Heart size and maximal cardiac output are limited by the pericardium

1992 ◽  
Vol 263 (6) ◽  
pp. H1675-H1681 ◽  
Author(s):  
H. K. Hammond ◽  
F. C. White ◽  
V. Bhargava ◽  
R. Shabetai
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Diastolic Pressure ◽  
Maximal Oxygen Consumption ◽  
Left Ventricular ◽  
Treadmill Running ◽  
Oxygen Utilization ◽  
End Diastolic Volume ◽  
Maximal Cardiac Output ◽  
Heart Size

We tested the hypothesis that the pericardium, by restricting heart size, limits maximal cardiac output and oxygen consumption. We studied 15 pigs. Five underwent maximal treadmill running before and 14–21 days after thoracotomy and pericardiectomy; these pigs also received sequential volume infusions to determine end-diastolic pressure-dimension relationships. Five underwent maximal treadmill running before and 14–21 days after thoracotomy (pericardium undisturbed) to determine the effect of thoracotomy on exercise performance. Finally, five underwent thoracotomy, instrumentation, loose closure of the pericardium, and sequential volume infusions to determine the effect of thoracotomy without pericardiectomy on end-diastolic pressure-dimension relationships. Pericardiectomy caused similar increases in maximal cardiac output (29% increase; P = 0.007) and maximal oxygen consumption (31% increase; P = 0.02). These results were associated with increased left ventricular end-diastolic dimension (10% increase; P = 0.01) and an estimated 33% increase in end-diastolic volume. In addition, left ventricular mass was increased by pericardiectomy (18% increase; P < 0.04). Thus the pericardium, by limiting utilization of the Starling mechanism, limits maximal cardiac output, and the limit to cardiorespiratory performance lies not in oxygen utilization, but in oxygen delivery. Furthermore, removal of pericardium is associated with myocardial hypertrophy.

Heart functional responses to pressure overload in exercised and sedentary rats

1976 ◽  
Vol 230 (1) ◽  
pp. 199-204 ◽  
Author(s):  
RT Dowell ◽  
AF Cutilletta ◽  
MA Rudnik ◽  
PC Sodt
Keyword(s):  
Cardiac Output ◽  
Diastolic Pressure ◽  
Heart Function ◽  
Pressure Overload ◽  
Normal Growth ◽  
Left Ventricular ◽  
Treadmill Running ◽  
Female Rats ◽  
Heart Weight ◽  
Functional Responses

Female rats that had been subjected to a moderate treadmill running program were compared with sedentary animals on the basis of heart weight, selected biochemical measurements, and heart function. Exercised animals maintained normal growth rate, and cardiac hypertrophy was not present. Left ventricular RNA, DNA, and cytochrome c levels were unchanged. Heart functional measurements obtained in situ were similar in sedentary and exercised animals under control conditions. When subjected to sustained (1-3 days) aortic constriction pressure overload, exercised animals maintained or increased myocardial contractility. Contractility was depressed in sedentary animals. Both sedentary and exercised animals increased left ventricular end diastolic pressure without changing contractility during acute (1-3 min) pressure overload. However, exercised animals were able to fully regain normal cardiac output when the acute overload was relieved. Cardiac output remained approximately 10% below control in sedentary animals. The improved ability of previously exercised animals to withstand pressure overload appears to be due to alterations in adaptation rather than preliminary augmentation of metabolism or function.

Effect of small vs large muscle mass endurance training on maximal oxygen uptake in organ transplanted recipients

2021 ◽  
pp. 1-10
Author(s):  
Alessio del Torto ◽  
Carlo Capelli ◽  
Roberto Peressutti ◽  
Adriana di Silvestre ◽  
Ugolino Livi ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Oxygen Uptake ◽  
Endurance Training ◽  
Maximal Oxygen Consumption ◽  
Factors Affecting ◽  
Maximal Cardiac Output ◽  
Leg Cycling ◽  
Before And After ◽  
Large Muscle

Maximal oxygen consumption (V̇O2max) is impaired in heart (HTx), kidney (KTx), and liver (LTx) transplanted recipients and the contribution of the cardiovascular, central, and peripheral (muscular) factors in affecting V̇O2max improvement after endurance training (ET) has never been quantified in these patients. ET protocols involving single leg cycling (SL) elicit larger improvements of the peripheral factors affecting O2 diffusion and utilization than the double leg (DL) cycling ET. Therefore, this study aimed to compare the effects of SL-ET vs DL-ET on V̇O2max. We determined the DL-V̇O2max and maximal cardiac output before and after 24 SL-ET vs DL-ET sessions on 33 patients (HTx = 13, KTx = 11 and LTx = 9). The DL-V̇O2max increased by 13.8% ± 8.7 (p < 0.001) following the SL-ET, due to a larger maximal O2 systemic extraction; meanwhile, V̇O2max in DL-ET increased by 18.6% ± 12.7 (p < 0.001) because of concomitant central and peripheral adaptations. We speculate that in transplanted recipients, SL-ET is as effective as DL-ET to improve V̇O2max and that the impaired peripheral O2 extraction and/or utilization play an important role in limiting V̇O2max in these types of patients. Novelty: SL-ET increases V̇O2max in transplanted recipients because of improved peripheral O2 extraction and/or utilization. SL-ET is as successful as DL-ET to improve the cardiorespiratory fitness in transplanted recipients. The model of V̇O2max limitation indicates the peripheral factors as a remarkable limitation to the V̇O2max in these patients.

Volume overload hypertrophy in a closed-chest model of mitral regurgitation

1988 ◽  
Vol 254 (6) ◽  
pp. H1034-H1041 ◽  
Author(s):  
J. P. Kleaveland ◽  
W. G. Kussmaul ◽  
T. Vinciguerra ◽  
R. Diters ◽  
B. A. Carabello
Keyword(s):  
Cardiac Output ◽  
Mitral Regurgitation ◽  
Diastolic Pressure ◽  
Volume Ratio ◽  
Volume Overload ◽  
Canine Model ◽  
Left Ventricular ◽  
Closed Chest ◽  
Cardiac Decompensation ◽  
End Diastolic Volume

Chronic volume overload hypertrophy as seen in mitral regurgitation in humans eventually may cause left ventricular dysfunction. Longitudinal study of the mechanisms leading to such dysfunction is difficult in humans and more easily performed in an animal model. In this study, we describe a canine model of volume overload hypertrophy produced by mitral regurgitation. An arterially placed grasping forceps was used to disrupt mitral chordae or leaflets; thus mitral regurgitation was produced without the need for thoracotomy. Eleven of 22 dogs had severe mitral regurgitation (regurgitant fraction greater than 0.50) and survived for greater than or equal to 3 mo (average 9.2 +/- 6 mo) after the production of mitral regurgitation. At 3 mo, end-diastolic volume increased from 48 +/- 9 to 85 +/- 19 ml, P less than 0.01. Left ventricular mass increased from 71 +/- 13 to 90 +/- 10 g, P less than 0.01. Left ventricular end-diastolic pressure increased from 9 +/- 3 to 19 +/- 6 mmHg, P less than 0.01. Cardiac output decreased from 2.3 +/- 0.61 to 1.80 +/- 0.64 l/min, P less than 0.05. The mass-to-volume ratio decreased from 1.44 +/- 0.17 to 1.09 +/- 0.13, P less than 0.01. We conclude that this closed-chest model of chronic mitral regurgitation produces significant eccentric cardiac hypertrophy. Despite a doubling of end-diastolic volume, there was a fall in cardiac output and a rise in left ventricular end-diastolic pressure, suggesting cardiac decompensation.

Hypertonic saline is a negative inotropic agent in normovolumic dogs

1994 ◽  
Vol 267 (2) ◽  
pp. H667-H677 ◽  
Author(s):  
P. D. Constable ◽  
W. W. Muir ◽  
P. F. Binkley
Keyword(s):  
Cardiac Output ◽  
Hypertonic Saline ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Inotropic Agent ◽  
Inotropic Effects ◽  
End Diastolic Volume

The inotropic effects of hypertonic saline (HS) and hyperosmotic dextrose (HD; 2,400 mosmol/l, 4 ml/kg) were determined in normovolumic, chloralose-anesthetized, intact (n = 14) and autonomically blocked (n = 8) dogs. Solutions were infused intravenously over 3 min. HS and HD rapidly increased preload in both intact and autonomically blocked dogs, as assessed by significant (P < 0.05) increases in plasma volume, end-diastolic volume, and end-diastolic pressure. In intact dogs, HS produced a nonsignificant decrease in end-systolic elastance (Ees) and a nonsignificant increase in the maximal rate of change of left ventricular pressure (dP/dtmax) and cardiac output, whereas HD produced a significant increase in Ees, dP/dtmax, and cardiac output. In autonomically blocked dogs, HS significantly decreased Ees and significantly increased dP/dtmax but did not alter cardiac output, whereas HD significantly increased Ees, dP/dtmax, and cardiac output. We conclude that in normovolumic animals, HS is a negative inotropic agent, HD is a positive inotropic agent, and the in vivo effect of an ionic hyperosmotic agent (HS) differs from that of a nonionic hyperosmotic agent (HD).

scholarly journals The effect of pericardiectomy on maximal oxygen consumption and maximal cardiac output in untrained dogs.

1986 ◽  
Vol 58 (4) ◽  
pp. 523-530 ◽  
Author(s):  
J Stray-Gundersen ◽  
T I Musch ◽  
G C Haidet ◽  
D P Swain ◽  
G A Ordway ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Maximal Oxygen Consumption ◽  
Maximal Cardiac Output

Role of impaired myocardial relaxation in the production of elevated left ventricular filling pressure

2005 ◽  
Vol 288 (3) ◽  
pp. H1203-H1208 ◽  
Author(s):  
Ilan Hay ◽  
Jonathan Rich ◽  
Paul Ferber ◽  
Daniel Burkhoff ◽  
Mathew S. Maurer
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Myocardial Relaxation ◽  
End Diastolic Volume ◽  
Wide Range

Although present in many patients with heart failure and a normal ejection fraction, the role of isolated impairments in active myocardial relaxation in the genesis of elevated filling pressures is not well characterized. Because of difficulties in determining the effect of prolonged myocardial relaxation in vivo, we used a cardiovascular simulated computer model. The effect of myocardial relaxation, as assessed by τ (exponential time constant of relaxation), on pulmonary vein pressure (PVP) and left ventricular end-diastolic pressure (LVEDP) was investigated over a wide range of τ values (20–100 ms) and heart rate (60–140 beats/min) while keeping end-diastolic volume constant. Cardiac output was recorded over a wide range of τ and heart rate while keeping PVP constant. The effect of systolic intervals was investigated by changing time to end systole at the same heart rate. At a heart rate of 60 beats/min, increases in τ from a baseline to extreme value of 100 ms cause only a minor increase in PVP of 3 mmHg. In contrast, at 120 beats/min, the same increase in τ increases PVP by 23 mmHg. An increase in filling pressures at high heart rates was attributable to incomplete relaxation. The PVP-LVEDP gradient was not constant and increased with increasing τ and heart rate. Prolonged systolic intervals augmented the effects of τ on PVP. Impaired myocardial relaxation is an important determinant of PVP and cardiac output only during rapid heart rate and especially when combined with prolonged systolic intervals. These findings clarify the role of myocardial relaxation in the pathogenesis of elevated filling pressures characteristic of heart failure.

Time course of hemodynamic changes in rats with healed severe myocardial infarction

1989 ◽  
Vol 257 (1) ◽  
pp. H289-H296 ◽  
Author(s):  
A. DeFelice ◽  
R. Frering ◽  
P. Horan
Keyword(s):  
Myocardial Infarction ◽  
Blood Flow ◽  
Cardiac Output ◽  
Diastolic Pressure ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Male Rats ◽  
Coronary Artery Ligation ◽  
Sham Operation ◽  
Functional Changes

Male rats were monitored for 8 mo after severe myocardial infarction (MI) to chronicle hemodynamic and left ventricular (LV) functional changes. Blood pressure (BP), heart rate (HR), cardiac output index (CO), regional blood flow, and systemic vascular resistance (SVR) were measured with catheters and radiolabeled microspheres at 4, 7, 10, 20, and 35 wk after coronary artery ligation (n = 10–16/group) or sham operation (control; n = 9–14/group). At 4 wk, 43 +/- 1% of the LV circumference was scarred, peak LV BP, LV dP/dtmax, mean BP, SVR, and HR were 11–38% less than control (P less than 0.05), and LV end-diastolic pressure (LVEDP) was increased by 313% (P less than 0.05). Mean BP, LVEDP, LVBP, and LV dP/dtmax did not further deviate after 4 wk. However, CO and SVR changed progressively and were 67 and 33%, respectively, of control by 35 wk (P less than 0.05) when blood flow to stomach, small intestine, and kidney was 55, 38, and 27% of control. Lung and heart weights were significantly increased by 148 and 22% at 4 wk, and remained elevated, and lung dry weight-to-wet weight ratio was reduced at 7 and 10 wk. Thus the trajectory of rats with healed severe MI reflects progressive cardiac decompensation, cardiac output redistribution, and terminal heart failure.

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