Validation of a mouse conductance system to determine LV volume: comparison to echocardiography and crystals

Feldman, Marc D.; Erikson, John M.; Mao, Yi; Korcarz, Claudia E; Lang, Roberto M.; Freeman, Gregory L.

doi:10.1152/ajpheart.2000.279.4.h1698

Cited by 78 publications

(72 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Right ventricular pressures in this study were similar to several prior studies (ϳ25 mmHg) (17,37,38,50,51,65) but higher than others (ϳ18 mmHg) (32,61), which may be due to the significantly slower heart rates in those studies compared with the present study. CO measured from the right ventricle in this study was similar to CO measured previously in the right ventricular by thermodilution (10) and estimated by transesophageal echocardiography (51), as well as left ventricular output measured by a variety of techniques (3,4,15,18,53). End-diastolic volumes were also similar to those measured by echocardiography (51), but much lower than that found by Rockman et al (47) using X-ray contrast microangiography.…”

Section: Discussionsupporting

confidence: 87%

Measuring right ventricular function in the normal and hypertensive mouse hearts using admittance-derived pressure-volume loops

Tabima¹,

Hacker

Chesler

2010

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Tabima DM, Hacker TA, Chesler NC. Measuring right ventricular function in the normal and hypertensive mouse hearts using admittance-derived pressure-volume loops. Am J Physiol Heart Circ Physiol 299: H2069 -H2075, 2010. First published October 8, 2010 doi:10.1152/ajpheart.00805.2010.-Mice are a widely used animal model for investigating cardiovascular disease. Novel technologies have been used to quantify left ventricular function in this species, but techniques appropriate for determining right ventricular (RV) function are less well demonstrated. Detecting RV dysfunction is critical to assessing the progression of pulmonary vascular diseases such as pulmonary hypertension. We used an admittance catheter to measure pressure-volume loops in anesthetized, open-chested mice before and during vena cava occlusion. Mice exposed to chronic hypoxia for 10 days, which causes hypoxia-induced pulmonary hypertension (HPH), were compared with control (CTL) mice. HPH resulted in a 27.9% increase in RV mass (P Ͻ 0.005), a 67.5% increase in RV systolic pressure (P Ͻ 0.005), and a 61.2% decrease in cardiac output (P Ͻ 0.05). Preload recruitable stroke work (PRSW) and slope of the maximum derivative of pressure (dP/dtmax)-end-diastolic volume (EDV) relationship increased with HPH (P Ͻ 0.05). Although HPH increased effective arterial elastance (Ea) over fivefold (from 2.7 Ϯ 1.2 to 16.4 Ϯ 2.5 mmHg/l), only a mild increase in the ventricular end-systolic elastance (Ees) was observed. As a result, a dramatic decrease in the efficiency of ventricular-vascular coupling occurred (Ees/Ea decreased from 0.71 Ϯ 0.27 to 0.35 Ϯ 0.17; P Ͻ 0.005). Changes in cardiac reserve were evaluated by dobutamine infusion. In CTL mice, dobutamine significantly enhanced Ees and dP/dtmax-EDV but also increased Ea, causing a decrease in Ees/Ea. In HPH mice, slight but nonsignificant decreases in Ees, PRSW, dP/dtmax-EDV, and Ea were observed. Thus 10 days of HPH resulted in RV hypertrophy, ventricular-vascular decoupling, and a mild decrease in RV contractile reserve. This study demonstrates the feasibility of obtaining RV pressure-volume measurements in mice. These measurements provide insight into ventricular-vascular interactions healthy and diseased states. cardiopulmonary hemodynamics; catheterization; chronic hypoxia; inotropic agents MOUSE IS A WIDELY USED SPECIES for investigating a growing number of disease states. In particular, the availability of knockout and transgenic mice allows the molecular mechanisms of disease to be understood with ever more clarity. Cardiopulmonary status, including right ventricular function, pulmonary vascular function, and right ventricular-pulmonary vascular interactions, is an important facet of health and disease. Recently, different methods for assessing left ventricular function, systemic vascular function, and the efficiency of left ventricular-systemic vascular hemodynamic interactions in mice in situ have been described (13,16,17,39,41,47,53,54,64). However, the feasibility and utility of these techniques in ...

show abstract

Section: Discussionsupporting

confidence: 87%

Measuring right ventricular function in the normal and hypertensive mouse hearts using admittance-derived pressure-volume loops

Tabima¹,

Hacker

Chesler

2010

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…This methodology has been extensively validated in various species, including mice, which are substantially smaller than 4-wk-old rats (17)(18)(19). However, the experience with the conductance catheter applied in young rats is limited.…”

Section: Discussionmentioning

confidence: 99%

“…A 30 A, 10 kHz current is applied between electrodes 1 and 4 to generate an intracavitary electric field and the voltage gradient between electrodes 2 and 3 is measured to determine the instantaneous electrical conductance of the blood in the LV. The volume calibration of the conductance measurements was performed in vitro as described by Yang et al (18) and parallel conductance was determined by the hypertonic saline method (16,19,20).…”

mentioning

confidence: 99%

Neonatal Glucocorticosteroid Treatment Causes Systolic Dysfunction and Compensatory Dilatation in Early Life: Studies in 4-Week-Old Prepubertal Rats

et al. 2005

View full text Add to dashboard Cite

Glucocorticosteroid treatment is widely used to prevent chronic lung disease in premature infants. Recent studies in adult rats, treated with dexamethasone in the neonatal period, report negative long-term effects on the heart and severely reduced life expectancy. We treated neonatal rats with dexamethasone and studied cardiac function after 4 wk (prepubertal age) to investigate whether the late effects as previously described are preceded by detectable alterations in cardiac function at a younger age. Male rat pups (n ϭ 12) were injected intraperitoneally with dexamethasone on d 1, 2, and 3 (0.5, 0.3, and 0.1 g/g) of life. Control pups (n ϭ 10) received saline. At 4 wk the animals were anesthetized, and a pressure-conductance catheter was introduced into the left ventricle to measure pressure-volume loops. Cardiac function was measured and pressure-volume relations were determined to quantify intrinsic systolic and diastolic function. Subsequently, hearts were excised for histologic examination. Compared with saline-treated animals, dexamethasonetreated rats had a reduced ventricular weight (270 Ϯ 40 versus 371 Ϯ 23 mg, p Ͻ 0.001) and reduced systolic function (endsystolic elastance: 1.24 Ϯ 0.43 versus 2.50 Ϯ 1.39 mm Hg/L, p ϭ 0.028). Cardiac output was maintained and end-diastolic volume was increased (84 Ϯ 23 versus 59 Ϯ 19 L, p ϭ 0.012) indicating a state of compensatory dilatation. Heart rate, diastolic function, and systemic vascular resistance were unchanged. Neonatal dexamethasone treatment causes cardiac alterations that can be detected in the prepubertal period and that may precede severe cardiac dysfunction later in life. If our findings are confirmed in humans, this may have consequences for a large patient population and cardiac screening at young age may be indicated to enable secondary prevention. Glucocorticosteroids, in particular DEX, are widely used to treat or prevent chronic lung disease in preterm infants (1). Besides their antiinflammatory action, glucocorticosteroids stimulate lung maturation and enhance surfactant production (2,3). Thus, glucocorticosteroid treatment improves pulmonary function and enables early weaning from the ventilator and, consequently, increased survival of extremely premature neonates (4).In the past two decades DEX therapy in preterm infants has gained wide acceptance. However, despite the short-term beneficial effects, concerns have been raised about long-lasting negative side effects of glucocorticosteroids (5-7). Several studies describe neurodevelopmental impairments in infants treated with glucocorticosteroids in the neonatal period (8 -10).With regard to the cardiovascular system, hypertension and reversible myocardial hypertrophy have been reported (11-13), but possible long-term effects became apparent only recently. De Vries et al. (14) showed that rats treated with DEX in the neonatal period had decreased heart weights, as well as hypertrophy and signs of early degeneration of cardiomyocytes in 85-23, revised 1996).Pregnant Wistar rats (270 -300 g) we...

show abstract

“…We concluded that it wasn't and suggested that the active energy per beat in small animals (rats) was about 1/2 to 1/3 that in man, meaning that there would be no 4-fold difference in energy flux between rat and man or 8-fold difference between mouse and man. Since the hearts of nearly all mammals work against a blood pressure of 100 mmHg and the cardiac output and weight of human, rat, and mouse hearts are well known, it is easy to calculate that the work output per beat is about 3.3 mJ/g in man and about 1.2 mJ/g in mice (14 l stroke volume assumed, see Feldman et al [117]). If the mechanical efficiency is constant and about 20%, the energy per beat of the human heart would be about 16 mJ/g, and it would be about 6 mJ/g in a mouse.…”

Section: Species Differences In Basal Metabolismmentioning

confidence: 99%

Cardiac Basal Metabolism.

Gibbs

Loiselle²

2001

JJP

View full text Add to dashboard Cite

The cardiac basal metabolism is the rate of energy expenditure of the quiescent myocardium. It is also called the resting metabolism or the arrested heart metabolism. It has been measured in numerous ways, and in vivo there is good evidence that it accounts for about 1/5 to 1/3 of the total energy flux. The difficulty arises, however, when the heart is stopped because the magnitude of the basal metabolism depends, as blood viscosity, on how and under what physiological condition it is measured. It is possible for the in vivo basal value to fall to less than 1/5 of its original value without cellular damage or to increase to values 5 times greater than its probable in vivo magnitude (i.e., to rise to values in excess of the energy flux of the normally beating heart) by altering the composition of the perfusion medium. We have written on this subject several times [1][2][3], but believe that developments in knowledge now make it possible for us to speculate in a more informed manner. Since several million openheart operations are performed on arrested hearts worldwide each year, it would seem imperative that we understand the cellular mechanisms that can change the magnitude of basal metabolism.A. V. Hill [4] has pointed out that in examining physiological activities, it is necessary to assume a baseline from which some quantity or rate can be measured. If the energy flux produced by the beating heart were very large compared with the energy flux of the arrested heart, baseline ambiguity would be relatively unimportant. But this is not so in regard to the heart; its basal metabolism is high. Within a species, the basal metabolism of cardiac tissue is several-fold higher than the resting metabolism of skeletal muscle and is an order of magnitude greater than the resting metabolism of amphibian skeletal muscle.Species differences are clearly evident in the magnitude of cardiac basal metabolism, and we believe that the major reason for these differences relates to the leakiness of cell membranes, such as those of the sarcolemma and sarcoplasmic reticulum and those of Japanese Journal of Physiology, 51, 399-426, 2001 Key words: whole hearts, isolated preparations, biochemical contributors, modifiers, species difference, temperature, substrate, hypoxia. Abstract:We endeavor to show that the metabolism of the nonbeating heart can vary over an extreme range: from values approximating those measured in the beating heart to values of only a small fraction of normal-perhaps mimicking the situation of nonflow arrest during cardiac bypass surgery. We discuss some of the technical issues that make it difficult to establish the magnitude of basal metabolism in vivo. We consider some of the likely contributors to its magnitude and point out that the biochemical reasons for a sizable fraction of the heart's basal ATP usage remain unresolved. We consider many of the physiological factors that can alter the basal metabolic rate, stressing the importance of substrate supply. We point out that the protective effect of hypothermia ...

show abstract

Validation of a mouse conductance system to determine LV volume: comparison to echocardiography and crystals

Cited by 78 publications

References 41 publications

Measuring right ventricular function in the normal and hypertensive mouse hearts using admittance-derived pressure-volume loops

Measuring right ventricular function in the normal and hypertensive mouse hearts using admittance-derived pressure-volume loops

Neonatal Glucocorticosteroid Treatment Causes Systolic Dysfunction and Compensatory Dilatation in Early Life: Studies in 4-Week-Old Prepubertal Rats

Cardiac Basal Metabolism.

Contact Info

Product

Resources

About