Inconsistency of the slope and the volume intercept of the end-systolic pressure-volume relationship as individual indexes of inotropic state in conscious dogs: presentation of an index combining both variables.

Crottogini, Alberto J.; Willshaw, Peter; Barra, J. G.; Armentano, Ricardo L.; Fischer, Edmundo Cabrera; Pichel, R

doi:10.1161/01.cir.76.5.1115

Cited by 51 publications

(26 citation statements)

References 58 publications

(4 reference statements)

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“…Accurate evaluations of the contractile state of the heart are challenging. Different methods such as SV, ejection fraction, cardiothoracic ratio, circumferential shortening velocity, and dP/dt max , among others, are frequently used to study ventricular contractility, despite their major limitations: they are known to be sensitive not only to changes in contractility but also to loading conditions (9,23,41). Moreover, they also are influenced by changes in cardiac mass and morphology.…”

Section: Discussionmentioning

confidence: 99%

“…Ventricular contractility was assessed by employing the slope of the line intersecting the end-systolic pressure-volume relationships (E max : maximal elastance index) and preload-recruitable stroke work index (PRSW) calculated from the stroke work-end-diastolic volume relationship. Both have been shown to be sensitive to changes in ventricular contractility and relatively insensitive to loading conditions, and the latter measure (PRSW) has been shown to be independent of changes in ventricular chamber size (9,14,15,21,23,49,50). We hypothesized that in the HF state, the muscle metaboreflex-induced increase in LV contractility during mild and moderate dynamic exercise would be impaired as shown by a smaller rise or no change in E max and PRSW.…”

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confidence: 99%

“…These parameters are known to be sensitive not only to contractile state but also to loading conditions (9,23,41). To accurately evaluate the MMR effect on ventricular contractility during dynamic exercise under normal conditions, we recently investigated LV performance in the pressure-volume plane in conscious dogs during mild and moderate exercise (42).…”

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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%

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confidence: 99%

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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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“…Also, anesthesia and acute surgical trauma may affect cardiovascular reflexes. Furthermore, traditional measures of ventricular function, such as LV dP/dt max , SV, and ejection fraction, are affected not only by the contractile state but also by loading conditions (7,17,34). Thus an accurate evaluation of LV contractile function has been a long-standing problem.…”

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confidence: 99%

“…To overcome these limitations, LV contractility has been studied with the pressure-volume technique. The maximal elastance (E max ), measured as LV end-systolic pressure-volume relationship (ESPVR) obtained under different loading conditions, has been validated by several investigators as a model to evaluate LV contraction and is useful for quantifying inotropic state independent of preload and afterload under physiological conditions (7,10,11,15,17,40,41). Employing the pressure-volume analysis technique, we conducted this investigation in an effort to clarify how the MMR modifies LV contractility during mild and moderate dynamic exercise.…”

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confidence: 99%

Muscle metaboreflex control of ventricular contractility during dynamic exercise

Sala‐Mercado¹,

Hammond²,

Kim³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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When oxygen delivery to active skeletal muscle is insufficient for the metabolic demands, afferent nerves within muscles are activated, which elicit reflex increases in heart rate (HR), cardiac output (CO), and arterial pressure (AP), termed the muscle metaboreflex (MMR). To what extent the increases in CO are the result of increased ventricular contractility is unclear. A widely accepted index of contractility is maximal left ventricular elastance (Emax), the slope of the end-systolic pressure-volume relationship, such as during rapidly imposed reductions in preload. The objective of the present study was to determine whether MMR activation elicits increases in Emax. Experiments were performed using conscious dogs chronically instrumented to measure left ventricular pressure and volume at rest and during mild or moderate treadmill exercise with and without partial hindlimb ischemia to elicit MMR responses. At both workloads, MMR activation significantly increased CO, HR, AP, and maximum rate of change of left ventricular pressure. During both mild and moderate exercise, MMR activation increased Emax to 159.6 Ϯ 8.83 and 155.8 Ϯ 6.32% of the exercise value under free-flow conditions, respectively. We conclude that the increase of ventricular elastance associated with MMR activation indicates that a substantial increase in ventricular contractility contributes to the rise in CO during dynamic exercise. elastance; pressor response; cardiac function DURING DYNAMIC EXERCISE, when oxygen delivery to active skeletal muscle is insufficient to meet the metabolic demands, metabolites (e.g., lactic acid, adenosine, potassium, diprotonated phosphate, H ϩ , arachidonic acid products, and others) accumulate within the active muscle and stimulate group III and IV afferent neurons. These sensory neurons project to the central nervous system, eliciting a reflex pressor response consisting of increases in efferent sympathetic nerve activity (SNA), mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), plasma levels of vasoactive hormones, and peripheral vasoconstriction termed the muscle metaboreflex (MMR) (1, 2, 8, 12, 14, 19, 21, 25-28, 30, 32, 33, 35-38, 42, 44). These mechanisms act in concert to partially restore blood flow and arterial oxygen delivery to the hypoperfused muscles (27,31). Previous studies have shown that in normal dogs exercising at mild and moderate workloads, the increases in MAP elicited by this MMR activation are mainly due to increases in CO. The rise in CO likely results from increases in ventricular performance, HR, and central blood volume mobilization (26, 35). In this way the MMR-induced increases in ventricular performance act to sustain or slightly increase stroke volume (SV) despite decreases in ventricular filling time due to the reflex tachycardia (2, 26, 44). Furthermore, O'Leary an Augustyniak (26) showed that in normal dogs in which HR was fixed at 225 beats/min during mild exercise, MMR activation caused such a rise in SV that the increases in CO were approximately equal to t...

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Afterload Sensitivity of Nonlinear End-Systolic Pressure–Volume Relation vs Preload Recruitable Stroke Work in Conscious Dogs

McClain

Wright

Bose

et al. 1998

Journal of Surgical Research

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Inconsistency of the slope and the volume intercept of the end-systolic pressure-volume relationship as individual indexes of inotropic state in conscious dogs: presentation of an index combining both variables.

Cited by 51 publications

References 58 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

Muscle metaboreflex control of ventricular contractility during dynamic exercise

Afterload Sensitivity of Nonlinear End-Systolic Pressure–Volume Relation vs Preload Recruitable Stroke Work in Conscious Dogs

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