Showing papers on "Atropine published in 1984"
TL;DR: In this article, the degree of parasympathetic control of heart rate was assessed by the abolition of respiratory sinus arrhythmia with atropine, and the peak-to-peak variations in heart periods (VHP) before atropINE injection correlated significantly (r = 0.90, P less than 0.001) with parasathy control.
Abstract: The degree of parasympathetic control of heart rate was assessed by the abolition of respiratory sinus arrhythmia with atropine. Peak-to-peak variations in heart periods (VHP) before atropine injection correlated significantly (r = 0.90, P less than 0.001) with parasympathetic control, indicating that VHP alone may be used as a noninvasive indicator of the parasympathetic control of heart rate. Pharmacologic blockade of beta-adrenergic supply in a separate group of normal volunteers did not alter the relationship between VHP and parasympathetic control, indicating that the condition of the experiment (complete rest in a quiet atmosphere) allows the use of VHP alone without pharmacologic interventions to characterize the vagal control of heart rate in humans.
304 citations
TL;DR: The potency of the atropine-induced suppression of GH secretion by three different stimuli, each with presumably different mechanisms of action, suggests that acetylcholine plays an important role in the regulation ofGH secretion.
Abstract: The role of acetylcholine in human GH secretion was studied with atropine, which selectively blocks cholinergic muscarinic receptors and crosses the blood-brain barrier. Paired tests were performed in 22 normal subjects divided into 4 groups. The stimuli employed were arginine (30 g/30 min, iv), clonidine (300 micrograms, orally), physical exercise for 20 min, and saline. In the second test, atropine (1 mg, im) was administered before GH stimulation. Arginine elicited a GH secretory peak of 16.6 +/- 5 ng/ml (mean +/- SEM), which was completely blocked when atropine was administered with arginine (0.9 +/- 0.1 ng/ml). Atropine did not, however, modify the PRL secretory response; peak levels after arginine and atropine plus arginine were 16.3 +/- 3.1 and 16.8 +/- 2.5 ng/ml, respectively. Clonidine elicited a GH secretory peak (11.8 +/- 2.7 ng/ml) which also was blocked by pretreatment with atropine (1.2 +/- 0.2 ng/ml). Neither clonidine nor clonidine plus atropine altered PRL secretion. GH levels also were sharply increased after physical exercise, with a peak level of 19.4 +/- 4.9 ng/ml. Atropine completely blocked exercise-induced GH secretion (2 +/- 0.9 ng/ml). Atropine alone did not modify GH or PRL values compared with saline administration. The potency of the atropine-induced suppression of GH secretion by three different stimuli, each with presumably different mechanisms of action, suggests that acetylcholine plays an important role in the regulation of GH secretion.
144 citations
TL;DR: Pancuronium plus atropine was associated with lesser increases in intracranial pressure and with the least changes in heart rate in response to intubation, and there was no significant difference between the groups for changes in systemic blood pressure or transcutaneous PO2.
136 citations
TL;DR: Parallel effects of cholinomimetic drugs and anticholinergic agents, combined with the effect of stress on central acetylcholine activity, suggest a stress‐acetyl choline linkage.
Abstract: The cholinomimetic agents, physostigmine, neostigmine, and arecoline, and the anticholinergic agents, atropine, scopolamine, and methscopolamine, have been used to explore an acetylcholine hypothesis of affect disorders and stress. Cholinomimetic drugs cause many of the same effects as do naturally occurring stressors. These include increases in negative affect, the induction of affective disorders, increases in stress neuroendocrines including ACThH, cortisol, beta-endorphin, growth hormone, prolactin, epinephrine, and noprepinephrine, increases in blood pressure and pulse rate, and increases in analgesia. These parallel effects, combined with the effect of stress on central acetylcholine activity, suggest a stress-acetylcholine linkage.
126 citations
Journal Article•
TL;DR: In this article, the cardiovascular effects associated with the microinjection (100 nl) of carbachol, physostigmine and atropine into the pressor area in the ventrolateral medulla (VLPA) were studied.
Abstract: The cardiovascular effects associated with the microinjection (100 nl) of carbachol, physostigmine and atropine into the pressor area in the ventrolateral medulla (VLPA) were studied. In urethane anesthetized rats, VLPAs were functionally identified bilaterally by microinjection of the neuroexcitatory amino acid L-glutamate (300 ng/site). L-Glutamate microinjections into the VLPA cause a transient rise in blood pressure (BP) and heart rate (HR). The bilateral microinjection of carbachol into the VLPA caused a prolonged dose-related increase in BP and HR in the dose range of 0.8 to 400.0 ng/site. At higher doses (1-10 micrograms), carbachol caused a decrease in BP and HR; indicative of depolarization blockade. Acetylcholine esterase inhibition by physostigmine microinjections in the VLPA caused cardiovascular effects similar to those observed with carbachol. The hypertensive responses evoked by muscarinic receptor stimulation in the VLPA were mediated by increasing sympathetic outflow. The pathway by which cholinergic receptor stimulation in the VLPA activates vasomotor outflow appears to be entirely descending as coronal knife cuts at the level of the trapezoid body failed to alter the hypertensive responses. Pressor responses elicited by both physostigmine and carbachol were reversed completely by the i.v. administration of atropine sulfate (0.5-3 mg/kg i.v.). Muscarinic receptor blockade in the VLPA after atropine sulfate microinjection caused a dose-related (0.4-15.0 micrograms/site) fall in the BP and HR suggesting that cholinergic mechanisms in the VLPA are tonically active.
99 citations
TL;DR: The results suggest that acetylcholine release is decreased in synaptosomes prepared from old rats although the presynaptic muscarinic regulation of release is functional, suggesting that mus carinic receptor-mediated release-modulation is a potential site for pharmacologically altering ACh release.
88 citations
TL;DR: The present data suggest that both VIP and PHI may contribute to the atropine-resistant vasodilation seen upon stimulation of the chorda-lingual nerve, as indicated by an increase in output.
79 citations
TL;DR: Positron Emission Tomography was used to analyse in vivo antagonist binding to human myocardial muscarinic cholinergic receptor and 11C-MQNB kinetics were analysed with a mathematical model which assumes the existence of a boundary layer containing free ligand in the vicinity of the binding sites.
79 citations
TL;DR: The nerve agent soman, as well as other organophosphates such as paraoxon and phospholine in concentrations that caused cholinergic symptoms induced a progressive dose-related necrosis in rat skeletal muscle fibers, causing necrotic nerve fibers to be repaired within 1 week.
78 citations
TL;DR: It is concluded that this region contains premotor elements forming part of the internuncial network organizing oesophageal peristalsis, and the source of postulated cholinergic afferents to these neurones remains to be identified.
75 citations
TL;DR: Analysis of various cholinergic drugs revealed that the evoked efflux was susceptible to muscarinic ligands, it was enhanced by atropine and reduced by oxotremorine, which suggest a feed-back regulation of acetylcholine release via mus carinic autoreceptors.
TL;DR: It is suggested that the conspicuous pathology that follows a single, near-lethal dose of soman results from a depletion of energy flow along with an influx of Ca2+ which sets into motion a cascade of destructive reactions, such as activation of proteases.
TL;DR: It is concluded that opiate receptor stimulation by morphine causes inhibition of the vagally mediated component of water-induced bronchoconstriction.
Abstract: To determine whether morphine sulfate alters the bronchoconstrictive response to inhalation of distilled water, we gave 13 subjects with mild asthma 0.15 mg/kg morphine sulfate or normal saline intravenously, after which they inhaled increasing volumes of nebulized distilled water from an ultrasonic nebulizer. We constructed stimulus-response curves, and by interpolation determined the provocative output of the nebulizer that resulted in a 50% increase in SRaw from baseline (PO50). On a separate day the subjects inhaled 2.0 mg of atropine sulfate 30 min before they inhaled distilled water. We compared the bronchoconstrictive response after morphine and after atropine with the bronchoconstrictive response after saline by determining the ratio of the PO50 values. Atropine was considered effective in inhibiting bronchoconstriction in 7 of the 13 subjects in whom the ratio of PO50 after atropine to the PO50 after saline was greater than 2.0. By similar criteria, morphine was also considered effective in 5 of these 7 subjects. Neither atropine nor morphine was effective in the remaining 6 subjects. By chi-square analysis, we found a positive correlation between the inhibitory effects of morphine and those of atropine (p less than 0.05). In the 5 subjects in whom morphine was effective, naloxone reversed the inhibitory effect of morphine. Atropine caused significant baseline bronchodilation when compared with placebo (normal saline), whereas morphine did not. We conclude that opiate receptor stimulation by morphine causes inhibition of the vagally mediated component of water-induced bronchoconstriction.
TL;DR: Rabbit bladder body was stimulated to contract by a number of agonists, of which bradykinin was the most potent, and ATP one of the least potent substances tested, and the atropine-resistant component of the neurogenic response was unaffected by doses which suppressed responses to histamine or 5HT.
TL;DR: The evidence that neostigmine markedly aggravated gastric damage caused by low doses of absolute ethanol and that atropine completely prevented this damage postulates mechanisms involving specific muscarinic receptor interactions.
TL;DR: It is concluded that in the neostriatum presynaptic muscarinic receptors modulate nicotinic excitation since potassium-stimulated ACh release and intrinsically evoked synaptic excitation are influenced byMuscarinic drugs in the same way.
TL;DR: The results suggest that V is sensitive to manipulations of vagal influences on the heart, and often responds in a different manner from heart period and HPV.
Abstract: Changes in heart period, heart period variance (HPV), and the respiratory component of HPV were examined during enhanced negative chronotropic influences on the heart produced by aortic depressor nerve (ADN) stimulation in urethane anesthetized rabbits. Spectral analysis was used to quantify the respiratory component of HPV, respiratory sinus arrhythmia (RSA). The statistic derived from spectral analysis which describes RSA, V, has been proposed to be sensitive to vagal influences on the heart. Stimulation of the ADN significantly increased V, heart period, and HPV. However, unlike V and heart period, HPV values remained elevated following the end of stimulation. Propranolol administration did not alter the magnitude of the evoked increase in V, heart period, or HPV. In contrast, administration of atropine abolished the increases due to stimulation in all three measures. Heart period exhibited a monotonic relationship with stimulation current intensity. This relationship disappeared after propranolol administration suggesting sympathetic mediation. The results suggest that V is sensitive to manipulations of vagal influences on the heart. In addition, V often responds in a different manner from heart period and HPV.
TL;DR: Progesterone-induced maturation of follicle-enclosed and denuded Xenopus laevis oocytes was significantly shortened by a concomitant exposure to acetylcholine, which might reflect a physiological influence of the cholinergic system on an in vivo maturation process.
Abstract: Progesterone-induced maturation of follicle-enclosed and denuded Xenopus laevis oocytes was significantly shortened by a concomitant exposure to acetylcholine The promotion of maturation by acetylcholine was blocked by the specific muscarinic antagonist atropine The action of acetylcholine was dose dependent, and the neurotransmitter was effective at very low concentrations Progesterone progressively reduced the electrophysiological responses of X laevis oocytes to acetylcholine, which completely disappeared close to the time of germinal vesicle breakdown Progesterone alone did not elicit any electrophysiological responses The in vitro effect of acetylcholine on oocyte maturation might reflect a physiological influence of the cholinergic system on an in vivo maturation process
TL;DR: The results show that ET is produced by antimuscarinic agents in general and is not mediated by the beta-adrenergic system and is present only when the cervical vagi are intact, probably because ET is mediated by cholinergic vagal efferent fibers via a mechanism that has not yet been recognized in cardiac rate control.
Abstract: In conscious dogs the heart rate after atropine is higher than after bilateral vagotomy; we have termed the additional heart rate with atropine "excess tachycardia" (ET). In six dogs the cervical vagosympathetic trunks were exteriorized in skin tubes, and arterial and venous catheters were chronically implanted. Atropine sulfate (0.1 mg/kg iv) injected during cold blockade of the vagi increased the heart rate by only 6 +/- 4 (SE) beats/min (NS) but rewarming the vagi in five of the six dogs after atropine resulted in an additional heart rate increase (ET) of 26 +/- 6 beats/min (P less than 0.005). The ET (41 +/- 11 beats/min) tended to be larger when the animals were pretreated with 1 mg/kg propranolol (P = 0.09). Similar results were obtained when atropine methylbromide, a charged derivative of atropine sulfate, or glycopyrrolate, a synthetic antimuscarinic agent, was substituted for atropine sulfate (ET: 51 +/- 6 and 51 +/- 16 beats/min, respectively). Raising the arterial blood pressure with phenylephrine increased the heart rate further; lowering the blood pressure with sodium nitroprusside attenuated or abolished the ET. Our results show that ET is produced by antimuscarinic agents in general and is not mediated by the beta-adrenergic system. Furthermore, ET is present only when the cervical vagi are intact, probably because ET is mediated by cholinergic vagal efferent fibers via a mechanism that has not yet been recognized in cardiac rate control.
TL;DR: It is concluded that inhaled atropine (an anticholinergic drug) may be preferable to inhaled metaproterenol (a beta-adrenergic agonist) when additional bronchodilation is needed in patients with chronic obstructive pulmonary disease and high-normal serum theophylline levels.
TL;DR: It is suggested that a direct peripheral action may occur at κ-sites, located on the heart after intravenous injection of ethylketocyclazocine in the rat, which is associated with a fall in heart rate and blood pressure.
01 Jan 1984
TL;DR: Evidence is presented that implicates brain acetylcholine (ACh) in the control of blood pressure (BP) and in hypertension and central cholinergic stimulation by muscarinic agonists or inhibitors of acetyl cholinesterase evokes a hypertensive response in several animal species, including humans.
Abstract: Evidence is presented that implicates brain acetylcholine (ACh) in the control of blood pressure (BP) and in hypertension. Central cholinergic stimulation by muscarinic agonists or inhibitors of acetylcholinesterase (AChE) evokes a hypertensive response in several animal species, including humans. The elevation in BP after injection of AChE inhibitors is mediated centrally by ACh acting on muscarinic receptors and peripherally through increased sympathetic nerve activity. The pressor response is accompanied by inhibition of reflex tachycardia and potentiation of both reflex bradycardia and the pressor reflex to carotid artery occlusion. Intracerebroventricular injection of hemicholinium 3 in doses that deplete brain ACh lowers BP in the spontaneously hypertensive and the deoxycorticosterone acetate-salt hypertensive rat. Little or no reduction occurs in the normotensive rat or in animals made hypertensive by aortic coarctation. In addition, atropine and the selective central muscarinic receptor antagonist N-(4-diethylamino-2-butynyl)-succinimide lower BP in the spontaneously hypertensive rat but not in the normotensive rat.
TL;DR: It is concluded that atropine causes dose-dependent inhibition of histamine-induced bronchoconstriction and that this effect is not merely a function of the atropin-induced in baseline airway caliber.
Abstract: To determine whether treatment with atropine causes dose-dependent inhibition of histamine-induced bronchoconstriction, we constructed dose-response curves to inhaled histamine after inhalation of placebo and 0.26 and 2.08 mg of atropine in eight subjects with mild asthma. Both doses of atropine significantly inhibited histamine-induced bronchoconstriction, and 2.08 mg caused significantly greater inhibition than 0.26 mg. Baseline specific airway resistance was significantly reduced by both doses of atropine but was no different after 2.08 mg than after 0.26 mg. There were considerable differences in the efficacy of atropine among individuals. We conclude that atropine causes dose-dependent inhibition of histamine-induced bronchoconstriction and that this effect is not merely a function of the atropine-induced in baseline airway caliber. The large magnitude of the atropine effect in some subjects and the small magnitude of the effect in others suggest that there is variability in the degree of involvement of muscarinic mechanisms in the exaggerated bronchomotor response to histamine in asthmatic subjects.
TL;DR: Glycopyrrolate produces significant bronchodilation of long duration but free of the side effects of muscarinic blockade that characterize atropine inhalation.
Abstract: Bronchodilation was produced in normal subjects by inhalation of high doses of a quaternary parasympatholytic agent (glycopyrrolate), and responses were compared with those of atropine and a placebo. Both drugs induced significant increases in specific airway conductance (SGaw) and forced expiratory flows, but the effects of glycopyrrolate were sustained significantly longer (> 6 h). Whereas atropine produced an increased heart rate (26%) and severe dry mouth in all subjects, these symptoms were absent with glycopyrrolate and placebo. Therefore, glycopyrrolate produces significant bronchodilation of long duration but free of the side effects of muscarinic blockade that characterize atropine inhalation.
TL;DR: Results indicate that alpha-adrenergic receptors are present in the muscle cell membrane of the rat seminal vesicle and prevent the effects of acetylcholine, indicating that they are of the muscarinic type.
Abstract: Various autonomic drugs were placed on the peritoneal covering of the seminal vesicles of anaesthetized rats. Adrenaline (which stimulates the alpha-, beta 1- and beta 2-adrenoceptors) and phenylephrine (an alpha-stimulating agent) produced a sudden increase in tonus and in the amplitude and frequency of contractions. Phentolamine (an alpha-blocker) prevented these effects, whereas propranolol (a beta 1- and beta 2-blocker) did not. Phentolamine also abolished the seminal vesicle response to electrical stimulations. Terbutaline (a beta 2-stimulating agent) did not affect the spontaneous activity. There were no differences between the effects of terbutaline alone and those of terbutaline in the presence of propranolol. Moreover, propranolol did not block the contractile response of the gland to adrenaline or to electrical stimulation. These results indicate that alpha-adrenergic receptors are present in the muscle cell membrane of the rat seminal vesicle. The effects of acetylcholine were similar to those produced by adrenaline or phenylephrine although of smaller magnitude. Atropine prevented the effects of acetylcholine, indicating that they are of the muscarinic type.
TL;DR: Ninety adult patients about to undergo strabismus surgery received glycopyrrolate or atropine intramuscularly and the oculocardiac reflex was inhibited in a dose‐dependent manner by the drugs studied.
Abstract: Summary
Ninety adult patients about to undergo strabismus surgery received glycopyrrolate or atropine intramuscularly. Three doses of each anticholinergic were studied. Cardiac rate and rhythm were recorded during halothane anaesthesia. The oculocardiac reflex, defined as a fall of 20% in heart rate during traction of the extraocular muscle was inhibited in a dose-dependent manner by the drugs studied. The potency ratio of glycopyrrolate to atropine according to the oculocardiac reflex was established as 1:2.
TL;DR: The results indicate that interactions between VIP- and muscarinic receptors may be of importance in the rat cerebral cortex.
TL;DR: The organophosphorus nerve agents soman and tabun were tested in the hen at doses 120–150 times higher than their acute LD50, as it was assumed that these doses would produce delayed neuropathy.
Abstract: The organophosphorus nerve agents soman and tabun were tested in the hen at doses 120–150 times higher than their acute LD50, as it was assumed that these doses would produce delayed neuropathy. The animals were protected against the acute lethal effect of these agents by pretreatment with atropine, physostigmine, diazepam, and the oxime HI-6 or obidoxime. The surviving animals were followed for 30 days and the occurrence of delayed neuropathy was clinically diagnosed. Soman produced severe delayed neuropathy at a dose of 1.5 mg/kg, a dose which produced acute lethality in five animals out of six. Tabun elicited very mild neuropathic symptoms in one animal out of two at a dose of 6 mg/kg given on 2 consecutive days. Delayed neuropathy was not seen in the hens that survived the acute toxicity of a single dose of tabun, 12 mg/kg (three out of six) or 15 mg/kg (two out of six).
TL;DR: There is a substantial bradycardia due to an increase in vagal activity during hypoxia in the fetus and that blockade of this activity causes a marked tachycardia but no increase in fetal oxygen uptake.
01 Aug 1984
TL;DR: It appears that the prolonged time course of the cardiac responses to bursts of vagal activity is determined by a slow rate of transmitter inactivation (diffusion plus hydrolysis) in addition to slowly operating postsynaptic mechanisms mediated by activation of the muscarinic receptor.
Abstract: The occurrence of unhydrolyzed acetylcholine (ACh) in the cardiac perfusate during vagal stimulation in the absence of cholinesterase inhibition has been demonstrated by several methods. Because some ACh was found unhydrolyzed in the extracellular space for several seconds after vagal stimulation (half-time of decay 2.5 s), it appears that the prolonged time course of the cardiac responses to bursts of vagal activity is determined by a slow rate of transmitter inactivation (diffusion plus hydrolysis) in addition to slowly operating postsynaptic mechanisms mediated by activation of the muscarinic receptor. The neuronal uptake of choline in isolated heart preparations was found to be Na+ dependent, sensitive to hemicholinium 3, and activated by vagal stimulation. Activation occurred after a delay of 1 or 2 min and slowly faded within 5 min after stimulation. Resting release of ACh was insensitive to extracellular Ca2+ and to muscarinic feedback inhibition, in contrast to the evoked transmitter release. Inasmuch as atropine increased ACh release by vagal and field stimulation to the same extent, muscarinic feedback inhibition is likely to occur at postganglionic parasympathetic neurons. Adrenergic agonists and propranolol did not significantly change the release of ACh.