather, may depend on the increase in afterload and/or a direct effect of L-NAME on the heart and/or its vasculature.

Animals↗

PubMed2006

Effects of atropine and pirenzepine on heart rate turbulence.

BACKGROUND: It has been shown that mortality risk in patients after myocardial infarction could be estimated by heart rate turbulence (HRT), a short-term change in heart rate after ventricular premature beat (VPB), presumably caused by baroreceptor mechanism. We sought to determine whether pharmacological blockade with atropine, or augmentation of vagal tone with pirenzepine given in small doses would influence HRT. METHODS: In 30 patients with normal echocardiogram, and without signs or symptoms of coronary artery disease, after electrophysiologic examination or radiofrequency ablation for supraventricular arrhythmias was completed, turbulence onset (TO) and turbulence slope (TS) in basal state, after 1.3 mg IV pirenzepine and finally, after atropine in dose of 0.04 mg/kg of body weight were compared. RESULTS: As assessed by Friedman ANOVA test both pirenzepine and atropine caused a significant change in both TO (P < 0.01) and TS (P < 0.01). The mean basal TO of -3.6 +/- 2.9%, changed after pirenzepine to -5.99 +/- 5.6% (P < 0.01), and after atropine it changed to -3.3 +/- 18.1% (P < 0.01). The mean basal TS of 18.6 +/- 10.1 ms/R-R interval increased after pirenzepine to 26.8 +/- 19.9 ms/R-R interval (P < 0.05), and decreased after atropine to 1.2 +/- 0.8 ms/R-R interval (P < 0.01). Mean cycle length increased after pirenzepine from 706.8 +/- 106.8 to 830 +/- 151.9 ms (P < 0.01), and decreased after atropine to 454.2 +/- 58.1 ms (P < 0.01). CONCLUSION: A conclusion could be drawn that vagomymetic manipulation with intravenous pirenzepine increases HRT; vagal blockade with atropine decreases HRT. This finding suggests that a normal vagal innervation of heart is a prerequisite for the phenomenon of HRT.

Analysis of Variance↗