<i>Effects of Atropine on Heart Rate and Oxygen Intake in Working Man</i>

Robinson, S.; Pearcy, M.; Brueckman, F. R.; Nicholas, J. R.; Miller, DT

doi:10.1152/jappl.1953.5.9.508

Cited by 51 publications

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“…The increase in mean exercise heart rate of 10 or 11 beats/min produced by vagal blockade with atropine is similar to that demonstrated by other workers at similar exercise heart rates (Robinson et aL, 1953;Robinson et al, 1966;Chamberlain et al, 1967). The results of the present study show that atropine (0.04 mg/kg) given intravenously unfolds a component of vagal activity which is reproducible in the same subject for standardised exercise.…”

Section: Resultssupporting

confidence: 91%

Intrinsic Heart Rate on Exercise and the Measurement of Β‐adrenoceptor Blockade

Carruthers¹,

Shanks²,

McDevitt³

1976

Brit J Clinical Pharma

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1 Methods of expressing the effects of ,B-adrenoceptor blocking drugs on exercise heart rate have been evaluated using a standardised exercise test. 2 In six normal subjects given atropine (0.04 mg/kg) on two separate occasions, the mean + s.e. mean exercise heart rate rose by 10.3± 1.8 beats/min and by 11.0± 1.6 beats/min respectively. This increase was designated the 'vagal effect and was not significantly different in the two studies. 3 After atropinsation, propranolol (0.2 mg/kg) reduced mean ± s.e. mean exercise heart rate by 45.3 ± 2.6 beats/min and 0.4 mg/kg by 50.8 ±4.5 beats/min. This mean sympathetic blockade was not altered significantly by increasing the dose of propranolol but, in four of the six subjects, the larger dose produced an increased effect of 4, 6, 12 and 16 beats/min, suggesting that maximum sympathetic blockade may not have been produced by 0.2 mg/kg. 4 Knowledge of the vagal effect in each subject with standardised exercise enabled prediction to be made of the exercise heart rate after propranolol (0.4 mg/kg) without previous atropinisation. Propranolol (0.4 mg/kg) was then given intravenously to each subject and the actual exercise heart rate measured. There was no significant difference between the predicted and observed exercise heart rates. 5 Propranolol (0.6 mg/kg) without atropine was then given to the four subjects who had shown increased effect with (0.4 mg/kg) and the sympathetic blockade was measured. In one subject, a further increase in sympathetic blockade of 10 beats/min was found. 6 The intrinsic heart rate at rest and on exercise was measured for propranolol (0.2 and 0.4 mg/kg) and, for propranolol (0.6 mg/kg), the intrinsic heart rate on exercise was, calculated. At rest, although no significant difference was found between the two dose levels, three subjects did not appear to have maximum autonomic blockade at 0.2 mg/kg. Similarly, several subjects had lower intrinsic heart rates on exercise after 0.4 or 0.6 mg/kg than after 0.2 mg/kg. The intrinsic heart rate on exercise was significantly greater than that obtained at rest. 7 Using the maximum sympathetic blockade obtained in each subject as the sympathetic component of exercise, the effects of increasing oral doses of practolol on exercise heart were measured as percentage blockade of sympathetic effect and this was compared with other conventional methods of measuring j-adrenoceptor blockade. It was found that percentage blockade of sympathetic effect correlated most closely with both percentage and absolute reduction of exercise heart rate. Correlations with exercise heart rate after drug and percentage inhibition of tachycardia, whilst also significant, did not appear as good. 8 When the effects of practolol were expressed in terms of the potential blockade, a plateau occurred between 70 and 80% of 'maximum' sympathetic blockade. The failure to achieve higher levels with practolol may be the result of its partial agonist or intrinsic sympathomimetic activity.

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Section: Resultssupporting

confidence: 91%

Intrinsic Heart Rate on Exercise and the Measurement of Β‐adrenoceptor Blockade

Carruthers¹,

Shanks²,

McDevitt³

1976

Brit J Clinical Pharma

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“…9,29) This result was confirmed in a largescale trial conducted by Cole, et al 6) Several mechanisms have been proposed for the attenuation of HRR in coronary artery disease patients, such as an imbalance between sympathetic withdrawal and parasympathetic activation, the alteration of venous return, or stretch in the atrial wall. [1][2][3][4][5] The mechanism underlying the attenuation of HRR in heart failure patients may be much more complicated. The decreased resting vagal tonus, increased resting and exercise sympathetic tonus, and attenuation of autonomic regulatory mechanisms by increasing age are possible mechanisms proposed for the attenuation of HRR in heart failure patients.…”

Section: Discussionmentioning

confidence: 99%

Decreased Heart Rate Recovery in Patients With Heart Failure Effect of Fluvastatin Therapy

et al. 2005

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SUMMARYHeart rate recovery is the difference in heart rate at peak exercise and at a specific time interval following the onset of recovery. Attenuated heart rate recovery is an independent predictor of mortality in patients with a history of coronary artery disease. The aim of the present study was to evaluate the effect of a statin on heart rate recovery, particularly in patients with ischemic heart failure and hyperlipidemia. Twenty-nine consecutive hyperlipidemic, stable coronary artery disease patients with heart failure and 19 healthy subjects were enrolled. Heart rate recovery values at the 1st and 3rd minutes and lipid profiles of the patients were evaluated at baseline and following 3 months of treatment with fluvastatin. Compared with healthy subjects, the heart rate recovery values were significantly lower in the heart failure patients in both the 1st and 3rd minutes, respectively (31 ± 6 versus 19 ± 7, P < 0.0001; 66 ± 7 versus 47 ± 8, P < 0.0001). Heart rate recovery in the 1st and 3rd minutes increased from 19 ± 7 to 24 ± 9 and 47 ± 8 to 57 ± 11, respectively, following treatment (P < 0.001, P < 0.001). There were no significant correlations among the changes in lipid parameters or HRR in the first and third minutes in the recovery period. The results revealed an improvement in heart rate recovery in heart failure patients by fluvastatin treatment. If this association can be confirmed by other studies, it would be interesting to perform further studies into the mechanism underlying this finding. (Int Heart J 2005; 46: 845-854)

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“…This is true at the cardiac level where exercise-induced tachycardia is almost maximal, vagal tone being almost completely abolished (Robinson, Pearcy, Brueckman, Nicholas & Miller, 1953;Hicks, Arbab, Turner & Hills, 1972;Guigler, Hobel, Bodem & Dengler, 1975). It is also true at the pulmonary level where post-exercise PEFR values are always greater than pre-exercise values (Kumana et al, 1974;Marlin, Kumana, Kaye, Smith & Turner, 1975).…”

Section: Discussionmentioning

confidence: 99%

Comparative beta‐adrenoceptor blocking effects and pharmacokinetics of penbutolol and propranolol in man.

Jf¹,

Richer²,

Chauvin³

et al. 1977

Brit J Clinical Pharma

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1The ,B-adrenoceptor blocking effects of penbutolol were compared with those of propranolol and a placebo in a double-blind trial involving six healthy volunteers. 2 Heart rate (HR), systolic blood pressure (SBP) and peak expiratory flow rate (PEFR) were measured at rest and during vigorous exercise before and at intervals up to 7 h after oral administration of the drugs. In addition, plasma renin activity (PRA) at rest and plasma levels of penbutolol and propranolol were determined. 3 Penbutolol proved to be a non-cardioselective,-adrenoceptor blocking drug, antagonizing exercise-induced tachycardia, reducing exercise-induced increase in PEFR and decreasing PRA. The ,B-adrenolytic potency of penbutolol was shown to be four-fold that of propranolol but the duration of its effect was similar. 4 The peak plasma level of penbutolol was reached 1 h after administration and its half-life was 4.5 h. 5 Comparison of plasma levels and biological activity of penbutolol revealed that after oral administration this drug is transformed into an active metabolite in man.

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Effects of Atropine on Heart Rate and Oxygen Intake in Working Man

Cited by 51 publications

References 0 publications

Intrinsic Heart Rate on Exercise and the Measurement of Β‐adrenoceptor Blockade

Intrinsic Heart Rate on Exercise and the Measurement of Β‐adrenoceptor Blockade

Decreased Heart Rate Recovery in Patients With Heart Failure Effect of Fluvastatin Therapy

Comparative beta‐adrenoceptor blocking effects and pharmacokinetics of penbutolol and propranolol in man.

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