Relative systolic dysfunction in female spontaneously hypertensive rat myocardium

2007 ◽  
Vol 103 (1) ◽  
pp. 353-358 ◽  
Author(s):  
Brian F. Renna ◽  
Scott M. MacDonnell ◽  
Patricia O. Reger ◽  
Deborah L. Crabbe ◽  
Steven R. Houser ◽  
...  
Keyword(s):  
Exercise Training ◽  
Spontaneously Hypertensive Rat ◽  
Systolic Function ◽  
Isolated Heart ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Lv Function ◽  
Spontaneously Hypertensive ◽  
Heart Preparation ◽  
Wistar Kyoto

Hypertension and exercise independently induce left ventricular (LV) remodeling and alter LV function. The purpose of this study was to determine systolic and diastolic LV pressure-volume relationships (LV-PV) in spontaneously hypertensive rats (SHR) with and without LV hypertrophy, and to determine whether 6 mo of exercise training modified the LV-PV in SHR. Four-month-old female SHR ( n = 20), were assigned to a sedentary (SHR-SED) or treadmill-trained (SHR-TRD) group (∼60% peak O2 consumption, 5 days/wk, 6 mo), while age-matched female Wistar-Kyoto rats (WKY; n = 13) served as normotensive controls. The LV-PV was determined using a Langendorff isolated heart preparation at 4 (no hypertrophy: WKY, n = 5; SHR, n = 5) and 10 mo of age (hypertrophy: WKY, n = 8; SHR-SED, n = 8; SHR-TRD, n = 7). At 4 mo, the LV-PV in SHR was similar to that observed in WKY controls. However, at 10 mo of age, a rightward shift in the LV-PV occurred in SHR. Exercise training did not alter the extent of the shift in the LV-PV relative to SHR-SED. Relative systolic function, i.e., relative systolic elastance, was ∼50% lower in SHR than WKY at 10 mo of age ( P < 0.05). Doppler-derived LV filling parameters [early wave (E), atrial wave (A), and the E/A ratio] were similar between groups. LV capacitance was increased in SHR at 10 mo ( P < 0.05), whereas LV diastolic chamber stiffness was similar between groups at 10 mo. Hypertrophic remodeling at 10 mo of age in female SHR is manifest with relative systolic decompensation and normal LV diastolic function. Exercise training did not alter the LV-PV in SHR.

scholarly journals Progression of myocardial remodeling and mechanical dysfunction in the spontaneously hypertensive rat

2012 ◽  
Vol 303 (11) ◽  
pp. H1353-H1365 ◽  
Author(s):  
Ian J. LeGrice ◽  
Adèle J. Pope ◽  
Gregory B. Sands ◽  
Gillian Whalley ◽  
Robert N. Doughty ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rat ◽  
Systolic Function ◽  
Three Dimensional ◽  
Hypertensive Heart Disease ◽  
Left Ventricular ◽  
Morphological Data ◽  
Systemic Hypertension ◽  
Myocardial Remodeling ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

The progression of hypertensive heart disease (HHD) to heart failure (HF) is associated with myocardial remodeling. Corresponding changes in three-dimensional organization of cardiac extracellular matrix have not been quantified or related fully to the development of HF. Spontaneously hypertensive rats (SHRs) and Wistar-Kyoto controls were studied at 3, 12, 18, and 24 mo. Hemodynamic and morphological data, brain natriuretic peptide levels, and echocardiography demonstrate four distinct disease stages: systemic hypertension, diastolic dysfunction, early systolic failure, and decompensated HF. Passive left ventricular (LV) pressure-volume relationships were determined in vitro. Transmural specimens from the anterior LV free wall were imaged using extended-volume confocal microscopy, and three-dimensional myocardial architecture was quantified. In SHRs, LV compliance was reduced at 12 mo and increased progressively thereafter. However, it was less than in controls for filling pressures <10 mmHg and not significantly different at ≥10 mmHg. Myocyte cross section was enlarged, with increased variability from 12 mo, while collagen fraction increased progressively. Perimysial collagen fraction remained unchanged with age, although endomysial collagen increased from 12 mo. Perimysial collagen between adjacent muscle layers fused at 12 mo and continued to thicken subsequently, while muscle layers became more dispersed and disordered. We conclude that LV dilatation, which accompanies decompensated HF in this model of HHD, is not due to LV “softening.” While perimysial (and endomysial) collagen networks are substantially remodeled, they are not dissolved, as has been proposed. We argue that progressive disruption of the laminar organization of LV myocardium may contribute to impaired systolic function in HHD.

scholarly journals Correlation between hemoglobin level and left ventricular systolic functions and dimensions in children with chronic severe anemia

2011 ◽  
Vol 51 (2) ◽  
pp. 79
Author(s):  
Erlina Masniari Napitupulu ◽  
Fera Wahyuni ◽  
Tina Christina L. Tobing ◽  
Muhammad Ali ◽  
Bidasari Lubis
Keyword(s):  
Systolic Function ◽  
Pearson Correlation ◽  
Systolic Dysfunction ◽  
Univariate Analysis ◽  
Left Ventricular Systolic Function ◽  
Left Ventricular ◽  
Lv Function ◽  
Severe Anemia ◽  
Cross Sectional ◽  
Lv Systolic Function

Background Chronic severe anemia is a connnon disease. Cardiac output may increase when the hemoglobin (Hb) level decreases to < 7 g/dL for 3 months or more. Alteration of left ventricular (LV) function occurs frequently in children 'With chronic severe anemia, in the {onn of concentric LV hypertrophy, LV dilatation with or v.ithout LV hypertrophy, or systolic dysfunction. Objective To examine the correlation between Hb level and alteration of LV systolic function in children with chronic severe anemia. Methods We conducted a cross-sectional study in Adam Malik Hospital from October to December 2009. Subjects were chronic severely anemic children. Left ventricular systolic function (ejection fraction/EF, fractional shortening/FS) and dimensions (left ventricular end diastolic diameter/LVEDD and left ventricular end systolic diameter/LVESD) were measured using Hitachi EUB 5500 echocardiography unit. Univariate analysis  and Pearson correlation were performed.Results Thirty children were enrolled in the study. The mean of age was 113.5 months (SD 53.24). Hb values ranged from 2.1 to 6.9 g/dL with mean value of 4.6 g/dL (SD 1.44). Mean duration of anemia was 3.9 months (SD 0.70). Chronic severe anemia was not associated \\lith decreased LV systolic function [EF 62.2% (SD 9.16), r =0.296, P=0.112; FS 33.8% (SD 7.26), r =0.115, P=0.545], nor LV dimension changes [LVEDD 40.2 mm (SD 6.85), r = -0.192, P=0.308; LVESD 26.2 mm (SD 4.98), r=-0.266, P=0.156]. Conclusion There was no correlation between Hb level in chronically anemic children and changes in LV systolic function or dimension.

Cardiomyocyte function associated with hyperactivity and/or hypertension in genetic models of LV hypertrophy

2006 ◽  
Vol 290 (1) ◽  
pp. H463-H473 ◽  
Author(s):  
Bradley M. Palmer ◽  
Zengyi Chen ◽  
Richard R. Lachapelle ◽  
Edith D. Hendley ◽  
Martin M. LeWinter
Keyword(s):  
Spontaneously Hypertensive Rat ◽  
Left Ventricular ◽  
Adult Males ◽  
Compensatory Response ◽  
Spontaneously Hypertensive ◽  
Hypertrophic Response ◽  
Rat Strain ◽  
Males And Females ◽  
Sarcomere Dynamics ◽  
Wistar Kyoto

We examined cardiomyocyte intracellular calcium ([Ca2+]i) dynamics and sarcomere shortening dynamics in genetic rat models of left ventricular (LV) hypertrophy associated with or without hypertension (HT) and with or without hyperactive (HA) behavior. Previous selective breeding of the spontaneously hypertensive rat (SHR) strain, which is HA and HT, with the Wistar-Kyoto (WKY) rat strain, which is not hyperactive (NA) and not hypertensive (NT), has led to two unique strains: the WKHA strain, selected for HA and NT, and the WKHT strain, selected for NA and HT. Cardiomyocytes were isolated from young adult males and females of each strain, paced at 2, 3, and 4 Hz in 1.2 mM external Ca2+ concentration at 37°C, and cardiomyocyte [Ca2+]i and sarcomere dynamics were recorded simultaneously. Under these conditions, LV cardiomyocyte systolic and diastolic [Ca2+]i dynamics and diastolic sarcomere dynamics in the WKHT were significantly enhanced compared with WKY controls, suggesting an underlying LV hypertrophic response that successfully compensated for HT in the absence of HA. LV cardiomyocyte [Ca2+]i dynamics in the WKHA and SHR were strikingly similar to each other and only slightly reduced compared with WKY. LV cardiomyocyte systolic and diastolic sarcomere dynamics, on the other hand, were significantly reduced in the SHR compare with WKHA and more so in male than in female SHR. We conclude from these data that HT alone is an insufficient descriptor of the cause of LV hypertrophy and diminished LV cardiomyocyte function in the SHR rat. These data further suggest that HA (augmented by male sex) in the SHR may interact with the HT state to initiate impaired cardiomyocyte function and thereby inhibit or undermine an otherwise compensatory response that may occur with HT in the absence of HA.

Plasma cardiotrophin-1 following acute myocardial infarction: relationship with left ventricular systolic dysfunction

2001 ◽  
Vol 102 (1) ◽  
pp. 9-14 ◽  
Author(s):  
Suneel TALWAR ◽  
Iain B. SQUIRE ◽  
Russell J. O'BRIEN ◽  
Paul F. DOWNIE ◽  
Joan E. DAVIES ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Function ◽  
Systolic Dysfunction ◽  
Clinic Visit ◽  
Left Ventricular ◽  
Lv Function ◽  
Ventricular Remodelling

The glycoprotein 130 (gp130) signalling pathway is important in the development of heart failure. Cardiotrophin-1 (CT-1), a cytokine acting via the gp130 pathway, is involved in the process of ventricular remodelling following acute myocardial infarction (AMI) in animals. The aims of the present study were to examine the profile of plasma CT-1 following AMI in humans, and its relationship with echocardiographic parameters of left ventricular (LV) systolic function. Serial measurements of plasma CT-1 levels were made in 60 patients at 14-48h, 49-72h, 73-120h and 121-192h following AMI and at a later clinic visit. LV function was assessed using a LV wall motion index (WMI) score on admission (WMI-1) and at the clinic visit (WMI-2). Compared with values in control subjects (29.5±3.6fmol/ml), the plasma CT-1 concentration was elevated in AMI patients at 14-48h (108.1±15.1fmol/ml), 49-72h (105.2±19.7fmol/ml), 73-120h (91.2±14.9fmol/ml) and 121-192h (118.8±22.6fmol/ml), and at the clinic visit (174.9±30.9 fmol/ml) (P < 0.0001). Levels were higher following anterior compared with inferior AMI. For patients with anterior AMI, CT-1 levels were higher at the clinic visit than at earlier times. WMI-1 correlated with CT-1 at all times prior to hospital discharge (P < 0.05). On best subsets analysis, the strongest correlate with WMI-1 was CT-1 level at 49-72h (R2 = 20%, P < 0.05). In conclusion, plasma levels of CT-1 are elevated soon after AMI in humans and rise further in the subsequent weeks in patients after anterior infarction. CT-1 measured soon after AMI is indicative of LV dysfunction, and this cytokine may have a role in the development of ventricular remodelling and heart failure after AMI.

Exercise training modifies myocardial mitochondria and myofibril growth in spontaneously hypertensive rats

1985 ◽  
Vol 248 (1) ◽  
pp. H8-H14
Author(s):  
R. P. Crisman ◽  
R. J. Tomanek
Keyword(s):  
Blood Pressure ◽  
Exercise Training ◽  
Spontaneously Hypertensive Rats ◽  
Pressure Overload ◽  
Volume Ratio ◽  
Volume Density ◽  
Left Ventricular ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

We tested the hypothesis that exercise training provides a stimulus that could modify the decrement in mitochondria-to-myofibril volume ratio characteristic of myocardial cells hypertrophied in response to a pressure overload. Spontaneously hypertensive rats (SHR) were trained 5 days/wk on a treadmill at 70-90% maximal VO2 between the ages of 6 and 16 wk corresponding to the development of hypertension and cardiac hypertrophy. The training program increased maximal VO2 and effected a resting bradycardia but did not alter blood pressure, left ventricular hypertrophy, or peak cardiac output. Our stereological data from electron micrographs shows that the decrement in mitochondrial volume density and the increase in myofibril volume density characteristic of SHR compared with their normotensive controls (WKY, Wistar-Kyoto rats) were reversed. Thus the relative volumes of mitochondria and myofibrils and their ratio in trained SHR were similar to those of the WKY group. The similarity was noted in myocytes from both the subepicardium and subendocardium. These data suggest that exercise training facilitates a proportional growth of energy-producing and energy-consuming organelles in SHR and that this effect is not secondary to modification of blood pressure or left ventricular mass.

Troponin I phosphorylation in spontaneously hypertensive rat heart: effect of beta-adrenergic stimulation

1997 ◽  
Vol 273 (3) ◽  
pp. H1440-H1451 ◽  
Author(s):  
B. K. McConnell ◽  
C. S. Moravec ◽  
I. Morano ◽  
M. Bond
Keyword(s):  
Troponin I ◽  
Ventricular Myocytes ◽  
Spontaneously Hypertensive Rat ◽  
Left Ventricular ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Spontaneously Hypertensive ◽  
Myosin Light Chain 2 ◽  
Wistar Kyoto ◽  
Phospholamban Phosphorylation

We compared baseline and protein kinase A (PKA)-dependent troponin I (TnI) phosphorylation in 32Pi-labeled left ventricular myocytes from hearts of 26-wk spontaneously hypertensive rats (SHR) and Wistar-Kyoto controls (WKY). TnI phosphorylation was normalized to myosin light chain 2 phosphorylation, which was invariant. There was no difference in baseline TnI phosphorylation in SHR and WKY, but stimulation with isoproterenol, norepinephrine plus prazosin, forskolin, chloroadenosine 3',5'-cyclic monophosphate, or 3-isobutyl-1-methylxanthine caused a greater increase in TnI phosphorylation in the SHR than in the WKY. This was observed both in the presence and absence of the phosphatase inhibitor calyculin A; thus the differences in TnI phosphorylation between SHR and WKY are not due to decreased phosphatase activity in the SHR. After stimulation of the beta-adrenergic pathway, phospholamban phosphorylation was not different in SHR and WKY, indicating that the observed differences may be specific for PKA phosphorylation of TnI. The increased PKA-dependent TnI phosphorylation in the SHR resulted in decreased Ca2+ sensitivity of actomyosin adenosinetriphosphatase activity as compared with the WKY. We conclude that increased PKA-dependent TnI phosphorylation in the SHR may contribute to the impaired response to sympathetic stimulation.

scholarly journals Peripartum Cardiomyopathy Presenting with Predominant Left Ventricular Diastolic Dysfunction: Efficacy of Bromocriptine

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Piercarlo Ballo ◽  
Irene Betti ◽  
Giuseppe Mangialavori ◽  
Leandro Chiodi ◽  
Gherardo Rapisardi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Diastolic Dysfunction ◽  
Diastolic Function ◽  
Systolic Function ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Peripartum Cardiomyopathy ◽  
Lv Function ◽  
Lv Diastolic Dysfunction ◽  
Lv Diastolic Function

Management of patients with peripartum cardiomyopathy (PPCM) is still a major clinical problem, as only half of them or slightly more show complete recovery of left ventricular (LV) function despite conventional evidence-based treatment for heart failure. Recent observations suggested that bromocriptine might favor recovery of LV systolic function in patients with PPCM. However, no evidence exists regarding its effect on LV diastolic dysfunction, which is commonly observed in these patients. Tissue Doppler (TD) is an echocardiographic technique that provides unique information on LV diastolic performance. We report the case of a 37-year-old white woman with heart failure (NYHA class II), moderate LV systolic dysfunction (ejection fraction 35%), and severe LV diastolic dysfunction secondary to PPCM, who showed no improvement after 2 weeks of treatment with ramipril, bisoprolol, and furosemide. At 6-week followup after addition of bromocriptine, despite persistence of LV systolic dysfunction, normalization of LV diastolic function was shown by TD, together with improvement in functional status (NYHA I). At 18-month followup, the improvement in LV diastolic function was maintained, and normalization of systolic function was observed. This paper might support the clinical utility of bromocriptine in patients with PPCM by suggesting a potential benefit on LV diastolic dysfunction.

Abstract 4833: Protective Effect of a Quinazoline-Type Poly(ADP-Ribose)Polymerase Inhibitor Against the Development of Hypertensive Cardiomyopathy and Heart Failure

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Eva Bartha ◽  
Klara Magyar ◽  
Izabella Solti ◽  
Laszlo Kereskai ◽  
Tamas Kalai ◽  
...  
Keyword(s):  
Heart Failure ◽  
Spontaneously Hypertensive Rat ◽  
Systolic Function ◽  
Parp Inhibitor ◽  
Left Ventricular ◽  
Parp Inhibition ◽  
Suitable Model ◽  
Spontaneously Hypertensive ◽  
Signal Transduction Proteins ◽  
Gsk 3Β

Purpose: Spontaneously hypertensive rat (SHR) is a suitable model for studies of hypertension and consequential left ventricular (LV) hypertrophy and heart failure. It is known, that activation of poly(ADP-ribose)polymerase enzyme (PARP) plays a role in the development of postinfarction myocardial remodeling. In our work we examined the effect of a PARP inhibitor (L-2286) against the development of hypertensive cardiopathy and heart failure in SHRs. Methods: Male 6-week-old SHR rats were treated with L-2286 (n=32, SHR-L) or placebo (n=32, SHR-C) for 50 weeks. Male CFY rats were used as aged-matched, normotensive controls (n=7, CFY). The phosphorylation state of signal transduction proteins were monitored by Western blotting. To detect the extent of fibrosis, histologic samples were stained with Masson’s trichrome. Plasma BNP activity was also determined. Before the study, after 24 weeks, and at the end of the treatment period echocardiography was performed. Results: L-2286 treatment enhanced the phosphorylation of the prosurvival factors Akt-1/GSK-3β and PKC ϵ (p<0.01), while phosphorylation of JNK, p-38 MAPK, PKC pan (p<0.01), PKC α/β, δ (p<0.05) were significantly ameliorated in SHR-L group. Interstitial collagen accumulation and plasma BNP activity were significantly elevated (p<0.05) in SHR-L and SHR-C groups compared to the CFY group. These parameters were improved due to L-2286 treatment (p<0.01 and p<0.05, respectively). Echocardiography showed that the measured parameters did not differ significantly among the three groups at baseline. After 24 weeks, LV end-diastolic and end-systolic volumes and LV wall thickness increased (p<0.05 SHR-L and SHR-C vs. CFY). All these parameters decreased by L-2286 treatment (p<0.05 SHR-L vs. SHR-C). At the end of the study in SHR-L group LV hypertrophy with preserved LV ejection fraction, however in the SHR-C group an excentric hypertrophy with poor systolic function was observable. As a hard endpoint, the survival rate was significantly better in SHR-L group (p<0.05) compared to SHR-C group. Conclusions: We demonstrated that PARP inhibition has a beneficial effect against the development of LV hypertrophy and heart failure in SHRs, due to the activation of PKC ϵ, and Akt-1/GSK-3β signaling pathways.

Angiotensin-converting enzyme inhibitor captopril prevents volume overload cardiomyopathy in experimental chronic aortic valve regurgitation

2004 ◽  
Vol 82 (3) ◽  
pp. 191-199 ◽  
Author(s):  
Eric Plante ◽  
Martin Gaudreau ◽  
Dominic Lachance ◽  
Marie-Claude Drolet ◽  
Élise Roussel ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Angiotensin Converting Enzyme ◽  
Enzyme Inhibitor ◽  
Systolic Function ◽  
Systolic Dysfunction ◽  
Volume Overload ◽  
Left Ventricular ◽  
Lv Function ◽  
Mrna Levels ◽  
Converting Enzyme

The efficacy of angiotensin-converting enzyme inhibitors (ACEIs) in the treatment of chronic aortic regurgitation (AR) is not well established and remains controversial. The mechanisms by which ACEIs may protect against left-ventricular (LV) volume overload are not well understood, and clinical trials performed until now have yielded conflicting results. This study was therefore performed to assess the effectiveness of two different doses of the ACEI captopril in a rat model of chronic AR. We compared the effects of a 6-month low-dose (LD) (25 mg/kg) or higher dose (HD) (75 mg/kg) treatment with captopril on LV function and hypertrophy in Wistar rats with severe AR. Untreated animals developed LV eccentric hypertrophy and systolic dysfunction. LD treatment did not prevent hypertrophy and provided modest protection against systolic dysfunction. HD treatment preserved LV systolic function and dimensions and tended to slow hypertrophy. The cardiac index remained high and similar among all AR groups, treated or not. Tissue renin–angiotensin system (RAS) analysis revealed that ACE activity was increased in the LVs of AR animals and that only HD treatment significantly decreased angiotensin II receptor mRNA levels. Fibronectin expression was increased in the LV or AR animals, but HD treatment almost completely reversed this increase. The ACE inhibitor captopril was effective at high doses in this model of severe AR. These effects might be related to the modulation of tissue RAS and the control of fibrosis.Key words: aortic valve, insufficiency, rat, echocardiography, volume overload, ACE inhibitors.

Adaptations in β-adrenergic cardiovascular responses to training in older women

2000 ◽  
Vol 89 (6) ◽  
pp. 2300-2305 ◽  
Author(s):  
Robert J. Spina ◽  
Saima Rashid ◽  
Victor G. Dávila-Román ◽  
Ali A. Ehsani
Keyword(s):  
Exercise Training ◽  
Older Women ◽  
Contractile Function ◽  
Systolic Function ◽  
Wall Stress ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Lv Function ◽  
Lv Systolic Function ◽  
Systolic Wall Stress

To determine whether endurance exercise training can alter the β-adrenergic-stimulated inotropic response in older women, we studied 10 postmenopausal healthy women (65.4 ± 0.9 yr old) who exercised for 11 mo. Left ventricular (LV) function was evaluated with two-dimensional echocardiography during infusion of isoproterenol after atropine. Maximal O2 consumption increased 23% in response to training (from 1.35 ± 0.06 to 1.66 ± 0.07 l/min; P = 0.004). Training had no effect on baseline LV function, end-diastolic diameter, LV wall thickness, or LV mass. The increase in LV systolic function in response to isoproterenol was unaffected by training. Furthermore, neither the systolic shortening-to-end-systolic wall stress relationship nor the end-systolic wall stress-to-end-systolic diameter relationship during isoproterenol infusion changed with training. We conclude that older postmenopausal women can increase their maximal O2consumption with exercise training without eccentric LV hypertrophy or enhancement of β-adrenergic-mediated LV contractile function. These observations provide an explanation for the finding that maximal cardiac output and stroke volume are not increased in older women in response to training.

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