Dependence of cardiac filling pressure on cardiac output during rest and dynamic exercise in dogs

Sheriff, Don D.; Zhou, Xuezhe; Scher, Allen M.; Rowell, L. B.

doi:10.1152/ajpheart.1993.265.1.h316

Cited by 56 publications

(66 citation statements)

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“…Komamura et al (20) demonstrated in dogs with pacing-induced HF that the failing ventricle is not able to increase SV in response to acute volume loads. In addition, in normal dogs, MMR activation causes substantial central blood volume mobilization (35), which maintains ventricular filling pressure that would otherwise decrease due to the rise in CO (43,45). In HF, this central blood volume mobilization still occurs, as evidenced by large increases in central venous pressure (11), but evidently even this increase in filling pressure is ineffective in raising CO during MMR activation.…”

Section: Discussionmentioning

confidence: 99%

Heart failure attenuates muscle metaboreflex control of ventricular contractility during dynamic exercise

Sala‐Mercado¹,

Hammond²,

Kim³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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DS. Heart failure attenuates muscle metaboreflex control of ventricular contractility during dynamic exercise. Am J Physiol Heart Circ Physiol 292: H2159 -H2166, 2007. First published December 22, 2006; doi:10.1152/ajpheart.01240.2006.-Underperfusion of active skeletal muscle elicits a reflex pressor response termed the muscle metaboreflex (MMR). In normal dogs during mild exercise, MMR activation causes large increases in cardiac output (CO) and mean arterial pressure (MAP); however, in heart failure (HF) although MAP increases, the rise in CO is virtually abolished, which may be due to an impaired ability to increase left ventricular contractility (LVC). The objective of the present study was to determine whether the increases in LVC seen with MMR activation during dynamic exercise in normal animals are abolished in HF. Conscious dogs were chronically instrumented to measure CO, MAP, and left ventricular (LV) pressure and volume. LVC was calculated from pressure-volume loop analysis [LV maximal elastance (E max) and preload-recruitable stroke work (PRSW)] at rest and during mild and moderate exercise under free-flow conditions and with MMR activation (via partial occlusion of hindlimb blood flow) before and after rapid ventricular pacing-induced HF. In control experiments, MMR activation at both workloads [mild exercise (3.2 km/h) and moderate exercise (6.4 km/h at 10% grade)] significantly increased CO, E max, and PRSW. In contrast, after HF was induced, CO, Emax, and PRSW were significantly lower at rest. Although CO increased significantly from rest to exercise, E max and PRSW did not change. In addition, MMR activation caused no significant change in CO, E max, or PRSW at either workload. We conclude that MMR causes large increases in LVC in normal animals but that this ability is abolished in HF. pressor response; elastance; preload recruitable stroke work WHEN EXERCISING SKELETAL MUSCLE does not receive sufficient blood flow to meet the ongoing metabolic demands, by-products of metabolism such as lactic acid, H ϩ , adenosine, potassium, diprotonated phosphate, and arachidonic acid products, among others, accumulate within the muscle and stimulate group III and IV afferent neurons, which evokes a reflex response known as the muscle metaboreflex (MMR). This reflex response consists of increases in efferent sympathetic nerve activity (SNA) and mean arterial pressure (MAP) (1, 3, 11, 17, 18, 24, 31-35, 39, 40, 43, 46, 47, 52, 53). In addition, MMR activation causes increases in cardiac output (CO), heart rate (HR), and plasma levels of vasoactive hormones and produces vasoconstriction in the renal and the nonischemic active skeletal muscle vasculature to partially restore arterial O 2 delivery and blood flow to the hypoperfused muscles (25,33,36). The rise in CO likely results from increases in ventricular performance, HR, and central blood volume mobilization (32,42,43). By this means the MMR-induced increases in ventricular performance act to slightly increase or sustain stroke volume (SV) despite decreas...

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Section: Discussionmentioning

confidence: 99%

Heart failure attenuates muscle metaboreflex control of ventricular contractility during dynamic exercise

Sala‐Mercado¹,

Hammond²,

Kim³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…To what extent the HR responses cause changes in CO can be variable, as a result of reciprocal changes in SV (17,48), which can likely be attributed to the changes in ventricular filling time. Furthermore, even if SV is initially maintained, an increase in CO will decrease central venous pressure, thereby, decreasing right ventricular filling pressure, which would ultimately limit the ability to sustain left ventricular SV and, therefore, sustain the rise in CO (6,30,40). Because of the capacitance of the pulmonary circulation, the fall in the ventricular filling does take time to occur, and therefore, transient changes in HR can still cause transient changes in CO (42).…”

Section: Discussionmentioning

confidence: 99%

“…However, we and others have observed that changes in HR do not necessarily elicit proportional changes in CO because stroke volume (SV) may also vary with the changes in ventricular filling time (17,34,48). Furthermore, transient increases in CO will lower ventricular filling pressure (and decreases in CO will raise filling pressure), thereby providing a self-limiting response (6,30,40). Furthermore, baroreflex control of HR may not functionally buffer high-frequency (Hi-F: above 0.15 Hz) blood pressure fluctuations (4,38,44).…”

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confidence: 99%

Dynamic cardiac output regulation at rest, during exercise, and muscle metaboreflex activation: impact of congestive heart failure

Ichinose

Sala‐Mercado

Coutsos

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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.2012.-We tested whether mild and moderate dynamic exercise and muscle metaboreflex activation (MMA) affect dynamic baroreflex control of heart rate (HR) and cardiac output (CO), and the influence of stroke volume (SV) fluctuations on CO regulation in normal (N) and pacing-induced heart failure (HF) dogs by employing transfer function analyses of the relationships between spontaneous changes in left ventricular systolic pressure (LVSP) and HR, LVSP and CO, HR and CO, and SV and CO at low and high frequencies (Lo-F, 0.04 -0.15 Hz; Hi-F, 0.15-0.6 Hz). In N dogs, both workloads significantly decreased the gains for LVSP-HR and LVSP-CO in Hi-F, whereas only moderate exercise also reduced the LVSP-CO gain in Lo-F. MMA during mild exercise further decreased the gains for LVSP-HR in both frequencies and for LVSP-CO in Lo-F. MMA during moderate exercise further reduced LVSP-HR gain in Lo-F. Coherence for HR-CO in Hi-F was decreased by exercise and MMA, whereas that in Lo-F was sustained at a high level (Ͼ0.8) in all settings. HF significantly decreased dynamic HR and CO regulation in all situations. In HF, the coherence for HR-CO in Lo-F decreased significantly in all settings; the coherence for SV-CO in Lo-F was significantly higher. We conclude that dynamic exercise and MMA reduces dynamic baroreflex control of HR and CO, and these are substantially impaired in HF. In N conditions, HR modulation plays a major role in CO regulation. In HF, influence of HR modulation wanes, and fluctuations of SV dominate in CO variations. arterial baroreflex; exercise reflexes; pressor response; impaired cardiac performance BEAT-TO-BEAT CARDIAC OUTPUT (CO) varies considerably across successive heart beats, whereas the average level remains remarkably constant under basal conditions (21, 50). This likely involves control mechanisms operating at markedly different frequencies. Rapid baroreflex control of heart rate (HR) is thought to play a crucial role in dynamic CO regulation. Previous studies suggest that low-frequency (Lo-F: 0.04 -0.15 Hz) blood pressure fluctuations are buffered by the dynamic baroreflex control of HR (25, 28). However, we and others have observed that changes in HR do not necessarily elicit proportional changes in CO because stroke volume (SV) may also vary with the changes in ventricular filling time (17,34,48). Furthermore, transient increases in CO will lower ventricular filling pressure (and decreases in CO will raise filling pressure), thereby providing a self-limiting response (6,30,40). Furthermore, baroreflex control of HR may not functionally buffer high-frequency (Hi-F: above 0.15 Hz) blood pressure fluctuations (4,38,44). In this case, Hi-F variations of CO could facilitate blood pressure variability via a feedforward mechanism rather than buffer arterial pressure. In addition, it has been shown that in anesthetized rats, the blood pressure response to cardiac pacing induced high-frequency oscillation of CO is smaller than that to low-frequency oscillation of CO (41). To our knowledge, however, the dynam...

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“…venous physiology; venous return; cardiac filling pressure THE DISTRIBUTION of cardiac output between compliant vasculature (e.g., splanchnic organs and skin) and noncompliant vasculature (e.g., skeletal muscle) is proposed to constitute an important determinant of the amount of blood available to the heart (e.g., central venous pressure, central blood volume) (6,13,16,17). The redistribution of cardiac output from compliant to noncompliant circulations is proposed to constitute a critical adjustment that permits cardiac output to increase in dynamic exercise (10,12,27,28), and redistribution of blood flow to the compliant skin circulation during heat stress is thought to reduce stroke volume and thereby impose a limitation on the ability to maintain or increase cardiac output in this setting (22). However, there is recent evidence against this idea (9); thus the concept remains controversial.…”

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confidence: 99%

“…Another approach has been to alter cardiac output distribution by evoking reflexes (8) or infusing drugs (16). The third approach has been to impose stresses that alter cardiac output distribution such as exercise (27,28) and combined exercise and heat stress (9,22). There are important limitations to each of these approaches.…”

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confidence: 99%

Diversion of blood flow from noncompliant to compliant vasculature in awake dogs: mechanical impact on right atrial pressure

Zidon

Sheriff

2006

American Journal of Physiology-Heart and Circulatory Physiology

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Dependence of cardiac filling pressure on cardiac output during rest and dynamic exercise in dogs

Cited by 56 publications

References 0 publications

Heart failure attenuates muscle metaboreflex control of ventricular contractility during dynamic exercise

Heart failure attenuates muscle metaboreflex control of ventricular contractility during dynamic exercise

Dynamic cardiac output regulation at rest, during exercise, and muscle metaboreflex activation: impact of congestive heart failure

Diversion of blood flow from noncompliant to compliant vasculature in awake dogs: mechanical impact on right atrial pressure

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