Inotropic responses of the left ventricle to changes in heart rate in anesthetized rabbits

1987 ◽  
Vol 65 (2) ◽  
pp. 179-184 ◽  
Author(s):  
Leonard B. Bell ◽  
D. Fred Peterson
Keyword(s):  
Heart Rate ◽  
Diastolic Pressure ◽  
Marked Change ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Resting Heart Rate ◽  
Ventricular Contractility ◽  
Inotropic Responses ◽  
Rate Infusion ◽  
Catecholamine Concentration

Factors known to influence left ventricular contractility include preload, afterload, circulating catecholamine concentration, efferent sympathethic discharge, and heart rate. Heart rate influences have been primarily determined in the dog, whereas the influence of heart rate in smaller mammals has not been determined. Eight pentobarbital-anesthetized rabbits were instrumented to measure electrocardiogram, heart rate, left ventricular pressure, end-diastolic pressure, dP/dt, and mean and pulsatile aortic pressures. Systematic bradycardia was induced by stimulating the peripheral end of the sectioned right vagus nerve. Between 293 and 235 beats/min, there was no change in (dP/dt)max as heart rate was decreased. Below this range there was a direct relationship between (dP/dt)max and heart rate. Preload remained unchanged down to 132 beats/min. There was a small but significant decrease in afterload (0.09 mmHg∙beat−1∙min−1; 1 mmHg = 133.32 Pa) throughout the decrease in heart rate. Infusion of propranolol (2.0 mg/kg) produced no marked change in the heart rate – (dP/dt)max relationship, although both resting heart rate and (dP/dt)max were reduced. This study demonstrates that (dP/dt)max is not influenced by changes in heart rate above 235 beats/min in the pentobarbital-anesthetized rabbit. These results differ from findings in other animals, and demonstrate that species and heart rate ranges must be considered when drawing conclusions regarding (dP/dt)max as a reliable index of contractility.

Enhanced sensitivity of diabetic hearts to alpha-adrenoceptor stimulation

1983 ◽  
Vol 245 (5) ◽  
pp. H808-H813 ◽  
Author(s):  
S. E. Downing ◽  
J. C. Lee ◽  
R. R. Fripp
Keyword(s):  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Receptor Activation ◽  
Left Ventricular ◽  
Adrenergic Blockade ◽  
Dependent Manner ◽  
Adrenergic Stimulation ◽  
Response Curves ◽  
Receptor System ◽  
Inotropic Responses

Inotropic responses to alpha-adrenergic stimulation with methoxamine were compared in 12 normal (N) and 12 diabetic (Db) lambs. Diabetes was produced by giving alloxan monohydrate (150 mg/kg iv). Measurements of maximal rate of rise of left ventricular pressure (dP/dtmax), left ventricular end-diastolic pressure (LVEDP), coronary flow, and myocardial O2 consumption were made simultaneously in hemodynamically controlled preparations. All animals were subjected to ganglionic blockade (tetraethylammonium chloride, 100 mg) and beta1-adrenergic blockade (practolol, 4 mg/kg). Methoxamine was given in incremental doses ranging from 0.4 to 6.0 mg/kg. dP/dtmax increased progressively to 126 +/- 4% of initial values in N. However, the increase was twice as large (150 +/- 4%) in the diabetics (P less than 0.005). LVEDP fell in both groups. These changes were abolished by phentolamine (2 mg/kg). Inotropic responses to methoxamine in lambs 2 and 3 wk after induction of diabetes did not differ from those with acute (2 days) diabetes. Dose-response curves obtained by infusing Ca2+ (2-8 mg X min-1 X kg-1) were identical in N and Db. It is concluded that lamb myocardium possesses an alpha-adrenergic receptor system that is stimulated by methoxamine in a dose-dependent manner and blocked by phentolamine. Db hearts are supersensitive to alpha-receptor activation. The mechanistic basis for this latter finding has not been examined but may relate to altered receptor density or nucleotide regulation.

Hemodynamic determinants of the maximal rate of rise of left ventricular pressure

1963 ◽  
Vol 205 (1) ◽  
pp. 30-36 ◽  
Author(s):  
Andrew G. Wallace ◽  
N. Sheldon Skinner ◽  
Jere H. Mitchell
Keyword(s):  
Heart Rate ◽  
Diastolic Pressure ◽  
Complex Function ◽  
Left Ventricular Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Maximal Rate ◽  
Pressure Development ◽  
Ventricular Activation

The maximal rate of left ventricular pressure development (max. dp/dt) was measured in an areflexic preparation which permitted independent control of stroke volume, heart rate, and aortic pressure. Max. dp/dt increased as a result of elevating ventricular end-diastolic pressure. Elevating mean aortic pressure and increasing heart rate each resulted in a higher max. dp/dt without a change in ventricular end-diastolic pressure. Aortic diastolic pressure was shown to influence max. dp/dt in the absence of changes in ventricular end-diastolic pressure or contractility. Increasing contractility increased max. dp/dt while changing the manner of ventricular activation decreased max. dp/dt. These findings demonstrate that changes in max. dp/dt can and frequently do reflect changes in myocardial contractility. These data also indicate that max. dp/dt is a complex function, subject not only to extrinsically induced changes in contractility, but also to ventricular end-diastolic pressure, aortic diastolic pressure, the manner of ventricular activation, and intrinsic adjustments of contractility.

Statistical analysis of effect of anoxia on rate of change of ventricular pressure

1982 ◽  
Vol 53 (3) ◽  
pp. 726-730 ◽  
Author(s):  
C. George ◽  
M. T. Kopetzky
Keyword(s):  
Heart Rate ◽  
Analysis Of Variance ◽  
Repeated Measures ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Aortic Flow ◽  
Ventricular Pressure ◽  
Ventricular Contractility ◽  
Sprague Dawley

Hearts from 32 male Sprague-Dawley rats were studied to determine effects of anoxia on ventricular contractility. Maximum rate of ventricular pressure changes with time (Pmax) were obtained from simultaneous recordings of right and left ventricular pressure curves. Peak aortic flow and heart rate were measured. Anoxia was produced by 100% N2 respiration. Statistical models were repeated-measures analysis of variance and randomized block factorial analysis of variance. Alpha was 0.05. Heart rate during anoxia was significantly lower than during the 1st min of recovery. Heart rate during both these periods was significantly lower than in preanoxia or the remainder of recovery. Peak aortic flow was not significantly altered. In left ventricles positive Pmax was significantly higher than negative Pmax. In right ventricles positive and negative Pmax were not significantly different. Left ventricular Pmax was significantly depressed during anoxia, whereas right ventricular Pmax was not. Significant differences in pressure developed per mass of tissue was a possible source of variation in right (0.12 +/- 0.002 mmHg/mg) and left (0.16 +/- 0.009 mmHg/mg) ventricular contractile maintenance.

Inotropic responses to digoxin during hypoxia and autonomic blockade

1975 ◽  
Vol 229 (2) ◽  
pp. 309-313 ◽  
Author(s):  
KH Halloran ◽  
SE Downing
Keyword(s):  
Stroke Volume ◽  
Autonomic Function ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Not Given ◽  
Ventricular Contractility ◽  
Left Ventricular Contractility ◽  
Autonomic Blockade ◽  
Inotropic Responses ◽  
Sustained Hypoxia

Inotropic responses to digoxin (0.08 mg/kg) were studied in dogs and compared with responses during hypoxemia and autonomic blockade. Changes in left ventricular contractility (VC) were assessed by constructing function curves relating left ventricular (dP/dt)max and stroke volume to end-diastolic pressure. Augmentation of VC was observed 20 min after digoxin infusion and continued to increase until termination of the experiment after 60 min. In animals subjected to autonomic blockade with practolol, TEAC, and atropine, the increases in VC after digoxin were substantially greater. Equally large increases occurred in blocked dogs during sustained hypoxia (Pao2 = 28 mmHg). However, in animals without blockade there was a progressive fall in VC during hypoxia despite digoxin infusion, although less than in those not given digoxin. Serum digoxin levels were measured by radioimmunoassay and did not differ significantly in blocked compared to unblocked dogs or in hypoxic compared to nonhypoxic animals. These findings indicate that digoxin protects the heart from the decrease in myocardial contractility which occurs during extended hypoxia. This protective effect is more pronounced in animals deprived of autonomic function, possibly reflecting the elimination of reflex sympathetic withdrawal ordinarily induced by digitalis.

Cardiovascular responses to metabolic acidosis

1965 ◽  
Vol 208 (2) ◽  
pp. 237-242 ◽  
Author(s):  
S. Evans Downing ◽  
Norman S. Talner ◽  
Thomas H. Gardner
Keyword(s):  
Heart Rate ◽  
Metabolic Acidosis ◽  
Vascular Resistance ◽  
Diastolic Pressure ◽  
Cardiovascular Responses ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Precise Control ◽  
Arterial Ph

The performance of the left ventricle was examined in a feline preparation which allowed precise control of aortic pressure, cardiac output, heart rate, and temperature. The arterial pH, Po2, and Pco2 were continuously measured with a Jewett flow-through electrode assembly. Reduction of arterial pH from 7.45 to 6.80 by HCl or lactic acid infusion was associated with a minimal reduction or no change of left ventricular contractility as measured by the stroke volume or mean ejection rate for a given left ventricular end-diastolic pressure at a constant aortic pressure and heart rate. No evidence for a diminished positive inotropic response to norepinephrine was found. Simultaneous systemic and pulmonary pressure-flow curves demonstrated that metabolic acidosis caused a reduction of systemic vascular resistance and a concurrent increase of pulmonary vascular resistance.

scholarly journals Electrophysiological effects of right and left vagal nerve stimulation on the ventricular myocardium

2014 ◽  
Vol 307 (5) ◽  
pp. H722-H731 ◽  
Author(s):  
Kentaro Yamakawa ◽  
Eileen L. So ◽  
Pradeep S. Rajendran ◽  
Jonathan D. Hoang ◽  
Nupur Makkar ◽  
...  
Keyword(s):  
Heart Rate ◽  
Nerve Stimulation ◽  
Regional Differences ◽  
Left Ventricular Pressure ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Ventricular Pressure ◽  
Electrophysiological Effects

Vagal nerve stimulation (VNS) has been proposed as a cardioprotective intervention. However, regional ventricular electrophysiological effects of VNS are not well characterized. The purpose of this study was to evaluate effects of right and left VNS on electrophysiological properties of the ventricles and hemodynamic parameters. In Yorkshire pigs, a 56-electrode sock was used for epicardial ( n = 12) activation recovery interval (ARI) recordings and a 64-electrode catheter for endocardial ( n = 9) ARI recordings at baseline and during VNS. Hemodynamic recordings were obtained using a conductance catheter. Right and left VNS decreased heart rate (84 ± 5 to 71 ± 5 beats/min and 84 ± 4 to 73 ± 5 beats/min), left ventricular pressure (89 ± 9 to 77 ± 9 mmHg and 91 ± 9 to 83 ± 9 mmHg), and dP/d tmax (1,660 ± 154 to 1,490 ± 160 mmHg/s and 1,595 ± 155 to 1,416 ± 134 mmHg/s) and prolonged ARI (327 ± 18 to 350 ± 23 ms and 327 ± 16 to 347 ± 21 ms, P < 0.05 vs. baseline for all parameters and P = not significant for right VNS vs. left VNS). No anterior-posterior-lateral regional differences in the prolongation of ARI during right or left VNS were found. However, endocardial ARI prolonged more than epicardial ARI, and apical ARI prolonged more than basal ARI during both right and left VNS. Changes in dP/d tmax showed the strongest correlation with ventricular ARI effects ( R2 = 0.81, P < 0.0001) than either heart rate ( R2 = 0.58, P < 0.01) or left ventricular pressure ( R2 = 0.52, P < 0.05). Therefore, right and left VNS have similar effects on ventricular ARI, in contrast to sympathetic stimulation, which shows regional differences. The decrease in inotropy correlates best with ventricular electrophysiological effects.

scholarly journals Elevated resting heart rate is a marker of subclinical left ventricular dysfunction in hodgkin lymphoma survivors

2021 ◽  
Vol 35 ◽  
pp. 100830
Author(s):  
Julius C. Heemelaar ◽  
Augustinus D.G. Krol ◽  
Marloes Louwerens ◽  
Saskia L.M.A. Beeres ◽  
Eduard R. Holman ◽  
...  
Keyword(s):  
Heart Rate ◽  
Hodgkin Lymphoma ◽  
Left Ventricular Dysfunction ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
Resting Heart Rate ◽  
Lymphoma Survivors

Abstract 15830: Elevated Resting Heart Rate is Associated With Impaired Quality of Life and Worse NYHA Functional Capacity in Patients With Chronic Heart Failure: Results From REALITY HF Study

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Yuksel Cavusoglu ◽  
Omer Kozan ◽  
Ahmet Temizhan ◽  
Serdar Kucukoglu
Keyword(s):  
Quality Of Life ◽  
Heart Failure ◽  
Heart Rate ◽  
Functional Capacity ◽  
Real Life ◽  
Left Ventricular ◽  
Summary Score ◽  
Treatment Modalities ◽  
Resting Heart Rate

Purpose: Resting heart rate (HR), health related quality of life (HQoL) and NYHA functional capacity are referred as important determinants of prognosis and targets of therapy in heart failure (HF). REALITY HF (Resting Heart Rate and Real Life Treatment Modality in Outpatients with Left Ventricular Systolic Dysfunction) study data were analyzed for the evaluation of any relationship of resting HR with HQoL assessed by Kansas City Cardiomyopathy Questionnaire (KCCQ) and NYHA functional class. Methods: REALITY HF was a multicenter, prospective registry designed to evaluate HF patients’ characteristics and effects of treatment modalities on resting HR and enrolled 1057 patients (age 61±12 years) with LVEF <40%. 781 (74%) patients in sinus rhythm were included in this analysis. Patients were classified into 4 groups according to the quartiles of HR: Q1:<68 bpm (n=234), Q2:69-75 bpm (n=189), Q3:76-87 bpm (n=194) and Q4:>87 bpm (n=164). KCCQ was completed in a random sample of 320 (Q1:n=27, Q2:n=99, Q3:n=125, Q4:n=69) patients, in which higher scores show better patient’s health status. Results: During enrollment, 82% of patients were receiving ≥2 drugs including ACE[[Unable to Display Character: &#304;]]/ARB, beta blocker, aldosterone blocker, diuretic or digoxin. Resting HR was 76±14 bpm and 68% of patients had a resting HR ≥70 bpm. KCCQ overall summary score (OSC) was found to be 75.7±13.2 in those in Q1, 65.5±20.8 in Q2, 64.4±20.6 in Q3 and 58.3±21.2 in Q4 (p=0.004) and KCCQ clinical summary score (CSS) was 80.4±15.7 in those in Q1, 70.0±22.4 in Q2, 69.9±21.9 in Q3 and 63.8±23.3 in Q4 (p=0.016). Also, there was a significant negative correlation between resting HR and OSC (p=0.008) or CSS (p=0.031). The distribution of NYHA-I patients for Q1, Q2, Q3 and Q4 were 40.7%, 22.8%, 23.8% and 12.7%, NYHA-II patients-30.8%, 23.1%, 27.2% and 18.9%, NYHA-III patients-21.2%, 23.9%, 24.3% and 30.6% and NYHA-IV patients-22.7%, 34.1%, 22.7% and 20.5%, respectively (p<0.001). Also, resting HR were found to gradually and significantly increase across NYHA categories (72.8±12 bpm in NYHA-I, 76.1±13 bpm in NYHA-II, 80.2±15 bpm in NYHA-III and 78.9±16 bpm in NYHA-IV, p<0.001). Conclusions: These results suggest that elevated resting HR in HF patients is associated with impaired HQoL and worse NYHA functional capacity.

Abstract 2135: Correlation between Resting Heart Rate and Defibrillation Energy Threshold in Patients Undergoing Implantable Cardioverter Defibrillator Device Implantation

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Ramtin Anousheh ◽  
David E Krummen ◽  
Navinder S Sawhney ◽  
Wei Chung Chen ◽  
Linda Tone ◽  
...  
Keyword(s):  
Heart Rate ◽  
Beta Blocker ◽  
Standard Of Care ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Resting Heart Rate ◽  
Icd Implantation ◽  
Ventricular Ejection Fraction ◽  
Blocker Therapy ◽  
Beta Blocker Therapy

To investigate the association between resting heart rate (HR) and defibrillation threshold (DFT) in patients (pts) undergoing ICD implantation. DFT testing is usually considered standard of care during ICD implantation. However, the risk factors for high DFTs remain ill defined and the extent of testing required at implant has not been well defined. Baseline HR has been associated with higher DFTs in prior studies. We studied 128 pts undergoing ICD implantation. Baseline HR and DFTs were determined. HR was determined using ECGs obtained in the resting position on the day of ICD implantation. DFT testing was done during ICD implantation. We excluded 13 pts who were on amiodarone. The baseline characteristics of pts in the study are shown below in the table below (values in parenthesis represents standard error of the mean): First, a multivariate analysis of the association between baseline HR and DFT was performed, adjusting for left ventricular ejection fraction (LVEF), gender, body surface area (BSA) and beta blocker therapy. For every 10 beat increase in heart rate, DFT increased by 1 joule (p=0.02). Gender and beta blocker therapy did not effect this association. Second, pts were dichotomized based on DFTs to low (<15 joules) and high (≥15 joules). Mean resting HR was significantly higher among pts with high DFT (79 bpm) compared to those with low DFT (70 bpm) after adjusting for LVEF and BSA (p=0.01). Baseline resting HR is a risk factor for high DFT and may help define a higher risk pt population undergoing DFT testing.

Interaction of interval-force relationship with aortic pressure and stroke volume

1976 ◽  
Vol 230 (4) ◽  
pp. 893-900 ◽  
Author(s):  
ER Powers ◽  
Foster ◽  
Powell WJ
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Cardiac Performance ◽  
Right Heart ◽  
Anesthetized Dogs ◽  
Right Heart Bypass ◽  
Force Relationship

The modification by aortic pressure and stroke volume of the response in cardiac performance to increases in heart rate (interval-force relationship) has not been previously studied. To investigate this interaction, 30 adrenergically blocked anesthetized dogs on right heart bypass were studied. At constant low aortic pressure and stroke volume, increasing heart rate (over the entire range 60-180) is associated with a continuously increasing stroke power, decreasing systolic ejection period, and an unchanging left ventricular end-diastolic pressure and circumference. At increased aortic pressure or stroke volume at low rates (60-120), increases in heart rate were associated with an increased performance. However, at increased aortic pressure or stroke volume at high rates (120-180), increases in heart rate were associated with a leveling or decrease in performance. Thus, an increase in aortic pressure or stroke volume results in an accentuation of the improvement in cardiac performance observed with increases in heart rate, but this response is limited to a low heart rate range. Therefore, the hemodynamic response to given increases in heart rate is critically dependent on aortic pressure and stroke volume.

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