Effect of Atropine on the Heart-Rate

Morton, H. J. V.; Thomas, E. T.

doi:10.1016/s0140-6736(58)90580-4

Cited by 70 publications

(26 citation statements)

References 13 publications

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“…The recruiting pattern of inhibition that occurs during inspiration appears to be blocked by atropine, which is consistent with evidence that ACh inhibits c.v.m.s and that this effect is antagonized by atropine. Our data obtained using the direct application of atropine onto c.v.m.s confirm earlier suggestions of a central action of atropine (McGuigan, 1921 ;Heinekamp, 1922;Morton & Thomas, 1958;Averill & Lamb, 1959). Katona, Lipson & Dauchot (1977) showed that minute doses of atropine given i.v.…”

Section: P Gilbey and Otherssupporting

confidence: 90%

Synaptic mechanisms involved in the inspiratory modulation of vagal cardio‐inhibitory neurones in the cat.

Gilbey¹,

Jordan²,

Richter³

et al. 1984

The Journal of Physiology

241

181

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SUMMARY1. The respiratory modulation of the activity of vagal cardio-inhibitory neurones of the nucleus ambiguus of the cat has been investigated by electrophysiological and neuropharmacological techniques.2. All twenty-four vagal efferent neurones studied had axons with conduction velocities indicative of B fibres and projected to the right cardiac branches of the vagus. Their spontaneous or DL-homocysteic acid (DLH)-evoked activity showed a marked reduction during the phase of inspiration and all showed signs of receiving a baroreceptor input.3. Ionophoretic application of DLH always excited cardiac vagal motoneurones (c.v.m.s). Application of acetylcholine to these same cells provoked a decrease in firing rate in twelve of the fifteen neurones tested. In ten of these twelve cells simultaneous application of atropine antagonized the effect of acetylcholine. Atropine applied alone enhanced neuronal firing, particularly in inspiration.4. Stable intracellular recordings have been made from two c.v.m.s. These were inhibited during inspiration. Input resistance fell markedly during inspiration and injection of chloride reversed this wave of hyperpolarization to a wave of depolarization indicating that this resulted from chloride-mediated inhibitory post-synaptic potentials (i.p.s.p.s).5. These c.v.m.s were activated during Stage I expiration, and showed a weak and variable wave of inhibition in Stage II expiration.6. Pulse-rhythmic depolarizing potentials were reduced in their amplitudes during the periods of decreased neurone input resistance.7. It is concluded that c.v.m.s receive an excitatory input during post-inspiration and a powerful inhibitory synaptic input during inspiration. The implications of these observations for the physiology of cardiorespiratory reflexes are discussed.

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Section: P Gilbey and Otherssupporting

confidence: 90%

Synaptic mechanisms involved in the inspiratory modulation of vagal cardio‐inhibitory neurones in the cat.

Gilbey¹,

Jordan²,

Richter³

et al. 1984

The Journal of Physiology

241

181

View full text Add to dashboard Cite

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“…There was an insignificant slowing in heart rate but there was no tachycardia throughout the 6 h period of observation even with the highest doses employed in this investigation. The initial slowing of heart rate with small doses of atropine and similar drugs is considered to be a stimulant effect on medullary vagal nuclei and is not usually seen after large doses given intravenously (Morton & Thomas, 1958;Innes & Nickerson, 1975). It seems therefore that glycopyrronium per se does not have much effect on heart rate.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the anticholinergic actions of glycopyrronium bromide.

Mirakhur¹,

Dundee²,

Jones³

1978

Brit J Clinical Pharma

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1. Glycopyrronium was evaluated by intramuscular, intravenous and oral routes in six adult volunteers for its efficacy as an antisialogogue as also for its action on other aspects of cholinergic activity. 2. It was found to be an effective antisialogogue of long duration of action by all three routes. When given orally the effects were delayed in onset and persisted for too long. Intramuscular and intravenous routes were useful. The intramuscular absorption of the drug is rapid and consistent. 3. Sweat gland activity was affected in a similar fashion but less consistently and other parameters were mostly unaffected. 4. Glycopyrronium 0.2 mg intramuscularly was found to be the optimal dose. Larger doses produced subjective discomfort out of proportion to a further reduction in salivary secretion. 5. Intravenous administration causes no changes in cardiovascular stability.

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“…For example, the chronotropic response to high, fully parasympatholytic doses of atropine has been used to quantify resting cardiac vagal tone (Robinson et al, 1966). However, very low doses are parasympathomimetic reducing heart rate (Averill et al, 1959;McGuigan, 1921;Morton et al, 1958) and increasing variability (Raczkowska et al, 1983). The responses to vagotonic atropine may provide insight to mechanisms influencing resting cardiac vagal tone.…”

Section: Introductionmentioning

confidence: 99%

Effects of fitness and age on the response to vagotonic atropine

Lee¹,

Picard²,

Beske³

et al. 2008

Autonomic Neuroscience

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Previous work indicates compromised cardiac vagal control plays a prominent role in reducing arterial baroreflex gain with age, however older fit individuals display cardiovagal baroreflex responses similar to young individuals. The purpose of this study was to test the hypothesis that chronic aerobic exercise mitigates against age-related declines in cardiac parasympathetic receptor function. In forty-four young and old (fit and unfit) individuals, we used the parasympathomimetic responses to low doses of atropine to probe cardiac cholinergic receptor responses. Data was collected before and after eight doses of atropine sulfate from 0.4 to 7.2 ug/kg. Chronotropic responses were assessed from average RR intervals and heart rate variabilities were derived in time and frequency domains. All subjects exhibited bradycardia with at least one dose of atropine and peak bradycardia occurred at a similar dose in each group. However, changes in heart rate variability did not consistently track the chronotropic responses within subjects (r-square from 0.90 down to 0). As expected, basal RR interval was longer in the fit groups and was unaffected by age. However, the degree of RR interval lengthening with parasympathomimetic atropine was unaffected by physical fitness and was significantly less in all older subjects. These data indicate there are certain prepotent age-related declines in the cardiac parasympathetic system that cannot be prevented by regular physical activity. Keywordsatropine; vagal; heart rate variability; muscarinic receptor Our previous work indicates a decline in cardiac parasympathetic neural control compromises baroreflex gain with age (Kaushal et al., 2002) and this decline can be offset by regular physical activity (Hunt et al., 2001). This suggests a reduced cardiac vagal control accompanying physiologic aging may result essentially from progressive deconditioning (Goldsmith et al., 1997). Greater resting cardiac vagal tone is a distinguishing characteristic of physically fit individuals (Ekblom et al., 1973;Frick et al., 1967;Shi et al., 1995;Smith et al., 1989) and a vagally mediated resting bradycardia is observed in younger as well as older humans after exercise training (Stratton et al., 1994). Moreover, our prior work shows that older fit individuals can display baroreflex-mediated cardiac vagal control similar to young individuals (Hunt et al., 2001). In these individuals, baroreflex responses are maintained despite age-related Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Atropine sulfate is routinely used to probe the cardiac parasympathe...

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Effect of Atropine on the Heart-Rate

Cited by 70 publications

References 13 publications

Synaptic mechanisms involved in the inspiratory modulation of vagal cardio‐inhibitory neurones in the cat.

Synaptic mechanisms involved in the inspiratory modulation of vagal cardio‐inhibitory neurones in the cat.

Evaluation of the anticholinergic actions of glycopyrronium bromide.

Effects of fitness and age on the response to vagotonic atropine

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