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Atropine

About: Atropine is a research topic. Over the lifetime, 3461 publications have been published within this topic receiving 79434 citations. The topic is also known as: (+-)-Hyoscyamine & (+,-)-Tropyl tropate.


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Journal ArticleDOI
TL;DR: Baroreceptor-induced slowing of heart rate in normal subjects was shown to be mediated by the parasympathetic nervous system since it could be abolished with atropine.
Abstract: To define the state of the parasympathetic nervous system in heart failure, parasympathetic blockade with atropine was induced after adrenergic blockade with propranolol in 12 normal subjects and in nine patients with heart disease. Atropine elevated heart rate by 55 ± 9 per cent in normal subjects, but by only 23 ± 8 per cent in patients with heart disease (p less than 0.05). In 23 control subjects and 22 patients, transient elevations in arterial pressure were produced by intravenous injections of phenylephrine, and successive R-R intervals were plotted as a function of systolic pressure. The slowing of heart rate per unit rise in systolic arterial pressure averaged 16.0 ±1.8 msec per millimeter of mercury in normal subjects but only 3.70 ± 0.8 msec per millimeter of mercury in the patients (p less than 0.001). Baroreceptor-induced slowing of heart rate in normal subjects was shown to be mediated by the parasympathetic nervous system since it could be abolished with atropine. These findings poi...

963 citations

Journal ArticleDOI
TL;DR: The results indicate that T30 is mediated primarily by vagal reactivation, independent of sympathetic withdrawal, and is significantly smaller in athletes and significantly larger in patients with chronic heart failure than that in respective age-matched normal control subjects.

932 citations

Journal ArticleDOI
TL;DR: It appears that baroreceptor-induced alterations in heart rate may be mediated by increased or decreased activity of either efferent system; the ultimate balance is critically dependent on the preexisting level of background autonomic activity.
Abstract: The control of heart rate by the autonomic nervous system was investigated in conscious human subjects by observing the effects of β-adrenergic blockade with propranolol, of parasympathetic blockade with atropine, and of combined sympathetic and parasympathetic blockade. The increase in heart rate with mild exercise in supine men was mediated predominantly by a decrease in parasympathetic activity; at higher levels of work, however, sympathetic stimulation also contributed to cardiac acceleration. When the response to 80° head-up tilt was compared with the response to exercise in the same subject supine, it appeared that the attainment of an equivalent heart rate was associated with a significantly greater degree of sympathetic activity during tilting than during exercise. Although heart rate was always higher at any given pressure during exercise than it had been at rest, the changes in heart rate that followed alterations in arterial pressure were found to be of similar magnitudes at rest and during exe...

838 citations

Journal ArticleDOI
TL;DR: The aim of this study was to determine the effect of varying concentrations of acetylcholine on the vasoconstriction of the perfused mesenteric arteries of the rat caused by stimulation of their sympathetic postganglionic nerves.
Abstract: The aim of this study was to determine the effect of varying concentrations of acetylcholine on the vasoconstriction of the perfused mesenteric arteries of the rat caused by stimulation of their sympathetic postganglionic nerves. Perfusion was carried out with a peristaltic pump, and the constriction caused by stimulation was measured by the rise of pressure in the cannula tied in the artery. Two effects were found. At rates of stimulation between 2 and 8/sec, acetylcholine added to the perfusion fluid in very low concentrations (50 pg/ml) caused an increase in the vasoconstriction. An increase was also caused by adding a concentration of 2 ng/ml for 15 seconds. If, however, this or a greater concentration was added for a longer time, it had the opposite effect and the vasoconstriction was greatly reduced or blocked. This reduction or block was not due in the main to a reduction or block of the vasoconstrictor action of norepinephrine. Block of response to stimulation was also produced by guanethidine. The block produced by acetylcholine resembled the block produced by guanethidine in two respects. The block was removed by raising the calcium concentration, and it was also removed by adding d -amphetamine to the perfusion fluid. The block produced by a given concentration of acetylcholine was abolished by a much higher concentration of atropine or hyoscine.

376 citations

Journal ArticleDOI
15 Apr 1983-Science
TL;DR: Administration of pilocarpine or physostigmine to rats treated with lithium chloride produced sustained limbic seizures, widespread brain damage, and increased concentrations of D-myo-inositol-1-phosphate in the brain.
Abstract: Administration of pilocarpine or physostigmine to rats treated with lithium chloride produced sustained limbic seizures, widespread brain damage, and increased concentrations of D-myo-inositol-1-phosphate (a metabolite of the phosphoinositides, lipids involved in membrane receptor function) in the brain. The syndrome was preventable with atropine. The physostigmine doses and concentrations of blood lithium that caused the syndrome are similar to those considered appropriate for psychiatric chemotherapy.

365 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20243
2023137
2022237
202120
202019
201918