Effect of excitement on coronary and systemic energetics in unanesthetized dogs

1965 ◽  
Vol 209 (4) ◽  
pp. 680-688 ◽  
Author(s):  
Claudia R. Rayford ◽  
Edward M. Khouri ◽  
Donald E. Gregg
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Coronary Flow ◽  
Cardiac Cycle ◽  
Myocardial Metabolism ◽  
Aortic Pressure ◽  
Moderate Increase ◽  
Sizeable Increase

The effect of excitement on phasic aortic pressure and flow, phasic left coronary flow, and myocardial metabolism has been studied in dogs 1–8 weeks after implantation of appropriate flowmeters and other devices. The rapid increase in heart rate and mild increase in blood pressure in the first few seconds tend to maintain coronary flow per minute despite a decrease in stroke cardiac output and coronary flow throughout the cardiac cycle. The main response is a delayed rise in coronary flow per minute resulting from further elevation of heart rate and blood pressure, a moderate increase in stroke cardiac output and a sizeable increase in stroke coronary flow, the latter being divided fairly evenly between systole and diastole. From 60 to 90% of the increase in mean coronary flow arises from the increase in stroke coronary flow, and the remainder from the increased number of heartbeats per minute. Some of the possible mechanisms concerned are discussed.

Cardiovascular system

2011 ◽  
pp. 443-462
Author(s):  
Dr Mark Harrison
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Cardiovascular System ◽  
Cardiac Cycle ◽  
Peripheral Circulation ◽  
Pharmacological Manipulation ◽  
System P

2.1 Control of blood pressure and heart rate, 445 2.2 Control of heart rate, 446 2.3 Cardiac output (CO), 447 2.4 Measurement of cardiac output (CO), 450 2.5 Blood flow peripherally, 451 2.6 The cardiac cycle, 454 2.7 ECG, 458 2.8 Pharmacological manipulation of the heart and peripheral circulation, ...

A Method to Personalize the Lumped Parameter Model of Coronary Artery

2019 ◽  
Vol 16 (03) ◽  
pp. 1842004 ◽  
Author(s):  
Bao Li ◽  
Wenxin Wang ◽  
Boyan Mao ◽  
Youjun Liu
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Coronary Artery ◽  
Coronary Flow ◽  
Systemic Circulation ◽  
Aortic Pressure ◽  
Physiological Parameters ◽  
Lumped Parameter Model ◽  
Non Invasive ◽  
Lumped Parameter

A method which can personalize the lumped parameter model of coronary artery and cardiovascular system based on the non-invasive physiological parameters has been developed. The parameters of system were determined by different physiological parameters. The heart module was determined by aortic pressure and heart rate; the systemic circulation module was determined by cardiac output, height and cardio-ankle vascular index (CAVI), while the CAVI was determined by age and aortic pressure; the coronary module was determined by the target waveforms of coronary flow rate predicted from cardiac output. The considerable results proved that this method could be applied to each patient.

Effect of Catecholamines, l-Epinephrine and l-Norepinephrine on Coronary Flow and Oxygen Metabolism of the Myocardium

1958 ◽  
Vol 193 (1) ◽  
pp. 151-156 ◽  
Author(s):  
Harold Feinberg ◽  
Louis N. Katz
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Oxygen Consumption ◽  
Coronary Flow ◽  
Myocardial Oxygen Consumption ◽  
Oxygen Metabolism ◽  
Aortic Pressure ◽  
Coronary Vasodilatation ◽  
Oxygen Difference ◽  
Mean Aortic Pressure

The effect of continuously infused intravenous l-epinephrine and l-norepinephrine (0.1–2.5 gamma/kg/min.) was determined in the open-chest, anesthetized dog prepared for measurement of total coronary flow. Coronary blood flow, myocardial oxygen availability and coronary venous oxygen content consistently increased after catecholamine administration despite wide fluctuations, above and below control values, in heart rate and mean aortic pressure at constant cardiac output. Thus, there was a significant decrease in the coronary arteriovenous oxygen difference after catecholamine administration. The increase in coronary flow and decrease in the coronary A-V oxygen difference were seen even when blood pressure and heart rate were lowered. It is concluded that the departure from the usual relationship between coronary flow and myocardial oxygen consumption is attributable to coronary vasodilatation. However, myocardial oxygen consumption is still the primary factor controlling coronary flow during catecholamine action.

A Comparison of the Acute Haemodynamic Effects of Propranolol and Pindolol at Rest and during Supine Exercise in Man

1980 ◽  
Vol 59 (s6) ◽  
pp. 465s-468s ◽  
Author(s):  
T. L. Svendsen ◽  
J. E. Carlsen ◽  
O. Hartling ◽  
A. McNair ◽  
J. Trap-Jensen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Response Curves ◽  
Receptor Blocking ◽  
Artery Pressure ◽  
Arterial Blood ◽  
Β Receptor

1. Dose-response curves for heart rate, cardiac output, arterial blood pressure and pulmonary artery pressure were obtained in 16 male patients after intravenous administration of three increasing doses of pindolol, propranolol or placebo. All patients had an uncomplicated acute myocardial infarction 6–8 months earlier. 2. The dose-response curves were obtained at rest and during repeated bouts of supine bicycle exercise. The cumulative dose amounted to 0.024 mg/kg body weight for pindolol and to 0.192 mg/kg body weight for propranolol. 3. At rest propranolol significantly reduced heart rate and cardiac output by 12% and 15% respectively. Arterial mean blood pressure was reduced by 9.2 mmHg. Mean pulmonary artery pressure increased significantly by 2 mmHg. Statistically significant changes in these variables were not seen after pindolol or placebo. 4. During exercise pindolol and propranolol both reduced cardiac output, heart rate and arterial blood pressure to the same extent. After propranolol mean pulmonary artery pressure was increased significantly by 3.6 mmHg. Pindolol and placebo did not change pulmonary artery pressure significantly. 5. The study suggests that pindolol may offer haemodynamic advantages over β-receptor-blocking agents without intrinsic sympathomimetic activity during low activity of the sympathetic nervous system, and may be preferable in situations where the β-receptor-blocking effect is required only during physical or psychic stress.

Characterization of baroreflex impairment in conscious dogs with pacing-induced heart failure

1993 ◽  
Vol 265 (5) ◽  
pp. R1132-R1140 ◽  
Author(s):  
N. B. Olivier ◽  
R. B. Stephenson
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Open Loop ◽  
Ventricular Pacing ◽  
Baroreflex Control ◽  
Rapid Ventricular Pacing ◽  
Reflex Control

Open-loop baroreflex responses were evaluated in eight conscious dogs before and during congestive heart failure to determine the effects of failure on baroreflex control of blood pressure, heart rate, cardiac output, and total peripheral resistance. Heart failure was induced by rapid ventricular pacing. Baroreflex function was determined by calculation of the range and gain of the open-loop stimulus-response relationships for the effect of carotid sinus pressure on blood pressure, heart rate, cardiac output, and total peripheral resistance. The range and gain of blood pressure responses were substantially reduced as early as 3 days after induction of heart failure (161 +/- 6 to 99 +/- 8 mmHg and -2.7 +/- 0.3 to -1.5 +/- 0.1, respectively) and remained depressed for the 21 days of heart failure. This depression in baroreflex control of blood pressure was associated with similar depressions in reflex range and gain for heart rate (125 +/- 9 to 78 +/- 11 beats/min and -2.05 +/- 0.2 to -1.16 +/- 0.2 beats/min, respectively) and cardiac output (1.74 +/- 0.2 to 0.46 +/- 0.2 l/min and -0.81 +/- 0.02 to -0.027 +/- 0.008 l/min, respectively). The group-averaged range and gain for reflex control of vascular resistance were not altered by heart failure. In three dogs, discontinuation of rapid ventricular pacing led to resolution of heart failure within 7 days and partial restoration of the range and gain of reflex control of blood pressure. We conclude that heart failure reversibly depresses baroreflex control of blood pressure principally through a concurrent reduction in reflex control of cardiac output, whereas reflex control of vascular resistance is not consistently affected.

Hemodynamic Determinants of Coronary Flow: Effect of Changes in Aortic Pressure and Cardiac Output on the Relationship Between Myocardial Oxygen Consumption and Coronary Flow

1957 ◽  
Vol 192 (1) ◽  
pp. 157-163 ◽  
Author(s):  
E. Braunwald ◽  
S. J. Sarnoff ◽  
R. B. Case ◽  
W. N. Stainsby ◽  
G. H. Welch
Keyword(s):  
Cardiac Output ◽  
Coronary Flow ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Ventricular Filling Pressure ◽  
Heart Preparation ◽  
Ventricular Filling ◽  
The Relationship ◽  
Hemodynamic Determinants

Although the general dependence of coronary flow on myocardial qo2 was confirmed in an in situ heart preparation, changes in aortic pressure and cardiac output were observed to be capable of influencing this relationship. Neither myocardial qo2 nor coronary flow were found to be dependent on left ventricular filling pressure.

The Chanages of Blood Pressure , Heart Rate and Cardiac Output During Awake Fiberoptic Nasotracheal and Orotracheal Intubation

1991 ◽  
Vol 24 (3) ◽  
pp. 505
Author(s):  
Young Jin Lim ◽  
Jae Hyon Bahk ◽  
Kook Hyun Lee ◽  
Jin Kyu Park ◽  
Kwang Won Yum
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Orotracheal Intubation

Pet CO2 inversely affects MSNA response to orthostatic stress

2001 ◽  
Vol 281 (3) ◽  
pp. H1040-H1046 ◽  
Author(s):  
J. Kevin Shoemaker ◽  
Debbie D. O'Leary ◽  
Richard L. Hughson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Orthostatic Intolerance ◽  
Muscle Sympathetic Nerve Activity ◽  
Peripheral Resistance ◽  
Burst Frequency ◽  
Head Up Tilt ◽  
End Tidal ◽  
Combined Data

Arterial hypocapnia has been associated with orthostatic intolerance. Therefore, we tested the hypothesis that hypocapnia may be detrimental to increases in muscle sympathetic nerve activity (MSNA) and total peripheral resistance (TPR) during head-up tilt (HUT). Ventilation was increased ∼1.5 times above baseline for each of three conditions, whereas end-tidal Pco 2 (Pet CO2 ) was clamped at normocapnic (Normo), hypercapnic (Hyper; +5 mmHg relative to Normo), and hypocapnic (Hypo; −5 mmHg relative to Normo) conditions. MSNA (microneurography), heart rate, blood pressure (BP, Finapres), and cardiac output (Q, Doppler) were measured continuously during supine rest and 45° HUT. The increase in heart rate when changing from supine to HUT ( P < 0.001) was not different across Pet CO2 conditions. MSNA burst frequency increased similarly with HUT in all conditions ( P < 0.05). However, total MSNA and the increase in total amplitude relative to baseline (%ΔMSNA) increased more when changing to HUT during Hypo compared with Hyper ( P < 0.05). Both BP and Q were higher during Hyper than both Normo and Hypo (main effect; P < 0.05). Therefore, the MSNA response to HUT varied inversely with levels of Pet CO2 . The combined data suggest that augmented cardiac output with hypercapnia sustained blood pressure during HUT leading to a diminished sympathetic response.

Cardiovascular functions in the dog rewarmed rapidly and slowly from deep hypothermia

1960 ◽  
Vol 198 (2) ◽  
pp. 333-335 ◽  
Author(s):  
H. E. D'Amato ◽  
Suzanne Kronheim ◽  
B. G. Covino
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Superior Vena ◽  
Vena Cava ◽  
Deep Hypothermia ◽  
Cardiovascular Collapse ◽  
Cardiovascular Failure ◽  
Myocardial Failure ◽  
Cardiovascular Functions

Heart rate, blood pressure, cardiac output and cardiac minute work were measured in pentobarbitalized dogs prior to induction of hypothermia, at rectal temperatures of 25°C or 20°C and following rapid rewarming in warm water or slow rewarming by wrapping in heated sheeting. During rapid rewarming from either 25°C or 20°C no consistent failure in recovery of normal cardiovascular function was observed, although 1 out of 10 dogs did suffer cardiovascular collapse during rapid rewarming. Slow rewarming from 25° and 20°C resulted in consistent failure of some or all of these functions to recover to prehypothermic levels. Moreover, 5 out of 15 slowly rewarmed dogs suffered cardiovascular collapse during the rewarming process. In five dogs slowly rewarmed from 20°C saline was infused into the superior vena cava. This procedure resulted in moderate increases in blood pressure but dramatic increases in cardiac output and minute work (200% and 270%, respectively), thereby negating myocardial failure as the primary cause of the occasionally observed cardiovascular failure.

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