scholarly journals Modulation of β-adrenoceptor signaling in the hearts of 4-wk simulated weightlessness rats

2008 ◽  
Vol 105 (2) ◽  
pp. 569-574 ◽  
Author(s):  
Wen Yin ◽  
Jin-Cheng Liu ◽  
Rong Fan ◽  
Xi-Qing Sun ◽  
Jin Ma ◽  
...  
Keyword(s):  
Adenylyl Cyclase ◽  
Systolic Function ◽  
Left Ventricular ◽  
Biologically Active ◽  
Heart Weight ◽  
Control Group ◽  
Simulated Weightlessness ◽  
Camp Production ◽  
Arterial Blood

The modulation of β-adrenoceptor signaling in the hearts of hindlimb unweighting (HU) simulated weightlessness rats has not been reported. In the present study, we adopted the rat tail suspension for 4 wk to simulate weightlessness; then the effects of simulated microgravity on β-adrenoceptor signaling were studied. Mean arterial blood pressure (ABP), left ventricular pressure (LVP), systolic function (+dP/d tmax), and diastolic function (−dP/d tmax) were monitored in the course of the in vivo experiment. Single rat ventricular myocyte was obtained by the enzymatic dissociation method. Hemodynamics, myocyte contraction, and cAMP production in response to β-adrenoceptor stimulation with isoproterenol or adenylyl cyclase stimulation with forskolin were measured, and Gs protein was also determined. Compared with the control group, no significant changes were found in heart weight, body weight and ABP, while LVP and ±dP/d tmax were significantly reduced. The ABP decrease, LVP increase, and ±dP/d tmax in response to isoproterenol administration were significantly attenuated in the HU group. The effects of isoproterenol on electrically induced single-cell contraction and cAMP production in myocytes of ventricles in the HU rats were significantly attenuated. The biologically active isoform, Gsα (45 kDa) in the heart, was unchanged. Both the increased electrically induced contraction and cAMP production in response to forskolin were also significantly attenuated in the simulated weightlessness rats. Above results indicated that impaired function of adenylyl cyclase causes β-adrenoceptor desensitization, which may be partly responsible for the depression of cardiac function.

Modulation of intracellular calcium transient in response to β-adrenoceptor stimulation in the hearts of 4-wk-old rats during simulated weightlessness

2010 ◽  
Vol 108 (4) ◽  
pp. 838-844 ◽  
Author(s):  
Yan Cui ◽  
Shu-Miao Zhang ◽  
Quan-Yu Zhang ◽  
Rong Fan ◽  
Juan Li ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Intracellular Calcium ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Left Ventricular ◽  
Heart Weight ◽  
Control Group ◽  
Simulated Weightlessness ◽  
Arterial Blood ◽  
Over Time

Modulation of intracellular calcium ([Ca2+]i) transient in response to β-adrenoceptor stimulation in the hearts of hindlimb unweighted (HLU) rats during simulated weightlessness has not been reported. In the present study, we adopted the rat tail suspension for 4 wk to simulate weightlessness. Effects of simulated microgravity on β-adrenoceptor responsiveness were then studied. Mean arterial blood pressure, left ventricular pressure (LVP), systolic function [maximum positive change in pressure over time (+dP/d tmax)], and diastolic function [maximum negative change in pressure over time (−dP/d tmax)] were monitored during the in vivo experiment. β-Adrenoceptor density was quantitated by radioactive ligand binding. Single rat ventricular myocyte was obtained by enzymatic dissociation method. ±dP/d tmax, myocyte contraction, intracellular [Ca2+]i transient, and L-type calcium current in response to β-adrenoceptor stimulation with isoproterenol were measured. Compared with the control group, no significant changes were found in heart weight, body weight, and mean arterial blood pressure, whereas LVP and ±dP/d tmax were significantly reduced. LVP and ±dP/d tmax were significantly attenuated in the HLU group in response to isoproterenol administration. In the in vitro study, the β-adrenoceptor density was unchanged. Effects of isoproterenol on electrically induced single-cell contraction and [Ca2+]i transient in myocytes of ventricles in HLU rats were significantly attenuated. The enhanced L-type Ca2+ current elicited by isoproterenol in cardiomyocytes was significantly decreased in the HLU group. The above results indicate that impaired function of L-type Ca2+ current and decreased [Ca2+]i transient cause the depressed responsiveness of the β-adrenoceptor stimulation, which may be partially responsible for the depression of cardiac function.

scholarly journals Hemodynamic characterization of a transgenic rat strain stably expressing the calcium sensor protein GCaMP2

2019 ◽  
Vol 316 (5) ◽  
pp. H1224-H1228 ◽  
Author(s):  
Attila Oláh ◽  
Mihály Ruppert ◽  
Tamás István Orbán ◽  
Ágota Apáti ◽  
Balázs Sarkadi ◽  
...  
Keyword(s):  
Systolic Function ◽  
Left Ventricular ◽  
Heart Weight ◽  
Transgenic Rat ◽  
Calcium Sensor ◽  
Transgenic Rats ◽  
Sensor Protein ◽  
Rat Strain

A novel transgenic rat strain has recently been generated that stably expresses the genetically engineered calcium sensor protein GCaMP2 in different cell types, including cardiomyocytes, to investigate calcium homeostasis. To investigate whether the expression of the GCaMP2 protein itself affects cardiac function, in the present work we aimed at characterizing in vivo hemodynamics in the GCaMP2 transgenic rat strain. GCaMP2 transgenic rats and age-matched Sprague-Dawley control animals were investigated. In vivo hemodynamic characterization was performed by left ventricular (LV) pressure-volume analysis. Postmortem heart weight data showed cardiac hypertrophy in the GCaMP2 group (heart-weight-to-tibial-length ratio: 0.26 ± 0.01 GCaMP2 vs. 0.23 ± 0.01 g/cm Co, P < 0.05). We detected elevated mean arterial pressure and increased total peripheral resistance in transgenic rats. GCaMP2 transgenesis was associated with prolonged contraction and relaxation. LV systolic function was not altered in transgenic rats, as indicated by conventional parameters and load-independent, sensitive indices. We found a marked deterioration of LV active relaxation in GCaMP2 animals (τ: 16.8 ± 0.7 GCaMP2 vs. 12.2 ± 0.3 ms Co, P < 0.001). Our data indicated myocardial hypertrophy, arterial hypertension, and impaired LV active relaxation along with unchanged systolic performance in the heart of transgenic rats expressing the GCaMP2 fluorescent calcium sensor protein. Special caution should be taken when using transgenic models in cardiovascular studies. NEW & NOTEWORTHY Genetically encoded Ca2+-sensors, like GCaMP2, are important tools to reveal molecular mechanisms for Ca2+-sensing. We provided left ventricular hemodynamic characterization of GCaMP2 transgenic rats and found increased afterload, cardiac hypertrophy, and prolonged left ventricular relaxation, along with unaltered systolic function and contractility. Special caution should be taken when using this rodent model in cardiovascular pharmacological and toxicological studies.

Abstract 3430: Left Ventricular Hypertrophy and Diastolic Dysfunction in Mice Lacking All Nitric Oxide Synthase Isoforms

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Masato Tsutsui ◽  
Kiyoko Shibata ◽  
Hiroaki Shimokawa ◽  
Yasuko Yatera ◽  
Yumi Furuno ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Diastolic Dysfunction ◽  
Cardiac Fibrosis ◽  
Systolic Function ◽  
Left Ventricular ◽  
Functional Changes ◽  
Arterial Blood ◽  
Oxide Synthase

We have recently succeeded in developing mice in which all three nitric oxide synthase isoforms (nNOS, iNOS, and eNOS) are completely disrupted ( PNAS 2005). In this study, we examined cardiac morphology and function in those mice. Cardiac echocardiography and left ventricular (LV) hemodynamic measurement were performed in male wild-type (WT), singly nNOS −/− , iNOS −/− , eNOS −/− , and triply n/i/eNOS −/− mice at 2 and 5 months of age (n=5–8). At 2 months of age, no significant cardiac morphological or functional changes were detected in any strains studied. However, at 5 months of age, significant LV hypertrophy (wall thickness, mm) were noted in the triply n/i/eNOS −/− mice (1.3±0.1, P <0.01) and to a lesser extent in the singly eNOS −/− mice (1.1±0.1, P <0.05), but not in the singly nNOS −/− (0.8±0.1) or iNOS −/− mice (1.0±0.1), as compared with the WT mice (1.0±0.2). Furthermore, significant LV diastolic dysfunction (as evaluated by echocardiographic E/A ratio and by hemodynamic peak negative dP/dt), with preserved LV systolic function (as assessed by echocardiographic ejection fraction and by hemodynamic peak positive dP/dt), was noted only in the 5-month-old triply n/i/eNOS −/− mice (2.7±0.1 and 2505±60, both P <0.05), but not in any singly nNOS −/− (2.1±0.2 and 3833±402), iNOS −/− (2.0±0.1 and 3773±747), or eNOS −/− mice (2.0±0.3 and 2934±122), as compared with the WT mice (1.9±0.1 and 4038±344). In addition, significant cardiac fibrosis (fibrosis area, %, Masson-trichrome staining) was also detected only in the 5-month-old triply n/i/eNOS −/− mice (1.4±0.2, P <0.05) compared with the WT mice (0.3±0.1). Importantly, arterial blood pressure (mmHg, tail-cuff method) was significantly elevated in the triply n/i/eNOS −/− (143±3.1, P <0.05) than in the WT mice (104±7.3), but the hypertensive level was comparable to that in the singly eNOS −/− mice (140±8.5). Thus, mechanism(s) other than hypertension appears to be involved in the cardiac abnormalities of the triply n/i/eNOS −/− mice. These results provide the first evidence that genetic disruption of all NOSs results in LV hypertrophy and diastolic dysfunction in mice in vivo, suggesting a pivotal role of the NOS system in maintaining cardiac homeostasis.

The Pattern of Ventricular Remodeling Influences the Level of Oxidative Stress in Heart Failure Patients

2017 ◽  
Vol 68 (7) ◽  
pp. 1506-1511
Author(s):  
Cerasela Mihaela Goidescu ◽  
Anca Daniela Farcas ◽  
Florin Petru Anton ◽  
Luminita Animarie Vida Simiti
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Ventricular Remodeling ◽  
Clinical Laboratory ◽  
Left Ventricular ◽  
Control Group ◽  
Reactive Protein ◽  
Lv Mass ◽  
Few Data

Oxidative stress (OS) is increased in chronic diseases, including cardiovascular (CV), but there are few data on its effects on the heart and vessels. The isoprostanes (IsoP) are bioactive compounds, with 8-iso-PGF25a being the most representative in vivo marker of OS. They correlate with the severity of heart failure (HF), but because data regarding OS levels in different types of HF are scarce, our study was aimed to evaluate it by assessing the urinary levels of 8-iso-PGF2aand its correlations with various biomarkers and parameters. Our prospective study included 53 consecutive patients with HF secondary to ischemic heart disease or dilative cardiomyopathy, divided according to the type of HF (acute, chronic decompensated or chronic compensated HF). The control group included 13 hypertensive patients, effectively treated. They underwent clinical, laboratory - serum NT-proBNP, creatinine, uric acid, lipids, C reactive protein (CRP) and urinary 8-iso-PGF2a and echocardiographic assessment. HF patients, regardless the type of HF, had higher 8-iso-PGF2a than controls (267.32pg/�mol vs. 19.82pg/�mol, p[0.001). The IsoP level was directly correlated with ejection fraction (EF) (r=-0.31, p=0.01) and NT-proBNP level (r=0.29, p=0.019). The relative wall thickness (RWT) was negatively correlated with IsoP (r=-0.55, p[0.001). Also 8-iso-PGF25a was higher by 213.59pg/�mol in the eccentric left ventricular (LV) hypertrophy subgroup comparing with the concentric subgroup (p=0.014), and the subgroups with severe mitral regurgitation (MR) and moderate/severe pulmonary hypertension (PAH) had the highest 8-iso-PGF2a levels. Male sex, severe MR, moderate/severe PAH, high LV mass and low RWT values were predictive for high OS level in HF patients.Eccentric cardiac remodeling, MR severity and PAH severity are independent predictors of OS in HF patients.

scholarly journals Remodeling of the heart and main vessels in patients with marfanoid habitus

2020 ◽  
Vol 10 (5) ◽  
pp. 27-34
Author(s):  
Eugene V. Timofeev ◽  
Eduard G. Malev ◽  
Nina N. Parfenova ◽  
Eduard V. Zemtsovsky
Keyword(s):  
Marfan Syndrome ◽  
Aortic Root ◽  
Structural Changes ◽  
Systolic Function ◽  
Interventricular Septum ◽  
Age Groups ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Control Group ◽  
Left Ventricular Myocardium

For many hereditary connective tissue disorders (HCTD), especially Marfan syndrome, remodeling of the heart and main vessels is described, which is manifested by a decrease in the systolic function of the left ventricle and expansion of the thoracic aorta. Evaluation of morphometric characteristics of the heart and main vessels in patients with other HCTD, in particular marfanoid habitus (MH) has not been previously carried out. Materials and methods. Weexamined 90 young men and 74 young women between the ages of 18 to 25 years, 111 patients older age groups with stable over coronary heart disease (mean age 64.66.2 years) and 9 patients with verified Marfan syndrome (mean age 27.99.3years). All survey phenotypic and performed anthropometric survey identifying bone signs of dysembryogenesis as well as Echocardiography study on standard protocol. The results.Patients with MH as compared with control group revealed a relatively larger diameter of aortic root (30.44.7 vs 28.03.6 mm,p= 0.03) and the ascending aorta (26.64.9 vs 24.63.2 mm,p= 0.05). Also young with MH turned out to be significantly thicker myocardium of left ventricular posterior wall (8.30.8 vs 7.71.1 mm,p= 0.02) and interventricular septum (8.81.2vs 8.21.1mm,p= 0.04). When performing correlation analysis identified reliable positive correlation between such highly specialized bone signs as high palate (r= 0.31), infundibular deformation of the chest (r= 0.43), arachnodactyly (r= 0.45) andZ-test (p 0.05 for all). Expansion of the aorta (Z-criterion 2.0) have found 24% of older patients with MH. Conclusion.Inpatients with MH revealed significant structural changes of heart and main vessels which are progredient character thickening of the left ventricular myocardium and expansion of the aortic root.

scholarly journals Contractile protein phosphorylation predicts human heart disease phenotypes

2013 ◽  
Vol 304 (12) ◽  
pp. H1644-H1650 ◽  
Author(s):  
Lori A. Walker ◽  
David A. Fullerton ◽  
Peter M. Buttrick
Keyword(s):  
Heart Failure ◽  
Heart Disease ◽  
Protein Phosphorylation ◽  
Protein Phosphatase ◽  
Human Heart ◽  
Troponin I ◽  
Systolic Function ◽  
Left Ventricular ◽  
Control Group ◽  
Lv Function

Human heart failure has been associated with a low level of thin-filament protein phosphorylation and an increase in calcium sensitivity of contraction relative to both “control” human heart tissue and tissue from small animal models. However, diverse strategies of human tissue procurement and the reliance on tissue obtained from subjects with end-stage heart failure suggest this may be an incomplete characterization. Therefore, we evaluated cardiac left ventricular (LV) biopsy samples from patients with aortic stenosis undergoing valve replacement who presented either with LV hypertrophy and preserved systolic function (Hyp) or with LV dilation and reduced ejection fraction (Dil). In Hyp, total troponin I (TnI) phosphorylation was markedly increased and myosin light chain 2 (MLC2) phosphorylation was unchanged relative to a control group of patients with normal LV function. Conversely, in Dil, total TnI phosphorylation was significantly reduced compared with control subjects and MLC2 phosphorylation was increased. Site-specific analysis of TnI phosphorylation revealed phenotype-specific differences such that Hyp samples demonstrated significant increases in phosphorylation at serine 22/23 and Dil samples had significant decreases at serine 43. The ratio of phosphorylation at the two sites was biased toward serine 22/23 in Hyp and toward serine 43/45 in Dil. Western blot analysis showed that protein phosphatase-1 was reduced in Hyp and protein phosphatase-2 was reduced in Dil. These data suggest that posttranslational modifications of sarcomeric proteins, both singly and in combination, are stage specific. Defining these changes in progressive heart disease may provide important diagnostic and treatment information.

Electrophysiologic properties and ventricular fibrillation in normal and myopathic hearts

1999 ◽  
Vol 77 (7) ◽  
pp. 510-519 ◽  
Author(s):  
Katherine M Kavanagh ◽  
Patricia A Guerrero ◽  
Bodh I Jugdutt ◽  
Francis X Witkowski ◽  
Jeffrey E Saffitz
Keyword(s):  
Ventricular Fibrillation ◽  
Myocardial Dysfunction ◽  
Myocardial Cell ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Functional Abnormality ◽  
Ventricular Ejection Fraction ◽  
Anisotropic Properties

This study tests the hypothesis that moderate myocardial dysfunction is associated with altered myocardial anisotropic properties and structurally altered ventricular fibrillation (VF). Mongrel dogs were randomized to either a control group or a group that was rapidly paced at 250 beats/min until the left ventricular ejection fraction was [Formula: see text] 40%. Changes in anisotropic properties and the electrical characteristics of VF associated with the development of moderate myocardial dysfunction were assessed by microminiature epicardial mapping studies. In vivo conduction, refractory periods, and repolarization times were prolonged in both longitudinal and transverse directions in myopathic animals versus controls. VF was different in myopathic versus control animals. There were significantly more conducted deflections during VF in normal hearts compared with myopathic hearts. Propagated deflection-to-deflection intervals during VF were significantly longer in myopathic hearts compared with controls (125.5 ± 49.06 versus 103.4 ± 32.9 ms, p = 0.009). There were no abnormalities in cell size, cell shape, or the number of intercellular gap junctions and there was no detectable change in the expression of the gap junction proteins Cx43 and Cx45. Moderate myocardial dysfunction is associated with significant electrophysiological abnormalities in the absence of changes in myocardial cell morphology or intercellular connections, suggesting a functional abnormality in cell-to-cell communication.Key words: cardiomyopathy, anisotropy, fibrillation, defibrillation.

Abstract 321: Cardiac Function Improvement Following In vivo Intracoronary Adeno-Associated Virus Type 1 Vector Gene Transfer of SERCA2a in a Pre-Clinical Model of Heart Failure

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Hung Q Ly ◽  
Yoshiaki Kawase ◽  
Fabrice A Prunier ◽  
Djamel Lebeche ◽  
Yafen Shi ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Ventricular Remodeling ◽  
Systolic Function ◽  
Left Ventricular ◽  
Internal Diameter ◽  
Adeno Associated Virus ◽  
Inotropic Effects ◽  
Clinical Model ◽  
Virus Serotype

Background: Reduced activity and expression of sarcoplasmic reticulum Ca 2+ ATPase (SERCA2a) is known to occur in HF. Method: Our 4-month study examined the effects of SERCA2a gene transfer in a swine volume-overload HF (VO-HF) model. Using Yorkshire-Landrace swine, HF was created by severing mitral apparatus chordae to induce mitral regurgitation. Results: At 2 months (M), a compensated state of VO-HF was found: prolongation of the rate of isovolumic relaxation (Tau), increased left ventricular internal diameter diastolic and systolic diameters (LVIDd, LVIDs). At 2M, intracoronary injection of adeno-associated virus serotype 1 vector carrying SERCA2a under a cytomegalovirus promoter (AAV1.SERCA2a) (n = 10) vs. saline (n = 6) was performed. At 4M, gene transfer resulted in (A) positive LV inotropic effects: (dP/dt)/P, 15.5 ± 3.0 sec − 1 SERCA2a-group vs. 21.2 ± 3.2 sec − 1 controls; p < 0.01; (B) a favorable trend in LV lusitropic effects: Tau, 0.037 ± 0.019 vs. 0.051 ± 0.01 msec, p = 0.09; (C) improvement in LV geometry: % change in LVIDs, +15 ± 11% controls vs. −3.0 ± 10% SERCA2a-group, p < 0.01. At 4M, BNP levels remained stable in post- SERCA2a gene transfer, in contrast to the progressive rising levels among controls. Further, cardiac SERCA2a expression was significantly decreased in controls whereas it was restored to normal levels in the SERCA2a group (Figure ). Lastly, there was no histopathological evidence of myocardial inflammatory reaction or necrosis. Conclusion: Overexpression of SERCA2a by in vivo AAV1-mediated intracoronary gene transfer preserved systolic function, potentially prevented diastolic dysfunction and improved ventricular remodeling.

Abstract 16771: Longitudinal Segmental Shape Analysis of the Remodeling Left Ventricle in Chronic Mitral Regurgitation

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Daniella Corporan ◽  
Muralidhar Padala
Keyword(s):  
Mitral Regurgitation ◽  
Systolic Function ◽  
Left Ventricular ◽  
Control Group ◽  
Adult Rats ◽  
Mitral Valve Leaflet ◽  
Area Index ◽  
Sphericity Index ◽  
Left Ventricular Shape ◽  
Apical Area

Introduction: Severe mitral regurgitation (MR) initiates left ventricular (LV) dilatation, but preserves systolic function. Due to preserved EF, patients are not referred for correction of their MR, and the ventricle continues to enlarge. Identifying patients at risk of heart failure, just from assessing LV size is challenging. In this study, we sought to investigate if ventricular shape and sphericity can represent the pathological remodeling process in this disease. Methods: Sixty adult rats (N=60) were induced with severe MR by puncturing the mitral valve leaflet with a 23G needle on the beating heart, using echo guidance (Fig.A1). Transthoracic echocardiography was performed at 2, 10, 20, and 40 weeks (n=15 rats/group) for analysis of the left ventricular shape. Fifteen healthy rats (N=15) were used as a sham group for comparison. Results: Severe MR was confirmed in all the rats in the MR group with a MR jet area of 40.99±9.40% ( Fig.A2 ), MR volume of 119.50±32.43μl ( Fig.A3 ), and pulmonary flow reversal ( Fig.A4 ). None of these were observed in the control group. LV dilation was observed in MR rats compared to sham ( Fig.B ). Diastolic sphericity index, LV area, and diastolic apical area index was significantly increased at 2, 10, 20, and 40 weeks after MR compared to sham (p<0.05) ( Fig.C1-C3 ). Systolic sphericity index was not significantly increased compared to sham at any time-point ( Fig.D1 ). LV area was unchanged at 2 weeks, and was significantly increased at 10, 20, and 40 weeks ( Fig.D2 ). Systolic apical area index was significantly increased at 2, 20, and 40 weeks compared to sham (p<0.05) ( Fig.D3 ). Conclusions: Analysis of left ventricular shape and its longitudinal changes can help detect remodeling patterns that are not visible using traditional functional indices.

Inotropic sensitivity to beta-adrenergic stimulation in early sepsis

1988 ◽  
Vol 255 (4) ◽  
pp. H699-H703 ◽  
Author(s):  
L. W. Smith ◽  
K. H. McDonough
Keyword(s):  
Contractile Function ◽  
Plasma Catecholamines ◽  
Left Ventricular ◽  
Adrenergic Stimulation ◽  
Maximal Increase ◽  
Beta Adrenergic ◽  
Arterial Blood ◽  
Myocardial Contractile ◽  
Early Sepsis

In early sepsis, maintenance of in vivo cardiovascular performance is at least partly dependent on sympathetic support to hearts with intrinsic contractile defects. Yet prolonged sympathetic stimulation, as occurs in sepsis, would be expected to alter the heart's ability to respond to this stimulation. We have investigated myocardial inotropic sensitivity to beta-adrenergic stimulation in a model of sepsis in which animals, at the time studied, exhibited bacteremia, normal arterial blood pressure and cardiac output, elevated heart rate, and elevated plasma catecholamines. Intrinsic myocardial contractile function, as assessed by the maximal rate of left ventricular pressure development (LV dP/dtmax) in an isovolumically contracting heart preparation, was significantly depressed in septic animals. To determine whether hearts from septic animals could respond normally to beta-adrenergic stimulation, we studied inotropic response to a bolus of isoproterenol in these isolated hearts. With maximal isoproterenol stimulation, hearts from septic animals were able to attain the same dP/dtmax as were hearts from control animals. With lower levels of isoproterenol, there was also no difference in inotropic indexes between the two groups when response was expressed as a percent of the maximal increase in dP/dtmax achieved with isoproterenol. These results suggest that in early sepsis, despite intrinsic myocardial contractile dysfunction, the ability of the heart to modulate its inotropic state in response in beta-adrenergic stimulation is intact.

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