Mechanisms of tachycardia caused by atropine in conscious dogs

Donald, DE; Samueloff, SL; Ferguson, Diane

doi:10.1152/ajplegacy.1967.212.4.901

Cited by 41 publications

(18 citation statements)

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“…In the dog non-myelinated fibres are reported to have no action on the heart (Donald, Samueloff & Ferguson, 1967), but in the rat both myelinated and non-myelinated fibres are reported to produce a bradyeardia (Nosaka, Yasunaga & Kawano, 1979). The cardioinhibitory actions of non-myelinated fibres in the rat were blocked by hexamethonium and thus the mechanism underlying their action appears to be different to that in the rabbit.…”

Section: Discussionmentioning

confidence: 95%

The effects of electrical stimulation of myelinated and non‐myelinated vagal fibres on heart rate in the rabbit.

Ford¹,

McWilliam²

1986

The Journal of Physiology

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SUMMARY1. The bradyeardia evoked by electrical stimulation of the peripheral end of the rabbit vagus nerve is mediated by both myelinated and non-myelinated fibres.2. Stimulation of myelinated fibres at 5 Hz for 20 s resulted in a fall in heart rate from a control value of 204 + 1-3 to 182 + 1-2 beats min-1 (means + S.E. of means). On stimulation of both myelinated and non-myelinated fibres, heart rate fell to 169 + 2 1 beats min-1. Heart rate returned rapidly to control value following stimulation of myelinated fibres but only slowly after stimulation of both myelinated and non-myelinated fibres. Thus recruitment of non-myelinated fibres increased both the magnitude and duration of the bradyeardia.3. Atropine abolished all effects ofvagal stimulation on heart rate. Hexamethonium abolished the effect of myelinated fibres on heart rate; however, recruitment of non-myelinated fibres still produced a bradyeardia.4. It is suggested that the prolonged effect following stimulation of non-myelinated fibres may reflect the persistent action of a non-cholinergic excitatory transmitter at the ganglion.

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Section: Discussionmentioning

confidence: 95%

The effects of electrical stimulation of myelinated and non‐myelinated vagal fibres on heart rate in the rabbit.

Ford¹,

McWilliam²

1986

The Journal of Physiology

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“…A potential criticism of the above protocol involving Chreceptor blockade is whether the reported central excitatory effects of atropine sulfate (Donald et al, 1967) may have influenced the results obtained. In two of the six baboons undergoing autonomic blockade, therefore, the HR-MABP relationship in the normothermic and hyperthermic states, the change in control HR, and the change in HR observed during heat stress were compared for equivalent bolus doses (0.15 mg/kg) and infusion rates (2 ng/kg per min) of atropine sulfate and atropine methylnitrate, a cholinergic antagonist that does not readily cross the blood-brain barrier (Innes and Nickerson, 1975).…”

Section: Experimental Protocolmentioning

confidence: 99%

Influence of heat stress on arterial baroreflex control of heart rate in the baboon.

Gorman¹,

Proppe²

1982

Circulation Research

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SUMMARY. The influence of environmental heat stress on the arterial baroreflex control of heart rate (HR) was studied in eight conscious, chronically instrumented baboons. Inflations of balloon occluders around the inferior vena cava (IVC) and thoracic descending aorta (DA) were used to produce acute, graded changes in mean arterial blood pressure (MABP) in 5 mm Hg intervals ranging from ±5 to ±25 mm Hg. After determination of the HR responses to changes in MABP in the normothermic baboon (blood temperature <37.6°C), the animal was subjected to environmental heating to produce hyperthermia. When blood temperature reached approximately 39.5°C, HR responses to graded DA and IVC occlusions were again determined. During hyperthermia, the HR sensitivity (AHR/AMABP) to MABP changes was markedly diminished for reductions in MABP and significantly enhanced for increases in MABP. To determine whether these alterations in the HR response to changes in MABP were due to an alteration of the baroreflex control of HR, full, sigmoid-shaped HR-MABP curves for both the normothermic and hyperthermic states were constructed and characterized by total HR range, estimated slope of the steep portion of the curve, and MABP at the midpoint of the HR range (BPM). During hyperthermia (1) the whole HR-MABP curve shifted significantly upward by 35-40 beats/min, (2) total HR range, the estimated slope, and BP50 did not change, and (3) the control point (pre-occlusion HR-MABP value) shifted upward along the steep portion of the HR-MABP curve. In six of the eight baboons, full HR-MABP curves were also constructed during either /?-adrenergic blockade or cholinergic (Ch)-receptor blockade in the normothermic and hyperthermic state. Similar to that seen for the unblocked heart, the whole HR-MABP curves were also shifted upward during hyperthermia in this group of baboons with no alteration in the total HR range, the estimated slope, or BP r , 0 . The upward shift in the HR-MABP curve during Ch-receptor blockade, unlike during /S-receptor blockade, was much greater than that which could be attributed only to the local effect of blood temperature. Although the control point was also shifted upward along the steep portion of the curve during /?-or Ch-receptor blockade, the upward shift observed during /S-adrenergic blockade was similar to that observed in the unblocked state. Thus, a heat stress-induced hyperthermia produces a rise in HR without significantly altering the characteristics of the reflex control of HR by arterial baroreceptors. To rely solely on changes in HR sensitivity may lead to erroneous conclusions as to the effect of a particular stress on the baroreceptor reflex control of HR. Further, these results indicate that: (1) the upward shift in the HR-MABP curve is mediated by both the local effect of blood temperature on HR and cardiac sympathetic efferent neurons which are independent of the baroreceptor reflex, and (2) the upward shift in the control point is mediated predominantly by vagal withdrawal, probably as part of the comp...

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“…Comparison of the tachycardiac effect of elliptinium in thoracotomized dogs with that in unthoracotomized dogs supports this reflex mechanism. In the former, the cardiomoderator tone is depressed and the tachycardia due to elliptinium is less marked than in unthoracotomized dogs (+28 • 10 against +74 + 13 beats/rain); the difference in response of the cholinergic system according to the experimental conditions is wellestablished [15,16,17]. However, the heart rate level reached in anesthetized dogs after atropine or atropine-propranolol association (163 • 20 and 163 :t: 14 beats/rain, respectively) makes any additional tachycardia more difficult.…”

Section: Discussionmentioning

confidence: 97%

Acute hemodynamic effects of an antitumoral agent: elliptinium. Involvement of histamine release

et al. 1986

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This work reports a study of cardiovascular effects of elliptinium, a recently-acquired antitumoral agent, acutely administered i.v. in the dog. Its hemodynamic effects (10 parameters) are detailed, and their mechanism of action is investigated by antagonist administration and determination of blood and plasma histamine levels. Elliptinium induces vasodilation and tachycardia. The former is mainly due to histamine release, and a brief and slight release of prostaglandins; the latter is due to a reflex to hypotension and release of catecholamines. These results agree with others using various compounds of the ellipticine family and anthracycline antitumoral agents. They suggest treatment to prevent anaphylactoid side effects observed with this drug in man and they raise the question of the usefulness, in antitumoral agent, of histamine releasing properties.

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Mechanisms of tachycardia caused by atropine in conscious dogs

Cited by 41 publications

References 0 publications

The effects of electrical stimulation of myelinated and non‐myelinated vagal fibres on heart rate in the rabbit.

The effects of electrical stimulation of myelinated and non‐myelinated vagal fibres on heart rate in the rabbit.

Influence of heat stress on arterial baroreflex control of heart rate in the baboon.

Acute hemodynamic effects of an antitumoral agent: elliptinium. Involvement of histamine release

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