Action of Digitalis on the Nonfailing Heart of the Dog

1957 ◽  
Vol 192 (1) ◽  
pp. 114-120 ◽  
Author(s):  
Marion deV. Cotten ◽  
Phyllis E. Stopp
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Left Atrial ◽  
Venous Return ◽  
Contractile Force ◽  
Left Ventricular ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Right Atrial ◽  
Stroke Work

Ouabain induces a moderate increase in the contractility of the nonfailing heart of the dog with a complete circulatory system in doses which do not produce electrocardiographic signs of digitalis intoxication. The increased contractility was demonstrated both by the increase in ventricular contractile force and by the higher ventricular function curves obtained after administration of ouabain. The drug also increased systemic peripheral resistance and blood pressure, decreased systemic output, heart rate, left and right atrial pressures, and produced only small, variable changes in left ventricular stroke work. The reduction in systemic output and left atrial pressure and the absence of substantial changes in stroke work after ouabain appeared to be the result of a decrease in venous return to the heart. Evidence for this interpretation was obtained from experiments in which left atrial pressure was kept constant during the actions of ouabain by infusing 100–300 cc of whole blood. Under these conditions, ouabain brought about moderate increases in systemic output and left ventricular stroke work as well as in contractile force even though the changes in heart rate and blood pressure were comparable to those obtained in experiments in which left atrial pressure was uncontrolled. The data presented indicate that ouabain has two primary hemodynamic effects in the normal animal, namely, a direct cardiac stimulant action and a peripheral action resulting in a decreased venous return. The relationship of these findings to the mechanism of action of digitalis in congestive heart failure is discussed.

Desflurane, Sevoflurane, and Isoflurane Affect Left Atrial Active and Passive Mechanical Properties and Impair Left Atrial–Left Ventricular Coupling In Vivo 

2001 ◽  
Vol 95 (3) ◽  
pp. 689-698 ◽  
Author(s):  
Meir Gare ◽  
David A. Schwabe ◽  
Douglas A. Hettrick ◽  
Judy R. Kersten ◽  
David C. Warltier ◽  
...  
Keyword(s):  
Left Atrial ◽  
Minimum Alveolar Concentration ◽  
Left Ventricular ◽  
Atrial Function ◽  
Left Atrial Function ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Stroke Work ◽  
Ventricular Elastance

Background The effects of volatile anesthetics on left atrial function in vivo have not been described. The authors tested the hypothesis that desflurane, sevoflurane, and isoflurane alter left atrial mechanics evaluated with invasively derived pressure-volume relations. Methods Barbiturate-anesthetized dogs (n = 24) were instrumented for measurement of aortic, left atrial, and left ventricular pressures (micromanometers) and left atrial volume (orthogonal sonomicrometers). Left atrial contractility and chamber stiffness were assessed with end-systolic and end-reservoir pressure-volume relations, respectively, obtained from differentially loaded diagrams. Relaxation was determined from the slope of left atrial pressure decline after contraction. Stroke work and reservoir function were assessed by A and V loop areas, respectively. Left atrial-left ventricular coupling was determined by the ratio of left atrial contractility and left ventricular elastance. Dogs received 0.6, 0.9, and 1.2 minimum alveolar concentration desflurane, sevoflurane, or isoflurane in a random manner, and left atrial function was determined after 20-min equilibration at each dose. Results Desflurane, sevoflurane, and isoflurane decreased heart rate, mean arterial pressure, and maximal rate of increase of left ventricular pressure and increased left atrial end-diastolic, end-systolic, and maximum volumes. All three anesthetics caused dose-related reductions in left atrial contractility, relaxation, chamber stiffness, and stroke work. Administration of 0.6 and 0.9 minimum alveolar concentration desflurane, sevoflurane, and isoflurane increased V loop area. All three anesthetics decreased the ratio of stroke work to total left atrial pressure-volume diagram area, increased the ratio of conduit to reservoir volume, and reduced left atrial contractility-left ventricular elastance to equivalent degrees. Conclusions The results indicate that desflurane, sevoflurane, and isoflurane depress left atrial contractility, delay relaxation, reduce chamber stiffness, preserve reservoir and conduit function, and impair left atrial-left ventricular coupling in vivo.

Effects of hypocapnia and hypercapnia on myocardial contractility

1960 ◽  
Vol 199 (6) ◽  
pp. 1121-1124 ◽  
Author(s):  
R. Grier Monroe ◽  
Gordon French ◽  
James L. Whittenberger
Keyword(s):  
Heart Rate ◽  
Ventricular Function ◽  
Myocardial Contractility ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Stroke Work ◽  
Control Value

Moderate elevations of pCO2 (61–75 mm Hg) did not consistently depress myocardial contractility as determined by standard ventricular function curves. With an altered preparation in which heart rate and left atrial pressure were held constant, a pCO2 of 60–75 mm Hg was accompanied by an average reduction in stroke work to 73.6% of its control value, while hypocapnia with an alveolar pCO2 of 6–13 mm Hg was unaccompanied by any consistent reduction in stroke work.

Cardiovascular effects of increasing airway pressure in the dog

1977 ◽  
Vol 232 (1) ◽  
pp. H35-H43 ◽  
Author(s):  
S. M. Scharf ◽  
P. Caldini ◽  
R. H. Ingram
Keyword(s):  
Lung Volume ◽  
Airway Pressure ◽  
Left Atrial ◽  
Venous Return ◽  
Pressure Rise ◽  
Cardiovascular Effects ◽  
Atrial Pressure ◽  
Pleural Pressure ◽  
Left Atrial Pressure ◽  
Right Atrial

In paralyzed anesthetized dogs the cardiovascular effects of increasing positive end-expiratory pressure (PEEP) were explored under two conditions: a) end-expiratory lung volume increasing, b) end-expiratory lung volume kept nearly constant by matching pleural pressure rise to end-expiratory airway pressure rise. Two series of experiments were done: I) xenous return was allowed to fall, II) venous return was kept constant by infusion of volume. Right atrial pressure, pulmonary arterial pressure, and left atrial pressure increased under all conditions when measured relative to atmospheric pressure, but increased relative to pleural pressure only under condition a. The rise in left atrial relative to pleural pressure may indicate a degree of left ventricular dysfunction associated with increasing end-expiratory lung volume. Furthermore, when end-expiratory lung volume increased, inequality of the rise in pulmonary artery wedge pressure exceeded the rise in left atrial pressure in series I. From plots of cardiac output as a function of right atrial pressure it was possible to conclude that the decrease in venous return is partially offset by an increase in mean circulatory pressure.

THE INOTROPIC EFFECT OF l-NORADRENALINE IN EXPERIMENTAL CARDIOGENIC SHOCK

1965 ◽  
Vol 43 (1) ◽  
pp. 55-68 ◽  
Author(s):  
Robert F. P. Cronin ◽  
Eng H. Tan
Keyword(s):  
Cardiac Output ◽  
Cardiogenic Shock ◽  
Left Atrial ◽  
Left Ventricular ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Inotropic Effect ◽  
Stroke Work ◽  
Noradrenaline Infusion ◽  
Arterial Blood

The hemodynamic effects of noradrenaline infusion (1 μg/kg min) were studied in five normal dogs and in five dogs in whom cardiogenic shock had been produced by closed-chest coronary embolization.Noradrenaline infusion caused a significant increase in arterial blood pressure, cardiac output, and mean left-atrial pressure in all animals. In the shocked group, the observed increase in cardiac output was significantly less than in the control group.The inotropic effect of infused noradrenaline was quantitated in each animal by comparing the increase in left-ventricular stroke work evoked by noradrenaline with the increase in stroke work which occurred when the mean left-atrial pressure was elevated by autologous transfusion to the level previously attained during noradrenaline infusion. In the control animals, noradrenaline increased left-ventricular stroke work an average of 91% for an average increase in mean left-atrial pressure of 5.6 mm Hg while transfusion increased left-ventricular stroke work 72% for a similar rise in left-atrial pressure. In the shocked animals, noradrenaline increased left-ventricular stroke work 120% but transfusion increased it only 35% for a similar increase in mean left-atrial pressure.It is concluded that the inotropic effect of noradrenaline is enhanced in experimental cardiogenic shock.

P3835Improvement of myocardial energetic efficiency during treatment in hypertensive patients: the life study

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M A Losi ◽  
C Mancusi ◽  
E Gerdts ◽  
K Wachtell ◽  
S E Kjeldsen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Ejection Fraction ◽  
Stroke Volume ◽  
Left Ventricular ◽  
Energetic Efficiency ◽  
Stroke Work ◽  
Hypertensive Patients ◽  
Life Study ◽  
Over Time

Abstract Background Myocardial energetic efficiency (MEE) per unit of left ventricular (LV) mass significantly predicts composite of cardiovascular (CV) events in treated hypertensive patients and specifically heart failure in an event-free population-based cohort with normal ejection fraction, independently of LV hypertrophy (LVH). Purpose To investigate whether MEEi changes over time in treated hypertensive patients, and whether different treatments have different effects. Methods From the Losartan Intervention For Endpoint study (LIFE Echo Sub-study) we selected 744 hypertensive patients (age 66±7 years; 45% women) with LVH at ECG, without atrial fibrillation, previous or incident myocardial infarction and with normal echocardiographic ejection fraction (>50%). MEE was estimated as the ratio of stroke work to the “double” product of heart rate times systolic blood pressure (BP), simplified as the ratio of stroke volume to heart rate, as previously reported. MEE was normalized for LVM (MEEi) and analyzed in quartiles at baseline and at the end treatment, according to an “intention-to-treat” protocol. Results Age and proportion of women were not significantly different from the highest to the lowest quartiles (from 65±7 to 66±7 years, p for trend=0.352; from 45% to 42%, p=0.946, respectively), whereas diastolic blood pressure (from 97±8 to 100±9 mmHg, p=0.006), prevalence of obesity (from 14 to 31%, p=0.001) and diabetes (from 4 to 14%, 0.004) progressively increased. Prevalence of concentric LV geometry and echocardiographic LVH also progressively increased from the highest to the lowest quartile (from 14 to 70%, and 61 to 90%, both p<0.0001). MEEi increased over time (p<0.007), independently of initial diastolic BP, diabetes and obesity, significantly more in patients treated with atenolol than with losartan (p<0.0001) (Figure), due to both increased stroke volume and decreased heart rate (both p<0.0001). Figure 1 Conclusions In a randomized clinical study, MEEi improves with anti-hypertensive therapy. Improvement is more evident in patients with atenolol than with losartan-based treatment, possibly providing pathophysiologic explanation of the comparable performance in prevention of ischemic heart disease previously reported in the LIFE study.

Reference sites not influenced by hydrostatic pressure for right and left atrial pressures

1964 ◽  
Vol 207 (2) ◽  
pp. 357-360 ◽  
Author(s):  
George G. Armstrong ◽  
John C. Hancock
Keyword(s):  
Hydrostatic Pressure ◽  
Reference Point ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Right Atrial ◽  
Lateral Border ◽  
Zero Reference ◽  
The Right ◽  
Made In

Simultaneous recordings of left and right atrial pressures made in dogs being rotated into all positions in space allowed the location of rotational axes where right or left atrial pressure became independent of hydrostatic pressure. Utilization of these axes as zero reference levels made possible the measurement of right or left atrial pressure without the influence of hydrostatic factors. The right zero reference point lay 62.8% of the distance from the manubrium to the xiphoid, 61.2% of the posterior to anterior thoracic diameter, and 47.7% of the greatest transverse thoracic diameter as measured from the right lateral border. The left atrial zero reference point lay 62.1% of the manubrium to xiphoid distance, 57.2% of the posterior to anterior diameter of thorax, and 53.0% of the greatest transverse thoracic diameter as measured from the right lateral border. When referred to the anatomy of the dog, these points lay in the immediate vicinity of the right and left atrioventricular valves, respectively.

Myocardial performance and collateral flow after transient coronary occlusion in exercising dogs

1979 ◽  
Vol 237 (4) ◽  
pp. H520-H527
Author(s):  
M. V. Cohen ◽  
T. Yipintsoi
Keyword(s):  
Stroke Volume ◽  
Left Atrial ◽  
Exercise Group ◽  
Left Ventricular ◽  
Treadmill Running ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Collateral Flow ◽  
Group I ◽  
Group Ii

Fourteen dogs with prior constriction of the left circumflex (LCf) coronary artery were studied at rest and during treadmill running. Hemodynamics were measured before and after a 1-min LCf occlusion. Coronary and collateral flows were quantitated during occlusion both at rest and during exercise. Group I consisted of 4 dogs with resting collateral flow exceeding one-half (average 78%) of normal flow, and group II consisted of 10 dogs with collateral flows less than one-half (average 30%) of normal. At rest LCf occlusion caused no hemodynamic changes in group I, but stroke volume fell significantly in group II. During running, collateral flow after LCf occlusion doubled in group I, and there was only a small rise in left atrial pressure to 18 mmHg. In group II, collateral flow increased by 50% during running and actually decreased in 4 dogs. Significant cardiac failure developed as stroke volume halved, and left atrial pressure rose to an average 30 mmHg. Therefore exercise-induced depression of left ventricular function in the ischemic heart can be correlated to the amount of coronary collateral flow.

Vasopressin-induced changes in cardiac vagal tone and oxygen consumption in dogs

1994 ◽  
Vol 266 (3) ◽  
pp. R838-R849
Author(s):  
J. F. Liard
Keyword(s):  
Heart Rate ◽  
Left Atrial ◽  
Vagal Stimulation ◽  
Vagal Tone ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Beta Blockade ◽  
Cardiac Denervation ◽  
Anesthetized Dogs ◽  
Atropine Treatment

Experiments were conducted in 63 dogs to determine whether stimulation of vagal tone contributes to the decrease in O2 consumption (VO2) that results from arginine vasopressin (AVP) administration. Vagal stimulation with pilocarpine did not reduce VO2 in conscious dogs. In anesthetized dogs, bilateral electrical cervical efferent vagal stimulation lowered both cardiac output (CO; by 46%) and VO2 (by 22%) over the first 5 min. Between 7 and 11 min of stimulation, CO remained decreased, but VO2 returned to control. Significant increases in left atrial pressure, bradycardia, and a fall in mean arterial pressure accompanied vagal stimulation. All these effects of cervical vagal stimulation were abolished by cardiac denervation and also by pacing. Administration of a selective AVP V1 agonist led to significant reductions of CO and VO2. Cardiac denervation prevented the decrease in VO2 induced by AVP infusion, but not the decrease in CO. During AVP infusions, pacing at a rate slightly higher than control heart rate did not prevent the fall in CO or in VO2, whereas pacing at 150 beats/min prevented part of the fall in VO2. Sinoaortic denervation or atropine treatment prevented the decrease in VO2 resulting from AVP infusion. The combination of alpha- and beta-blockade did not affect the CO or the VO2 response to AVP infusion, nor did naloxone treatment. The administration of atrial or ventricular extracts, but not that of alpha-human atrial natriuretic peptide, led to a significant reduction in VO2. These results are compatible with the hypothesis that AVP infusion increases vagal tone to the heart, which, possibly as a result of increased left atrial pressure and reduced heart rate, may release a factor reducing VO2.

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