Academic literature on the topic 'Atropine Physiological effect'

Older adults exhibit reduced physiological responses to beta-adrenergic stimulation and parasympathetic inhibition. This study aimed to investigate the effect of reducing the incidence of bradycardia in the atropine and ephedrine pretreatment group compared to the control group in older adults who received spinal anesthesia with intravenous dexmedetomidine. Overall, 102 older adults aged over 65 years were randomly divided into three groups, and saline (control group), atropine at 0.5 mg (atropine group), and ephedrine at 8 mg (ephedrine group) were administered intravenously to each group as pretreatment. Immediately after spinal anesthesia, dexmedetomidine loading and study drug injections were commenced. The primary outcome was the incidence of bradycardia (<50 beats per min) within 60 min following dexmedetomidine loading. The incidence of bradycardia requiring atropine treatment was significantly higher in the control group than in the atropine and ephedrine groups (27.3% vs. 6.1% and 8.8%, respectively; p = 0.035), and no difference was noted between the atropine and ephedrine groups. Therefore, if ephedrine or atropine is selected and used according to the patient’s condition and clinical situation, it may be helpful in preventing bradycardia during spinal anesthesia using dexmedetomidine in older patients.

Analysis of heart rate variability (HRV) by nonlinear approaches has been gaining interest due to their ability to extract additional information from heart rate (HR) dynamics that are not detectable by traditional approaches. Nevertheless, the physiological interpretation of nonlinear approaches remains unclear. Therefore, we propose long-term (60 min) protocols involving selective blockade of cardiac autonomic receptors to investigate the contribution of sympathetic and parasympathetic function upon nonlinear dynamics of HRV. Conscious male Wistar rats had their electrocardiogram (ECG) recorded under three distinct conditions: basal, selective (atenolol or atropine), or combined (atenolol plus atropine) pharmacological blockade of autonomic muscarinic or β1-adrenergic receptors. Time series of RR interval were assessed by multiscale entropy (MSE) and detrended fluctuation analysis (DFA). Entropy over short (1 to 5, MSE1–5) and long (6 to 30, MSE6–30) time scales was computed, as well as DFA scaling exponents at short (αshort, 5 ≤ n ≤ 15), mid (αmid, 30 ≤ n ≤ 200), and long (αlong, 200 ≤ n ≤ 1,700) window sizes. The results show that MSE1–5 is reduced under atropine blockade and MSE6–30 is reduced under atropine, atenolol, or combined blockade. In addition, while atropine expressed its maximal effect at scale six, the effect of atenolol on MSE increased with scale. For DFA, αshort decreased during atenolol blockade, while the αmid increased under atropine blockade. Double blockade decreased αshort and increased αlong. Results with surrogate data show that the dynamics during combined blockade is not random. In summary, sympathetic and vagal control differently affect entropy (MSE) and fractal properties (DFA) of HRV. These findings are important to guide future studies. NEW & NOTEWORTHY Although multiscale entropy (MSE) and detrended fluctuation analysis (DFA) are recognizably useful prognostic/diagnostic methods, their physiological interpretation remains unclear. The present study clarifies the effect of the cardiac autonomic control on MSE and DFA, assessed during long periods (1 h). These findings are important to help the interpretation of future studies.

Condensed tannins (CTs) extracted from various plants have been shown to possess antioxidant, antidiabetic, anthelmintic, anti-palatable and anti-diarrhea activity. Black currant (Ribes nigrum L.), a native plant of northern Europe and Asia, is rich in phenolic compounds, including CTs. Among the biological activities of CTs, their astringent property is likely to affect gastrointestinal motility. This study aimed to investigate the physiological effect of CTs from black currant (R. nigrum L.) leaves on isolated rat duodenal contraction. Duodenal segments were fixed in organ baths containing carbogen aerated Krebs solution at the resting tension of 0.7 - 0.8 g. The frequency, amplitude, and tone of duodenal contraction were recorded. Either CTs or acetylcholine (ACh) were cumulatively added into the bath at the concentration of between 0.001 - 10 µg/mL and 10–8 - 10–4 M, respectively. The mechanisms of CTs and ACh actions were studied using muscarinic receptor antagonist (atropine, 1.55×10–5 M) and calcium channel blocker (verapamil, 10–6 M). It is found that CTs at the concentration between 0.001 - 10 µg/mL had no direct effect on duodenal frequency, amplitude, and tone of contraction, whereas ACh showed a significant increase in tonic contraction, was suppressed by atropine. Interestingly, in the presence of atropine and verapamil, CTs showed a further significant decrease in the amplitude of duodenal contraction compared to the effect of these 2 blockers alone. It is concluded that CTs would synergize the activity of the muscarinic receptor antagonist and the calcium channel blocker at duodenal enteric neurons or smooth muscle membrane. However, the use of CTs from black currant (R. nigrum L.) leaves to treat gastro-intestinal disorders while having muscarinic receptor antagonist or calcium channel blocker need cautions. HIGHLIGHTS Black currant (Ribes nigrum L.), a native plant of northern Europe and Asia, is rich in phenolic compounds including condensed tannins (CTs) and their astringent property is likely to affect gastrointestinal motility CTs isolated from leaves of black currant (R. nigrum L.) at the physiological doses (0.001 - 10.0 µg/mL) have no direct effect on isolated rat duodenal contraction CTs may possess the synergistic or additive effect with either atropine, a nonselective muscarinic receptor, or verapamil, a calcium channel blocker on duodenal amplitude of contraction GRAPHICAL ABSTRACT

To determine whether physiological differences exist between primary (swallow-induced) and secondary (distension-induced) peristalsis in humans, 10 healthy male volunteers underwent esophageal manometry on 2 consecutive days using a perfused intraluminal catheter system that incorporated a latex balloon. Initially the catheter was positioned so that the balloon was centered 16 cm above the lower esophageal sphincter (LES), and intraluminal pressures were recorded 21, 11, 6, and 1 cm above the LES. After a series of wet swallows, dry swallows, and balloon distensions, the catheter was repositioned so that the balloon was 6 cm above the LES and pressures were recorded 1 and 11 cm above the LES. A series of balloon distensions were repeated in this position, and the subject was then given either atropine (10 micrograms/kg iv) or placebo in a double-blind randomized fashion (on consecutive days). The protocol was then repeated in reverse order. Distension-induced responses aboral to the balloon with the balloon located 16 cm above the LES were 1) of lower amplitude, 2) more often nonperistaltic, and 3) less atropine sensitive than swallow-induced contractions at comparable sites. With the balloon located distally (6 cm above LES) contractions induced at the 11-cm site (i.e., orad to the balloon) were much more atropine sensitive than contractions induced at the same site when the balloon was located proximally (i.e., 16 cm above LES). These data suggest that, contrary to previous reports, secondary peristalsis differs significantly from primary peristalsis. Furthermore, atropine differentially effects these two types of peristalsis, suggesting that the neural pathways involved are dissimilar.

The purpose of this study was to test the hypothesis that muscarinic cholinergic receptors are involved in the initial vasodilation in red muscle vascular beds of conscious rats performing slow locomotory exercise. Atropine sulfate (1 mg/kg, ia) was administered to one group of rats in which distribution of cardiac output was estimated with radiolabeled microspheres immediately before exercise while the animals were standing on the treadmill and at 30 s and 5 min of treadmill walking at 15 m/min. Blood flows within and among muscles in the atropine-treated animals were compared with flows in control rats that were given a sham injection of an equal volume of physiological saline. Heart rates were elevated above those of control animals in the atropinized rats during preexercise (+17%) and at 30 s of exercise (+15%). However, distributions and magnitudes of blood flows in nonmuscular tissues and within and among skeletal muscles were the same (P greater than 0.05) in atropinized and control rats during preexercise and at both exercise times, indicating that atropine had no effect on the distribution of cardiac output in the rats. It is concluded that muscarinic cholinergic receptors do not play a significant role in elevating muscle blood flow in conscious rats, either during the preexercise anticipatory phase or during slow locomotory exercise.

In the present investigation, we have studied the effect of atropine on the pancreatic secretion stimulated by intraduodenal administration of either sodium oleate or exogenous cholecystokinin (CCK). In four dogs prepared with gastric and Thomas duodenal cannulas, pancreatic juice was collected for measurement of volume, bicarbonate, and protein output, and peripheral venous blood samples were obtained for radioimmunoassay of both secretin and CCK. Volume, bicarbonate, and protein output of the pancreatic juice increased significantly in response to sodium oleate (1-4 mmol/h) in a dose-dependent manner. The increase in pancreatic secretion paralleled the increments in both plasma CCK and secretin. Atropine given intravenously suppressed completely both pancreatic secretion and release of CCK stimulated by sodium oleate, whereas the release of secretin was not affected. Pancreatic secretion was significantly increased in a dose-dependent manner by exogenous CCK octapeptide (CCK-8) at 16, 32, and 64 micrograms (14, 28, and 56 pmol).kg-1.h-1. Atropine inhibited protein output only partially, but it did not influence bicarbonate output. In five additional dogs, the effect of atropine on L-tryptophan-stimulated pancreatic secretion was studied. Interestingly, atropine failed to influence the CCK release and pancreatic secretion of volume and bicarbonate, except for protein secretion, which was significantly inhibited. It was shown previously that atropine inhibited significantly the pancreatic secretion of bicarbonate stimulated by secretin in physiological doses. Thus we conclude that the inhibition by atropine of the pancreatic exocrine secretion stimulated by sodium oleate is mediated by both suppression of CCK release and inhibition of action of secretin on the exocrine pancreas.(ABSTRACT TRUNCATED AT 250 WORDS)

To evaluate the functional status of neuronal α2-adrenoceptors (ARs) and β2-ARs on ACh release in horses with recurrent airway obstruction (RAO), we examined the effects of the physiological agonists epinephrine (Epi) and norepinephrine (NE) and the β2-agonists RR- and RR/ SS-formoterol on ACh release from airway cholinergic nerves of horses with RAO. Because SS-formoterol, a distomer of the β2-agonist, increases ACh release from airways of control horses only after the autoinhibitory muscarinic receptors are blocked by atropine, we also tested the hypothesis that if there is an M2-receptor dysfunction in equine RAO, SS-formoterol should increase ACh release even in the absence of atropine. ACh release was evoked by electrical field stimulation and measured by HPLC. Epi and NE caused less inhibition of ACh release in horses with RAO than in control horses. At the catecholamine concentration achieved during exercise (10−7 M), the inhibition induced by Epi and NE was 10.8 ± 13.2 and 3.4 ± 6.8%, respectively, in equine RAO versus 41.0 ± 6.4 and 27.1 ± 5.6%, respectively, in control horses. RR- and RR/ SS-formoterol (10−8 to 10−5 M) increased ACh release to a similar magnitude as that in control horses. These results indicate that neuronal β2-ARs are functioning; however, the α2-ARs are dysfunctional in the airways of horses with RAO in response to circulating catecholamines. SS-formoterol (10−8 to 10−5 M) facilitated ACh release in horses with RAO even in the absence of atropine. Addition of atropine did not cause significantly more augmentation of ACh release over the effect of SS-formoterol alone. The magnitude of augmentation in horses with RAO in the absence of atropine was similar to that in control horses in the presence of atropine. The latter observations could be explained by neuronal muscarinic-autoreceptor dysfunction in equine RAO.

The physiological mechanism responsible for cholecystokinin (CCK)-induced gallbladder (GB) contraction is unclear. We investigated the relative roles of direct muscle stimulation and neural activation at physiological and supraphysiological levels of CCK-octapeptide (CCK-8) using an in vivo guinea pig model. GB pressure was measured by a pressure transducer inserted into the GB lumen. Infusion of CCK-8 (2.5-40 ng.kg-1.min-1) increased GB pressure in a dose-dependent fashion. Pretreatment with atropine or hexamethonium antagonized GB responses to low doses of CCK-8 (2.5-5 ng.kg-1.min-1) but had no effect on doses greater than 10 ng.kg-1.min-1. Bilateral truncal vagotomy also significantly reduced GB responses to low doses of CCK-8 (2.5-5 ng.kg-1.min-1) but did not affect responses to high doses (10-40 ng.kg-1.min-1). Atropine or hexamethonium had no further inhibitory effects on guinea pigs that had undergone truncal vagotomy. Fasted guinea pigs that were fed ad libitum produced a postprandial peak plasma CCK level of 7.8 +/- 1.8 pM. This level was most closely approximated by infusion of 5 ng.kg-1.min-1 of CCK-8 (8.4 +/- 2.6 pM). CCK-8 infusion at greater than or equal to 10 ng.kg-1.min-1 gave supraphysiological plasma CCK levels. These observations indicate that CCK stimulated GB contraction via both a neural and a direct smooth muscle effect. Doses of CCK-8 that produce physiological plasma CCK levels act via stimulation of presynaptic cholinergic neurons in a vagally mediated pathway, whereas doses of CCK-8 that produce supraphysiological CCK levels act directly on GB smooth muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Distension of the isolated mouse stomach stimulated gastric acid secretion. Atropine, cimetidine, or proglumide antagonized the actions of cholinomimetics, histamine, and gastrin, respectively. However, these antagonists and the nerve blocking agent, tetrodotoxin, were without effect on basal secretion or distension-stimulated secretion. It is concluded that in the isolated mouse stomach neither basal secretion nor secretion evoked by distension involve the release of any of the established "physiological" secretagogues or the activation of intramural nerves.

Here, we describe a human physiology laboratory class measuring changes in autonomic function over time in response to atropine. Students use themselves as subjects, generating ownership and self-interest in the learning as well as directly experiencing the active link between physiology and pharmacology in people. The class is designed to concomitantly convey the importance of bias in experimentation by adopting a double-blind placebo-controlled approach. We have used this class effectively in various forms with ∼600 students receiving atropine over the last 16 yr. This class has received favorable feedback from staff and students of medicine, pharmacy, and neuroscience, and we recommend it for such undergraduates. The learning objectives that students are expected to achieve are to be able to 1) know the ethical, safety, and hygiene requirements for using human volunteers as subjects; 2) implement and explain a double-blind placebo-controlled trial; 3) design, agree, and execute a protocol for making (and accurately recording) precise reproducible measurements of pulse rate, pupil diameter, and salivary flow; 4) evaluate the importance of predose periods and measurement consistency to detect effects (including any reversibility) after an intervention; 5) experience direct cause-and-effect relationships integrating physiology with pharmacology in people; 6) calculate appropriate summary statistics to describe the data and determine the data's statistical significance; 7) recognize normal variability both within and between subjects in baseline physiological parameters and also recognize normal variability in response to pharmacological treatment; 8) infer the distribution and role of muscarinic receptors in the autonomic nervous system with respect to the heart, eye, and mouth; 9) identify and explain the clinical significance of differences in effect due to the route and formulation of atropine; 10) produce and deliver a concise oral presentation of experimental findings; and 11) produce a written report in the form of a short scientific research article. The results of a typical study are presented, which demonstrate that the administration of atropine by a subcutaneous injection elicited a significant increase in pulse rate and pupil diameter and a significant decrease in salivary flow, whereas administration of atropine in an oral liquid elicited significant effects on pulse rate and salivary flow, and an oral solid format elicited a significant alteration in salivary flow alone. More detailed analysis of the salivary flow data demonstrated clear differences between the routes of administration and formulation in the onset and magnitude of action of atropine.

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O reconhecimento e o tratamento precoce da hemorragia intraoperatória é primordial para prevenir a morbidade e a mortalidade associada à perda aguda de volume circulante. Por outro lado, dexmedetomidina é um fármaco adjuvante da anestesia que, devido a sua ação vasoconstritora, poderia agravar estados de hipoperfusão regional associados à perda volêmica aguda. Objetivou-se avaliar os efeitos da infusão intravenosa contínua de dexmedetomidina associada à atropina sobre os índices globais de perfusão e sobre outras variáveis hemodinâmicas em cães anestesiados com isoflurano submetidos à hemorragia guiada a volume seguida pela reposição volêmica com sangue autólogo. Oito cães hígidos (19,5-29,2 kg) foram anestesiados em duas ocasiões com concentrações equipotentes (1,3 concentração alveolar mínima) de isoflurano administrado isoladamente (tratamento ISO) ou em associação com a dexmedetomidina intravenosa (bolus de 1,6 μg/kg, seguido por 2 μg/kg/h) (tratamento ISO-DEX) em um delineamento aleatório cruzado, aguardando-se 2 semanas de intervalo entre os tratamentos. A atropina (0,03 mg/kg, IM e 0,01 mg/kg, IV) foi administrada 30 minutos antes da hemorragia no tratamento ISO-DEX. A anestesia foi mantida em ambos os tratamentos sob ventilação com volume controlado (volume corrente: 12 mL/kg, pressão positiva no final de expiração: 7 cm H2O, frequência respiratória: 16-20 mov/min) com bloqueio neuromuscular produzido pelo atracúrio. Após a obtenção dos parâmetros pré-hemorragia (basal), foram retirados 10, 20, e 30% do volume sanguíneo total estimado (80 mL/kg) de forma progressiva, seguido por reposição volêmica com sangue autólogo nas mesmas proporções. Comparativamente ao valor basal, a hemorragia reduziu significativamente (p < 0,05) o índice de transporte de O2 (IDO2) e a saturação venosa mista (SvO2) em ambos os tratamentos. Embora a taxa de extração de O2 (TeO2) tenha se elevado ...
Early recognition and treatment of acute intraoperative hemorrhage is seminal for preventing the morbidity and mortality associated with circulating volume losses. On the other hand, dexmedetomidine is an adjuvant anesthetic drug that might aggravate global tissue hypoperfusion induced by acute hemorrage because of its vasopressor effects. This study aimed to evaluate the effects of a constant rate infusion of dexmedetomidine combined with atropine on global perfusion indexes and on other hemodynamic parameters in isoflurane anesthestized dogs that underwent a volume-guided hemorrhage model followed by volume replacement with autologous blood. Eight healthy dogs (19-30 kg) were anesthetized in two occasions with equipotent concentrations (1.3 minimum alveolar concentration) of isoflurne alone (treatment ISO) or isoflurane combined with dexmedetomidine (1.6 μg/kg bolus, followed by 2 μg/kg/h) (treatment ISO-DEX) in a randomized crossover design, allowing 2-week intervals between treatments. Atropine (0,03 mg/kg, IM and 0.01 mg/kg IV) was administered 30 minutes prior to hemorrhage in the dexmedetomidne treatment. Anesthesia was maintained in both treatments under neuromuscular blockade induced by atracurium and volume controlled ventilation (expired tidal volume: 12 mL/kg, positive end-expiratory pressure: 7 cm H2O, respiratory rate: 16-20 mov/min). After recording pre-hemorrhage data (baseline), stepwise withdrawal of 10, 20, and 30% of the estimated blood volume (80 mL/kg) was followed by volume replacement with autologous blood in the same proportion. When compared with baseline values, hemorrhage significantly (P < 0,05) reduced oxygen delivery índex (IDO2) and mixed-venous saturation (SvO2) in both treatments. Although the oxygen extraction ratio (O2ER) was increased (P < 0.05) from baseline during hemorrhage, the anaerobic threshold (point where the oxygen comsumption (IVO2) becomes dependent on the IDO2] was not reached in both ...

Orientador: Francisco José Teixeira Neto
Banca: Carlos Alan Candido Dias Junior
Banca: Denise Aya Otsuki
Resumo: O reconhecimento e o tratamento precoce da hemorragia intraoperatória é primordial para prevenir a morbidade e a mortalidade associada à perda aguda de volume circulante. Por outro lado, dexmedetomidina é um fármaco adjuvante da anestesia que, devido a sua ação vasoconstritora, poderia agravar estados de hipoperfusão regional associados à perda volêmica aguda. Objetivou-se avaliar os efeitos da infusão intravenosa contínua de dexmedetomidina associada à atropina sobre os índices globais de perfusão e sobre outras variáveis hemodinâmicas em cães anestesiados com isoflurano submetidos à hemorragia guiada a volume seguida pela reposição volêmica com sangue autólogo. Oito cães hígidos (19,5-29,2 kg) foram anestesiados em duas ocasiões com concentrações equipotentes (1,3 concentração alveolar mínima) de isoflurano administrado isoladamente (tratamento ISO) ou em associação com a dexmedetomidina intravenosa (bolus de 1,6 μg/kg, seguido por 2 μg/kg/h) (tratamento ISO-DEX) em um delineamento aleatório cruzado, aguardando-se 2 semanas de intervalo entre os tratamentos. A atropina (0,03 mg/kg, IM e 0,01 mg/kg, IV) foi administrada 30 minutos antes da hemorragia no tratamento ISO-DEX. A anestesia foi mantida em ambos os tratamentos sob ventilação com volume controlado (volume corrente: 12 mL/kg, pressão positiva no final de expiração: 7 cm H2O, frequência respiratória: 16-20 mov/min) com bloqueio neuromuscular produzido pelo atracúrio. Após a obtenção dos parâmetros pré-hemorragia (basal), foram retirados 10, 20, e 30% do volume sanguíneo total estimado (80 mL/kg) de forma progressiva, seguido por reposição volêmica com sangue autólogo nas mesmas proporções. Comparativamente ao valor basal, a hemorragia reduziu significativamente (p < 0,05) o índice de transporte de O2 (IDO2) e a saturação venosa mista (SvO2) em ambos os tratamentos. Embora a taxa de extração de O2 (TeO2) tenha se elevado ...
Abstract: Early recognition and treatment of acute intraoperative hemorrhage is seminal for preventing the morbidity and mortality associated with circulating volume losses. On the other hand, dexmedetomidine is an adjuvant anesthetic drug that might aggravate global tissue hypoperfusion induced by acute hemorrage because of its vasopressor effects. This study aimed to evaluate the effects of a constant rate infusion of dexmedetomidine combined with atropine on global perfusion indexes and on other hemodynamic parameters in isoflurane anesthestized dogs that underwent a volume-guided hemorrhage model followed by volume replacement with autologous blood. Eight healthy dogs (19-30 kg) were anesthetized in two occasions with equipotent concentrations (1.3 minimum alveolar concentration) of isoflurne alone (treatment ISO) or isoflurane combined with dexmedetomidine (1.6 μg/kg bolus, followed by 2 μg/kg/h) (treatment ISO-DEX) in a randomized crossover design, allowing 2-week intervals between treatments. Atropine (0,03 mg/kg, IM and 0.01 mg/kg IV) was administered 30 minutes prior to hemorrhage in the dexmedetomidne treatment. Anesthesia was maintained in both treatments under neuromuscular blockade induced by atracurium and volume controlled ventilation (expired tidal volume: 12 mL/kg, positive end-expiratory pressure: 7 cm H2O, respiratory rate: 16-20 mov/min). After recording pre-hemorrhage data (baseline), stepwise withdrawal of 10, 20, and 30% of the estimated blood volume (80 mL/kg) was followed by volume replacement with autologous blood in the same proportion. When compared with baseline values, hemorrhage significantly (P < 0,05) reduced oxygen delivery índex (IDO2) and mixed-venous saturation (SvO2) in both treatments. Although the oxygen extraction ratio (O2ER) was increased (P < 0.05) from baseline during hemorrhage, the anaerobic threshold (point where the oxygen comsumption (IVO2) becomes dependent on the IDO2] was not reached in both ...
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