Response to exercise in dogs with cardiac denervation

1963 ◽  
Vol 205 (2) ◽  
pp. 393-400 ◽  
Author(s):  
David E. Donald ◽  
John T. Shepherd
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Stroke Volume ◽  
Equivalent Dose ◽  
Cardiac Denervation ◽  
Modest Increase ◽  
Severe Exercise ◽  
Response To Exercise

Dogs with chronic cardiac denervation by the technic of regional neural ablation showed an unchanged capacity for work as measured by oxygen consumption. The relation of cardiac output to oxygen consumption during exercise remained unchanged from preoperational values. When the dogs started to run, the heart rate rose slowly over 1.5 min to reach a steady value proportional to the work performed. When exercise was stopped, the heart rate declined slowly. With mild exercise, the increase in cardiac output was mainly through stroke volume; with more severe exercise, increase in stroke volume and heart rate contributed equally, in contrast to the normal dog where the increase in rate predominates. Neither the pattern of the change in heart rate nor the plateau values were altered by adrenalectomy. The change in rate was not attributable to change in intravascular temperature. In an equivalent dose of base, norepinephrine caused tachycardia but little or no change in cardiac output, whereas epinephrine resulted in an increase in cardiac output with but a modest increase in heart rate.

Cardiovascular changes in the exercising emu

1983 ◽  
Vol 104 (1) ◽  
pp. 193-201 ◽  
Author(s):  
B. Grubb ◽  
D. D. Jorgensen ◽  
M. Conner
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Stroke Volume ◽  
Oxygen Content ◽  
Body Mass ◽  
Fold Increase ◽  
Exercise Heart Rate ◽  
Rate Of Oxygen Consumption ◽  
Cardiovascular Variables

Cardiovascular variables were studied as a function of oxygen consumption in the emu, a large, flightless ratite bird well suited to treadmill exercise. At the highest level of exercise, the birds' rate of oxygen consumption (VO2) was approximately 11.4 times the resting level (4.2 ml kg-1 min-1). Cardiac output was linearly related to VO2, increasing 9.5 ml for each 1 ml increase in oxygen consumption. The increase in cardiac output is similar to that in other birds, but appears to be larger than in mammals. The venous oxygen content dropped during exercise, thus increasing the arteriovenous oxygen content difference. At the highest levels of exercise, heart rate showed a 3.9-fold increase over the resting rate (45.8 beats min-1). The mean resting specific stroke volume was 1.5 ml per kg body mass, which is larger than shown by most mammals. However, birds have larger hearts relative to body mass than do mammals, and stroke volume expressed per gram of heart (0.18 ml g-1) is similar to that for mammals. Stroke volume showed a 1.8-fold increase as a result of exercise in the emus, but a change in heart rate plays a greater role in increasing cardiac output during exercise.

Cardiopulmonary effects of continuous pressure breathing in hypothermic dogs

1965 ◽  
Vol 20 (4) ◽  
pp. 669-674 ◽  
Author(s):  
J. Salzano ◽  
F. G. Hall
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Stroke Volume ◽  
Negative Pressure ◽  
Alveolar Ventilation ◽  
Positive Pressure ◽  
Negative Pressure Breathing ◽  
Continuous Positive Pressure ◽  
Respiratory Dead Space

Continuous pressure breathing was studied in hypothermic anesthetized dogs. Alveolar ventilation decreased during continuous positive-pressure breathing and increased during continuous negative-pressure breathing. The changes in alveolar ventilation were due to changes in respiratory rate as well as in respiratory dead space. Cardiac output fell significantly during continuous positive-pressure breathing due to a reduction in heart rate and stroke volume. During continuous negative-pressure breathing cardiac output was only slightly greater than during control as a result of a fall in heart rate and an increase in stroke volume. Oxygen consumption was reduced to 60% of control during continuous positive-pressure breathing of 16 cm H2O but was 25% greater than control during continuous negative-pressure breathing. Qualitatively, CO2 production changed as did O2 consumption but was different quantitatively during continuous negative-pressure breathing indicating hyperventilation due to increased respiratory rate. Mean pulmonary artery pressures and pulmonary resistance varied directly with the applied intratracheal pressure. The results indicate that the hypothermic animal can tolerate an imposed stress such as continuous pressure breathing and can increase its oxygen consumption during continuous negative-pressure breathing as does the normothermic animal. hypothermia; respiratory dead space; metabolic rate; cardiac output Submitted on December 8, 1964

Constancy of stroke volume in ventricular responses to exertion

1959 ◽  
Vol 196 (4) ◽  
pp. 745-750 ◽  
Author(s):  
Robert F. Rushmer
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Cardiac Response ◽  
Indirect Measurements ◽  
Increase Stroke Volume ◽  
Normal Man ◽  
The Right ◽  
Response To Exercise ◽  
Indicator Dilution Techniques

Diastolic and systolic dimensions of the left ventricle and the free wall of the right ventricle in intact dogs are affected little by spontaneous exercise. The concept that stroke volume and heart rate in normal man increase by about the same relative amounts was derived from estimations of cardiac output, particularly in athletes, based upon indirect measurements using foreign gases or CO2. Data for man obtained with the modern cardiac catheterization or indicator dilution techniques confirm the impression derived from intact dogs that increased stroke volume is neither an essential nor a characteristic feature of the normal cardiac response to exercise. Stroke volume undoubtedly increases whenever cardiac output is increased with little change in heart rate (e.g. in athletes or in patients with chronic volume loads on the heart). Tachycardia produced experimentally with an artificial pacemaker in a resting dog causes a marked reduction in diastolic and systolic dimensions and in the stroke change of dimensions. The factors generally postulated to increase stroke volume during normal exercise may prevent the reduction in stroke volume accompanying tachycardia.

Cardiac Manifestations of Systemic Diseases and Pregnancy

2016 ◽  
pp. 45-52
Author(s):  
Lori A. Blauwet ◽  
Rekha Mankad ◽  
Sabrina D. Phillips ◽  
Kyle W. Klarich
Keyword(s):  
Heart Rate ◽  
Weight Loss ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Stroke Volume ◽  
Myocardial Oxygen Consumption ◽  
The Elderly ◽  
Systemic Diseases ◽  
Exertional Dyspnea ◽  
Cardiac Manifestations

Cardiovascular manifestations of hyperthyroidism include increased heart rate, stroke volume, and cardiac output. Peripheral vascular resistance is decreased, and thus pulse pressure is widened. As a result, myocardial oxygen consumption increases, which may precipitate angina. Other symptoms include palpitations, presyncope or syncope, and exertional dyspnea. Arrhythmias may occur. Common symptoms include weight loss, weakness (especially in the elderly), and tachycardia or palpitations.

Role of arterial baroreceptors in mediating cardiovascular response to exercise

1976 ◽  
Vol 230 (1) ◽  
pp. 85-89 ◽  
Author(s):  
RJ McRitchie ◽  
SF Vatner ◽  
D Boettcher ◽  
GR Heyndrickx ◽  
TA Patrick ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Aortic Pressure ◽  
Severe Exercise ◽  
Response To Exercise ◽  
Arterial Baroreceptor

The role played by the major arterial baroreceptor reflexes in the cardiovascular response to exercise was examined by comparing the responses of untethered conscious dogs instrumented for the measurement of aortic pressure and cardiac output with those of dogs with total arterial barorecptor denervation (TABD). Moderately severe levels of exercise (12 mph) in intact dogs increased cardiac output from 111 +/- 17 ml/kg per min, increased heart rate from 101 +/- 5 to 265 +/- 8 beats/min, and reduced total peripheral resistance from 0.039 +/- 0.003 to 0.015 +/- 0.002 mmHg/ml per min. Dogs with TABD responded in a very similar fashion; exercise increased cardiac output from 119 +/- 8 to 356 /+- 23 ml/kg per min, increased heart rate from 122 +/- 7 to 256 +/- 5 beats/min, and decreased total peripheral resistance from 0.042 +/- 0.005 to +/- 0.015 +/- 0.001 mmHg/ml per min. The reflex heart rate responses to intravenous bolus doses of methoxamine were also examined in intact animals, both at rest and during exercise. Methoxamine caused striking bradycardia at rest, but little bradycardia during exercise. These results suggest that the arterial baroreceptor reflex is normally turned off during severe exercise and thus does not modify significantly the cardiovascular response to exercise.

Initial hemodynamic responses to mild exercise in trained dogs

1965 ◽  
Vol 20 (3) ◽  
pp. 437-442 ◽  
Author(s):  
Harold Smulyan ◽  
Richard P. Cuddy ◽  
William A. Vincent ◽  
Udomporn Kashemsant ◽  
Robert H. Eich
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Stroke Volume ◽  
Right Atrium ◽  
Initial Reaction ◽  
Hemodynamic Responses ◽  
Heart Rates ◽  
Infusion Method ◽  
The Right

The transient changes in cardiac output at the onset of mild exercise were measured in dogs trained to walk on a treadmill. Cardiac output was obtained using a krypton 85 infusion method, which permitted frequent determinations of flow. The first go sec of exercise were marked by a prompt rise and overshoot of heart rate and cardiac output, whereas increases in stroke volume occurred later after the onset of exercise, and to a lesser extent than heart rate. At rest, the right atrium was electrically driven at rates slightly faster than heart rates attained spontaneously with exercise and the studies repeated. Changes in cardiac output with exercise were similar to those in unpaced animals, but when the heart rate was fixed stroke volume increased immediately. These studies show a consistent rise in heart rate and cardiac output in the initial reaction to exercise, but when the prompt rise in heart rate was prevented by pacing from the right atrium, increases in stroke volume provided a comparable response in cardiac output. krypton 85; cardiac output; stroke volume; pacing of heart; oxygen consumption Submitted on September 23, 1964

Cardiac autonomic blockade in exercising dogs

1977 ◽  
Vol 42 (6) ◽  
pp. 878-883 ◽  
Author(s):  
J. M. Atkins ◽  
L. D. Horwitz
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Autonomic Control ◽  
Cardiac Denervation ◽  
Autonomic Blockade ◽  
Myocardial Contractile Force ◽  
Myocardial Contractile ◽  
Severe Exercise

Pharmacological blockade of autonomic control of the heart was studied in dogs performing mild, moderate, and severe running exercise on a level treadmill. The dogs were studied without drugs, after atropine, after propranolol, and after both atropine and propranolol. As compared with results without drugs, cardiac denervation resulted in elevated resting heart rate (+45 beats/min) but reduced heart rate during moderate (-17 beats/min) and severe exercise (-47 beats/min); no change in cardiac output at rest or during mild exercise but decreases (-23% and -25%) during moderate and severe exercise; and reduced first derivatives of left ventricular pressure at rest (-24%) and during exercise (-35, -41, and -52% for mild, moderate, and severe loads, respectively). Cardiac denervation did not alter end-diastolic left ventricular diameter but significantly increased end-systolic diameter during exercise. It is concluded that blockade of autonomic control of the heart diminishes cardiac output during exercise by reducing heart rate and myocardial contractile force but does not alter cardiac output at rest.

Circulatory response to hypoxia in unanesthetized dogs with and without cardiac denervation

1964 ◽  
Vol 207 (4) ◽  
pp. 753-758 ◽  
Author(s):  
Gerald Glick ◽  
William H. Plauth ◽  
Eugene Braunwald
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Acute Hypoxia ◽  
Stroke Volume Index ◽  
Systemic Arterial Pressure ◽  
Volume Index ◽  
Classical Concept ◽  
Circulatory Response ◽  
Cardiac Denervation

The generally held view that acute hypoxia stimulates the cardiovascular system was reinvestigated in ten normal, trained, unanesthetized dogs and in six dogs which had previously been subjected to total cardiac denervation. In the normal dogs, no significant or consistent changes were noted in cardiac output, stroke volume index, or in systemic arterial pressure 5 and 15 min after the onset of 8% O2 inhalation. Heart rate, however, rose significantly. The dogs which had been subjected to cardiac denervation responded with small elevations of cardiac output and heart rate during the late hypoxic period. Thus, these findings are contrary to the classical concept that hypoxia elevates the cardiac output. Moreover, despite the absence of both the sympathetic and parasympathetic innervations of the heart, subjecting the denervated animals to severe hypoxia revealed that they were at no apparent hemodynamic disadvantage in comparison to the intact animals.

Left ventricular dynamics during recovery from exercise

1975 ◽  
Vol 39 (3) ◽  
pp. 449-452 ◽  
Author(s):  
L. D. Horwitz ◽  
J. M. Atkins ◽  
S. A. Dunbar
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Treadmill Exercise ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Strenuous Exercise ◽  
First Derivative ◽  
Severe Exercise ◽  
Ventricular Dynamics

Left ventricular dynamics during recovery were measured in dogs, 3 min after brief periods of mild, moderate, and severe treadmill exercise. As compared with resting values, stroke volume was unchanged, and the maximum first derivative of the left ventricular pressure was either unchanged or slightly elevated. Increases in heart rate of 20, 26, and 46 beats/min for mild, moderate, and severe exercise appear to be the major factor in augmenting cardiac output during recovery. With moderate and severe exercise, left ventricular end-diastolic diameter increased and continued to be elevated during recovery, whereas end-systolic diameter decreased during exercise but was elevated above resting values during recovery. Therefore, with strenuous exercise, a sympathetic-mediated increase in contractility recedes promptly during the postexercise period but the Frank-Starling mechanism continues to be a factor.

CARDIOVASCULAR EFFECTS OF PRONETHALOL IN THE DOG

1965 ◽  
Vol 43 (3) ◽  
pp. 411-420 ◽  
Author(s):  
M. A. Chiong ◽  
P. F. Binnion ◽  
J. D. Hatcher
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Stroke Volume ◽  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Cardiovascular Effects ◽  
Stroke Work ◽  
Right Ventricular Systolic Pressure ◽  
Ventricular Systolic Pressure

The cardiovascular effects of an intravenous injection of pronethalol (2.5 mg/kg) and the effect of this agent on the cardiovascular changes induced by an infusion of adrenaline (0.2 μg/kg per minute) were investigated in intact anaesthetized dogs. Fifteen minutes after the administration of pronethalol, significant increases were observed in oxygen consumption, right ventricular systolic pressure, and haematocrit, and decreases in arterial blood pressure and total peripheral resistance. Arterial hypotension and a fall in stroke work were the only changes noted at 30 minutes. There was considerable variability in cardiac output, stroke volume, and heart rate but, on the average, no significant change was observed. Pretreatment with pronethalol abolished or significantly reduced the adrenaline-induced rises in cardiac output, heart rate, stroke volume, stroke work, oxygen consumption, right ventricular systolic pressure, and arterial haematocrit, and reversed the changes in diastolic arterial pressure and peripheral resistance. It is concluded that pronethalol is not devoid of sympathomimetic activity and that it effectively blocks the adrenaline responses mediated by β-receptors.

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