Validation of Conductance Catheter System for Quantification of Murine Pressure-Volume Loops

Yang, Bo; Larson, Douglas F.; Beischel, Julie; Kelley, Ryan; Shi, Jiaqi; Watson, Ronald R.

doi:10.1080/089419301753435710

Cited by 46 publications

(47 citation statements)

References 24 publications

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“…For either the systemic or the pulmonary circulation, E a can be calculated as the peak ventricular pressure divided by the stroke volume (48,49). The value of E a for the pulmonary circulation found here is approximately fourfold lower than the value of E a for the systemic vasculature of mice published previously (13,41,53,62). Given that the peak ventricular pressure in the right ventricle is approximately fourfold less than that in the left ventricle for the same CO, this result is good validation of the values obtained here.…”

Section: Discussionsupporting

confidence: 71%

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

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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 ...

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Section: Discussionsupporting

confidence: 71%

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

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“…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%

“…To determine parallel conductance, we performed intravenous hypertonic saline injections (10% saline, 20 L) (18,20). Parallel conductance was calculated as the mean of three consecutive assessments.…”

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

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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...

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“…The mitral valve flow was measured with Doppler, using a four-chamber view to compute the E-to-A ratios. After echo analysis, pressure-volume loops were acquired with our previously described Millar conductance catheter system methods (42,43).…”

mentioning

confidence: 99%

IL-18 induction of osteopontin mediates cardiac fibrosis and diastolic dysfunction in mice

Yu¹,

Vazquez²,

Khojeini³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Osteopontin (OPN), a key component of the extracellular matrix, is associated with the fibrotic process during tissue remodeling. OPN and the cytokine interleukin (IL)-18 have been shown to be overexpressed in an array of human cardiac pathologies. In the present study, we determined the role of IL-18 in the regulation of cardiac OPN expression and the subsequent interstitial fibrosis and diastolic dysfunction. We demonstrated parallel increases in IL-18, OPN expression, and interstitial fibrosis in murine models of left ventricular pressure and volume overload. Exogenous recombinant (r)IL-18 administered for 2 wk increased cardiac OPN expression, interstitial fibrosis, and diastolic dysfunction. Stimulation of the T helper (Th)1 lymphocyte phenotype with a selective toll-like receptor (TLR)9 agonist induced cardiac IL-18 and OPN expression, which was associated with increased cardiac fibrillar collagen concentrations and interstitial fibrosis resulting in diastolic dysfunction. rIL-18 induced OPN expression and protein levels in primary of cardiac fibroblast cultures. Conditioned media from TLR9-stimulated T lymphocyte cultures induced IL-18 and OPN expression in cardiac fibroblasts, while blockade of the IL-18 receptor with a neutralizing antibody abolished the increase in OPN expression. Furthermore, a mutation in the transcriptional factor interferon regulatory factor (IRF)1 or IRF1 small interfering RNA (siRNA) resulted in the decreased expression of IL-18 and OPN in cardiac fibroblasts. With pressure overload, IRF1-mutant mice showed downregulation of IL-18 and OPN expression in cardiac tissue, reduced cardiac fibrotic development, and increased left ventricular function compared with wild type. These results provide direct evidence that the induction of IL-18 regulates OPN-mediated cardiac fibrosis and diastolic dysfunction. extracellular matrix; remodeling; T lymphocyte; interferon regulatory factor 1; toll-like receptor-9; lysyl oxidase LEFT VENTRICULAR REMODELING in response to pressure and/or volume overload is associated with myocardial hypertrophy, fibroblast hyperplasia, and increased concentrations of fibrillar collagen in the extracellular matrix. Recent studies have shown that pathological myocardial fibrosis may cause diastolic dysfunction and heart failure (24), whereas myocyte hypertrophy in the absence of fibrosis is considered physiological remodeling (22, 46) if the mass-to-volume ratio is preserved (5). In this study, we investigated whether interleukin (IL)-18 regulates the gene and protein expression of the matricellular protein osteopontin (OPN), a component and regulator of cardiac extracellular matrix fibrillar collagen concentrations.As reviewed by Okamoto (26), OPN also plays a critical role in the regulation of cellular proliferation and differentiation, interstitial fibrosis, arteriosclerosis, and angiogenesis. Although OPN is ubiquitously expressed in many tissues and is increased during stress-induced cardiac remodeling, it participates as a cytokine or humoral factor in the in...

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Validation of Conductance Catheter System for Quantification of Murine Pressure-Volume Loops

Cited by 46 publications

References 24 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

IL-18 induction of osteopontin mediates cardiac fibrosis and diastolic dysfunction in mice

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