Left ventricular function during chronic endotoxemia in swine

1988 ◽  
Vol 254 (2) ◽  
pp. H324-H330 ◽  
Author(s):  
K. Lee ◽  
H. van der Zee ◽  
S. W. Dziuban ◽  
K. Luhmann ◽  
R. D. Goldfarb
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Salmonella Enteritidis ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Cardiac Performance ◽  
Inotropic State ◽  
Pressure Development ◽  
Hyperdynamic Sepsis

Cardiac performance was studied in 15 chronically instrumented awake pigs during chronic endotoxemia (CET) induced by intravenous infusion of low doses of endotoxin. We sought to test the hypothesis that left ventricular inotropic state was depressed during the stage of chronic endotoxemia when cardiac output, heart rate, and left ventricular systolic pressures are elevated, termed "hyperdynamic sepsis". Left ventricular pressure, internal short axis diameter (SAX), pulmonary artery blood flow, and electrocardiogram were recorded. After initial surgical preparation, each pig was observed for 7-10 days to measure representative basal values. Each pig was then reoperated on day 10 to implant an endotoxin-loaded osmotic pump whose output, infused Salmonella enteritidis endotoxin at a rate calculated to be 10 micrograms.kg-1.h-1 for up to 7 days. Cardiac performance was monitored by measuring dP/dt, heart rate, stroke volume, end-diastolic diameter, percent change in diameter, and the slope of the end-systolic pressure diameter relationship (ESPDR). Data from the basal days were pooled and compared with the data obtained each day of CET by two-way analysis of variance. Ten of 15 pigs survived more than 2 days of CET; 5 died before the morning of the second CET day. The surviving pigs demonstrated elevated systolic pressures, left ventricular maximum rate of pressure development (+dP/dtmax and -dP/dtmax), heart rates, and cardiac output. However, both ESPDR and percent SAX shortening were significantly depressed during both CET days. We conclude that cardiac inotropic state is depressed during hyperdynamic sepsis as indicated by the load-independent parameter ESPDR and confirmed by depressed percent SAX shortening.

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.

Left ventricular functional capacity in the endurance-trained rodent

1990 ◽  
Vol 69 (1) ◽  
pp. 305-312 ◽  
Author(s):  
D. P. Fitzsimons ◽  
P. W. Bodell ◽  
R. E. Herrick ◽  
K. M. Baldwin
Keyword(s):  
Heart Rate ◽  
Systolic Pressure ◽  
Force Production ◽  
Left Ventricular Pressure ◽  
Fold Increase ◽  
Work Load ◽  
Left Ventricular ◽  
Cardiac Myosin ◽  
O2 Uptake ◽  
Training Protocol

Cardiac myosin P-light chain phosphorylation [P-LC(P)] has been proposed to augment myocardial force production. This study was undertaken to examine the potential for cardiac myosin P-LC(P) for both equivalent heart rate and work load in exercising endurance-trained and nontrained rodents. A 10-wk training protocol elicited a significant reduction in submaximal running O2 uptake while enhancing peak O2 uptake (-17 and 10%, respectively, P less than 0.05). Left ventricular functional index during submaximal exercise, obtained with a high-fidelity Millar ultraminiature pressure transducer, indicated that the trained animals were able to maintain peak left ventricular pressure (LVP) in comparison to their sedentary counterparts, even though both heart rate and rate of LVP development were significantly reduced (P less than 0.05). When expressed on the basis of equivalent submaximal heart rate, peak LVP was augmented in the trained animals. Cardiac myosin P-LC(P) was examined under two conditions known to produce disparate responses in trained vs. sedentary animals. For an equivalent work load, we observed parallel increases in P-LC(P) (20%) and systolic pressure (17%) in both groups, even though the trained animals exhibited significantly lower heart rates (P less than 0.05). For an equivalent heart rate, training evoked a significant increase in systolic pressure (26%, P less than 0.05) and caused a slight increase in P-LC(P) relative to the nontrained controls. Cardiac myosin adenosinetriphosphatase was reduced approximately 10% in the trained animals (P less than 0.05), commensurate with a 2.0-fold increase in the V3 (low adenosinetriphosphatase) isomyosin.(ABSTRACT TRUNCATED AT 250 WORDS)

Experimental hypothermia and rewarming: changes in mechanical function and metabolism of rat hearts

1996 ◽  
Vol 80 (1) ◽  
pp. 291-297 ◽  
Author(s):  
T. Tveita ◽  
M. Skandfer ◽  
H. Refsum ◽  
K. Ytrehus
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Maximum Rate ◽  
Energy Charge ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Left Ventricular ◽  
Mechanical Function ◽  
Control Value

Rewarming from accidental hypothermia is associated with fatal circulatory derangements. To investigate potential pathophysiological mechanisms involved, we examined heart function and metabolism in a rat model rewarmed after 4 h at 15-13 degrees C. Hypothermia resulted in a significant reduction of left ventricular (LV) systolic pressure, cardiac output, and heart rate, whereas stroke volume increased. The maximum rate of LV pressure rise decreased to 191 +/- 28 mmHg/s from a control value of 9,060 +/- 500 mmHg/s. Myocardial tissue content of ATP, ADP, and glycogen was significantly reduced, whereas lactate content remained unchanged. After rewarming, heart rate returned to control value, whereas LV systolic pressure, cardiac output, and stroke volume all remained significantly depressed. The posthypothermic maximum rate of LV pressure rise was 5,966 +/- 1.643 mmHg/s. The posthypothermic myocardial lactate content was significantly increased (to 13.3 +/- 3.2 nmol/mg from control value of 5.7 +/- 1.9 nmol/mg), and ATP and glycogen remained significantly lowered. Creatine phosphate or energy charge did not change significantly during the experiment. The finding of deteriorated myocardial mechanical function and a shift in energy metabolism shows that the heart could be an important target during hypothermia and rewarming in vivo, thus contributing to the development of a posthypothermic circulatory collapse.

scholarly journals Muscle metaboreflex-induced increases in effective arterial elastance: effect of heart failure

2020 ◽  
Vol 319 (1) ◽  
pp. R1-R10 ◽  
Author(s):  
Joseph Mannozzi ◽  
Jasdeep Kaur ◽  
Marty D. Spranger ◽  
Mohamed-Hussein Al-Hassan ◽  
Beruk Lessanework ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Muscle Metaboreflex ◽  
Effective Arterial Elastance

Dynamic exercise elicits robust increases in sympathetic activity in part due to muscle metaboreflex activation (MMA), a pressor response triggered by activation of skeletal muscle afferents. MMA during dynamic exercise increases arterial pressure by increasing cardiac output via increases in heart rate, ventricular contractility, and central blood volume mobilization. In heart failure, ventricular function is compromised, and MMA elicits peripheral vasoconstriction. Ventricular-vascular coupling reflects the efficiency of energy transfer from the left ventricle to the systemic circulation and is calculated as the ratio of effective arterial elastance ( Ea) to left ventricular maximal elastance ( Emax). The effect of MMA on Ea in normal subjects is unknown. Furthermore, whether muscle metaboreflex control of Ea is altered in heart failure has not been investigated. We utilized two previously published methods of evaluating Ea [end-systolic pressure/stroke volume ( EaPV)] and [heart rate × vascular resistance ( EaZ)] during rest, mild treadmill exercise, and MMA (induced via partial reductions in hindlimb blood flow imposed during exercise) in chronically instrumented conscious canines before and after induction of heart failure via rapid ventricular pacing. In healthy animals, MMA elicits significant increases in effective arterial elastance and stroke work that likely maintains ventricular-vascular coupling. In heart failure, Ea is high, and MMA-induced increases are exaggerated, which further exacerbates the already uncoupled ventricular-vascular relationship, which likely contributes to the impaired ability to raise stroke work and cardiac output during exercise in heart failure.

Acute aortic stenosis in the conscious dog: effects of inotropic state on heart rate

1986 ◽  
Vol 250 (2) ◽  
pp. H159-H166
Author(s):  
I. H. Zucker ◽  
M. J. Niebauer ◽  
K. G. Cornish
Keyword(s):  
Heart Rate ◽  
Aortic Stenosis ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Control Group ◽  
Epinephrine Infusion ◽  
Arterial Baroreceptors ◽  
Inotropic State ◽  
Arterial Blood ◽  
Significant Difference

Effects of acute distension of the left ventricle on heart rate were studied in conscious, instrumented dogs. In intact dogs, increasing left ventricular (LV) systolic pressure by a maximum of 77.6 +/- 3.6 mmHg from a control of 123.1 +/- 3.6 and LV end-diastolic pressure by a maximum of 24.1 +/- 2.0 mmHg from a control of 8.5 +/- 1.3 did not result in any consistent change in heart rate. Reduction of arterial pressure with sodium nitroprusside caused an increase in heart rate to 143.9 +/- 13.8 beats/min. With baroreceptors unloaded, increasing LV pressure by a similar degree as in the control group now resulted in consistent and significant bradycardia. Removal of arterial baroreceptors in a final group of dogs abolished the baroreflex. Increasing LV pressure by aortic stenosis now resulted in a stimulus-dependent decrease in heart rate that was significantly greater than that in the nitroprusside group. Both administration of atropine and bilateral cervical vagotomy abolished bradycardia. The second part of this study was concerned with effects of increases in LV inotropic state on heart rate change evoked by aortic stenosis. Each group was infused with intracoronary epinephrine. Infusion of epinephrine (12.5-50.0 ng . kg-1 . min-1) significantly increased LV dP/dt without any significant change in heart rate or mean arterial blood pressure. Aortic stenosis during epinephrine infusion did not result in any significant difference in heart rate responses in any group studied. It is concluded that LV distension can cause a reduction in heart rate that is opposed by the presence of arterial baroreceptors and that increases in LV myocardial contractility do not have any effect on the magnitude of this response.

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.

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.

Cardiac performance of isolated perfused hearts from alloxan diabetic rats

1979 ◽  
Vol 236 (6) ◽  
pp. H808-H812 ◽  
Author(s):  
T. B. Miller
Keyword(s):  
Cardiac Output ◽  
Systolic Pressure ◽  
Aortic Pressure ◽  
Diabetic Rats ◽  
Cardiac Performance ◽  
Ventricular Performance ◽  
Glucose Levels ◽  
Pressure Development ◽  
Relative Inability ◽  
Perfused Hearts

Acute alloxan diabetes (3 days) in the rat resulted in a decreased ability of the isolated perfused working heart to respond to increased atrial filling pressure with normal systolic (aortic) pressure development, using a physiologic concentration of glucose (5 mM) as substrate. The diabetic heart also exhibited impaired cardiac output, which could be attributed entirely to decreased aortic output without any apparent effect on coronary flow. This decrease in ventricular performance was accompanied by a 40% reduction in glucose uptake and a 20% reduction in tissue ATP concentrations even though perfusate glucose levels remained at or near physiologic levels. Perfusion of hearts with 5 mM glucose plus 10(-8) M insulin, with 10 or 30 mM glucose, or 1 mM octanoate reversed the diabetes-related decrease in systolic pressure development, cardiac output, and tissue ATP content. These data demonstrate that the defect in cardiac performance with increased work loads associated with acute insulin deficiency is due to the relative inability of the heart to utilize physiologic concentrations of glucose as substrate for energy production.

Reflex sympathetic augmentation of left-ventricular inotropic state in the conscious dog

1981 ◽  
Vol 241 (6) ◽  
pp. H857-H863
Author(s):  
C. Yoran ◽  
L. Higginson ◽  
M. A. Romero ◽  
J. W. Covell ◽  
J. Ross
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Pressure Rise ◽  
Left Ventricular Pressure ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Adrenergic Blockade ◽  
Conscious Dog ◽  
Inotropic State ◽  
Simultaneous Decrease

Cardiac reflex responses to a series of partial inferior vena caval occlusions were studied in conscious previously instrumented dogs. Heart rate responses during the fall of systemic arterial pressure were mediated both by increased sympathetic tone and withdrawal of parasympathetic tone. Responses of the left-ventricular inotropic state, estimated from changes in left ventricular pressure rise (LV dP/dt), were studied early after release of a series of partial vena caval occlusions, and a positive linear relation between the prior fall in the systemic arterial pressure and the increase in LV dP/dt was demonstrated. Serial studies showed this effect of persist for at least 12 s beyond the reflex slowing of heart rate early after release of vena caval occlusion. The positive inotropic response was markedly attenuated by beta-adrenergic blockade and also occurred at a constant heart rate. It was present after adrenalectomy. These studies suggest that the integrated baroreceptor responses that are activated by a simultaneous decrease in the venous return and systemic arterial pressure play an important role in the regulation of left-ventricular inotropic state in the conscious dog.

Spontaneous baroreflex control of heart rate versus cardiac output: altered coupling in heart failure

2008 ◽  
Vol 294 (3) ◽  
pp. H1304-H1309 ◽  
Author(s):  
Javier A. Sala-Mercado ◽  
Masashi Ichinose ◽  
Robert L. Hammond ◽  
Matthew Coutsos ◽  
Tomoko Ichinose ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Baroreflex Control ◽  
Ventricular Systolic Pressure ◽  
Linear Relationships ◽  
Before And After ◽  
Spontaneous Baroreflex

Dynamic cardiac baroreflex responses are frequently investigated by analyzing the spontaneous reciprocal changes in arterial pressure and heart rate (HR). However, whether the spontaneous baroreflex-induced changes in HR translate into changes in cardiac output (CO) is unknown. In addition, this linkage between changes in HR and changes in CO may be different in subjects with heart failure (HF). We examined these questions using conscious dogs before and after pacing-induced HF. Spontaneous baroreflex sensitivity in the control of HR and CO was evaluated as the slopes of the linear relationships between HR or CO and left ventricular systolic pressure (LVSP) during spontaneous sequences of greater or equal to three consecutive beats when HR or CO changed inversely versus pressure. Furthermore, the translation of baroreflex HR responses into CO responses (HR-CO translation) was examined by computing the overlap between HR and CO sequences. In normal resting conditions, 44.0 ± 4.4% of HR sequences overlapped with CO sequences, suggesting that only around half of the baroreflex HR responses cause CO responses. In HF, HR-LVSP, CO-LVSP, and the HR-CO translation significantly decreased compared with the normal condition (−2.29 ± 0.5 vs. −5.78 ± 0.7 beats·min−1·mmHg−1; −70.95 ± 11.8 vs. −229.89 ± 29.6 ml·min−1·mmHg−1; and 19.66 ± 4.9 vs. 44.0 ± 4.4%, respectively). We conclude that spontaneous baroreflex HR responses do not always cause changes in CO. In addition, HF significantly decreases HR-LVSP, CO-LVSP, and HR-CO translation.

Sign in / Sign up

Export Citation Format

Share Document