Basal and maximal inotropic state in renal hypertensive dogs with cardiac hypertrophy

1983 ◽  
Vol 245 (1) ◽  
pp. H33-H41 ◽  
Author(s):  
A. Broughton ◽  
P. I. Korner
Keyword(s):  
Ventricular Hypertrophy ◽  
Weight Ratio ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Body Weight Ratio ◽  
Absolute Value ◽  
Inotropic State ◽  
Lv Mass ◽  
Autonomic Blockade ◽  
Mean Aortic Pressure

We studied three isovolumic indexes of contractility, i.e., dP/dtmax, dP/dtDP40, and (dP/dt)/TPmax, in normal dogs and in a matched group of chronically hypertensive dogs with left ventricular hypertrophy (LVH) [DP40, developed LV pressure of 40 mmHg; TP, total LV pressure above atmospheric]. The LVH was moderate in degree with the LV-to-body weight ratio 50% greater than in normal dogs. The experiments were performed under pentobarbital with open chest, autonomic blockade, and independent control of mean left atrial pressure (LAP) and mean aortic pressure (MAP). We found that dP/dtmax provided the most consistent comparison of inotropic state in the two groups under both basal conditions and with norepinephrine (NE). The other indexes occurred too early in systole to reflect complete LV activation, particularly during the infusion with NE. Under controlled conditions basal dP/dtmax of LVH dogs was 1.28 times the value of normal dogs, with the increase accounted for by the amplifier effect of the increase in LV mass. But with moderate lowering of aortic pressure, inotropic state was more easily compromised in LVH than in normal dogs. With steady-state stimulation by infusing increasing amounts of NE, dP/dtmax rose by 10 times basal in both LVH and normal dogs at maximum stimulation. The absolute value of the index was 1.31 times higher in the LVH group, with the amplifier effect thus the same as under basal conditions. The results suggest that basal and maximal inotropic states are normal in LVH under optimum loading conditions.

P0875INFLUENCE OF CHRONIC KIDNEY DISEASE AND LEFT VENTRICULAR HYPERTROPHY ON CHANGE IN FGF23 AND RENIN-ANGIOTENSIN-ALDOSTERONE-SYSTEM

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Kohei Okamoto ◽  
Hideki Fujii ◽  
Shunsuke Goto ◽  
Keiji Kono ◽  
Kentaro Watanabe ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Body Weight ◽  
Mrna Expression ◽  
Ventricular Hypertrophy ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Heart Weight ◽  
Control Group ◽  
Body Weight Ratio ◽  
Related Factors

Abstract Background and Aims Left ventricular hypertrophy (LVH) is a clinically important risk factor for mortality and often observed in patients with chronic kidney disease (CKD). Serum FGF23 levels are elevated in CKD patients, and the relationship between elevated FGF23 and LVH has been reported in the previous studies. However, whether elevated FGF23 is a cause or result of LVH and whether FGF23 directly or indirectly affects LVH remain unclear. Therefore, we investigated changes in heart weight, CKD-mineral and bone disorder (MBD) parameters, including FGF23, and renin-angiotensin-aldosterone system (RAAS) related-factors in the setting of LVH and CKD using a mouse model. Method In the present study, twenty-four C57BL/6J mice were used and divided into 4 groups; control group (N=6), CKD group (N=6), LVH group (N=6), and LVH+CKD group (N=6). The mice in the CKD group underwent left 2/3 nephrectomy at 11 weeks of age and right nephrectomy at 12 weeks of age. Those in the LVH group underwent transverse aortic constriction (TAC) at 10 weeks of age. Those in the LVH+CKD group, TAC at 10 weeks of age, and left 2/3 nephrectomy at 11 weeks of age, and right nephrectomy at 12 weeks of age were performed. At 16 weeks of age, echocardiography was performed for all the mice, and they were sacrificed for blood and urine analysis, histopathological analysis and evaluating mRNA expressions of CKD-MBD- and RAAS-related factors in the heart. Results The systolic blood pressure was significantly higher in the LVH+CKD group and the CKD group than in the control group. The heart weight/body weight ratio in the LVH+CKD group was the highest, and that in the LVH was higher than that in the CKD group. Although serum creatinine and phosphate levels increased in CKD condition, those were comparable between the CKD and LVH+CKD groups. The urinary albumin excretion also increased in the CKD and LVH+CKD groups compared to the LVH and control groups. Serum FGF23 levels increased in the LVH and CKD group compared to the control group, and those in the LVH+CKD group were the highest among all the study groups. The cardiac mRNA expressions of FGF23, angiotensinogen (ANG), angiotensin type 1 receptor (AT1R), and angiotensin-converting enzyme (ACE) were also increased by induction of LVH and CKD, and those in the LVH+CKD group significantly increased compared to other groups. Heart weight/body weight ratio was significantly correlated with serum FGF23 levels and mRNA expression of FGF23, ANG, AT1R, ACE. In addition, significant correlations of serum FGF23 levels and cardiac mRNA expression of FGF23 with cardiac mRNA expressions of RAAS-related factors were observed. Conclusion Our results suggest that serum FGF23 levels and cardiac mRNA expression of FGF23 increase with the development of LVH and CKD and the changes is possibly enhanced through the colocalized activation of RAAS.

The hypertrophic heart rat: a new normotensive model of genetic cardiac and cardiomyocyte hypertrophy

2002 ◽  
Vol 9 (1) ◽  
pp. 43-48 ◽  
Author(s):  
Stephen B. Harrap ◽  
Vennetia R. Danes ◽  
Justine A. Ellis ◽  
Cory D. Griffiths ◽  
Elizabeth F. Jones ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Ventricular Hypertrophy ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Cardiomyocyte Hypertrophy ◽  
Spontaneously Hypertensive ◽  
Fischer 344 ◽  
Lv Mass ◽  
Low Blood Pressure

We describe a new line of rats with inherited cardiomyocyte and ventricular hypertrophy. From a second-generation cross of spontaneously hypertensive and Fischer 344 rats, we selected for low blood pressure and either high or low echocardiographic left ventricular (LV) mass over four generations to establish the hypertrophic heart rat (HHR) and normal heart rat (NHR) lines, respectively. After 13 generations of inbreeding, HHR had significantly greater ( P < 0.0001) LV mass-to-body weight ratio (2.68 g/kg, SE 0.14) than NHR matched for age (1.94 g/kg, SE 0.02) or body weight (2.13 g/kg, SE 0.03). The isolated cardiomyocytes of HHR were significantly ( P < 0.0001) longer and wider (161 μm, SE 0.83; 35.6 μm, SE 2.9) than NHR (132 μm, SE 1.2; 29.5 μm, SE 0.35). Telemetric 24-h recordings of mean arterial pressure revealed no significant differences between HHR and NHR. The HHR offers a new model of primary cardiomyocyte hypertrophy with normal blood pressure in which to examine genotypic causes and pathogenetic mechanisms of hypertrophy and its complications.

Antihypertensive effect of thyroidectomy in SHR: associated changes in heart performance

1986 ◽  
Vol 250 (4) ◽  
pp. H600-H605
Author(s):  
R. L. Rodgers ◽  
J. H. McNeill
Keyword(s):  
Ventricular Hypertrophy ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Body Weight Ratio ◽  
Or Efficiency ◽  
Spontaneously Hypertensive ◽  
Heart Performance ◽  
Rat Hearts ◽  
Wistar Kyoto ◽  
Perfused Hearts

Effects of thyroidectomy (TX; 10 wk) on the performance of perfused hearts from spontaneously hypertensive rats (SHR) were compared with effects on hearts from normotensive Wistar-Kyoto (WKY) controls. TX prevented the development of hypertension in SHR and moderately reduced arterial pressure of WKY, confirming previous observations. TX also reduced heart-to-body-weight ratio (relative left ventricular hypertrophy) but not left-to-right ventricular weight ratio (absolute hypertrophy) of SHR. The performances of euthyroid SHR and WKY hearts were similar to each other. TX reduced maximum left ventricular pulse pressure to the same extent in both strains and had no effect on hydraulic work, O2 consumption, or efficiency of contraction in either strain. However, TX reduced maximum left ventricular +dP/dt of SHR but not of WKY hearts. The results show that hypothyroidism selectively depresses the contractility (LV +dP/dt) of SHR hearts but otherwise has similar effects on the performance of hypertensive and normotensive rat hearts.

EVALUATION OF LEFT VENTRICULAR MASS IN THE PREHYPERTENSIVES BY ELECTROCARDIOGRAPHY AND ECHOCARDIOGRAPHY

2011 ◽  
pp. 119-125
Author(s):  
Thi Thuy Hang Nguyen
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Left Ventricular Mass ◽  
Ventricular Hypertrophy ◽  
Structural Changes ◽  
Left Ventricular ◽  
Control Group ◽  
Concentric Left Ventricular Hypertrophy ◽  
Increased Risk ◽  
Lv Mass ◽  
Left Ventricular Morphology

Objective: Prehypertensive individuals are at increased risk for developing hypertension and their complication. Many studies show that 2/3 prehypertensive individuals develop hypertension after 4 years. ECG and echocardiography are the routine tests used to assess LV mass. The objective of the research to determine the percentage of change in left ventricular morphology in the ECG, echocardiography, which explore the characteristics of left ventricular structural changes by echocardiography in pre-hypertensive subjects. Materials and method: We studied a total of 50 prehypertensive, 30 males (60%) and 20 females (40%), mean age 48.20±8.47years. 50 normotensive volunteers as control participants. These subjects were examined for ECG and echocardiography. Results: In prehypertensive group, with 18% of left ventricular hypertrophy on electrocardiogram, 12% of left ventricular hypertrophy on echocardiography; in the control group, we did not find any subjects with left ventricular hypertrophy. In the group with left ventricular hypertrophy, mostly eccentric left ventricular hypertrophy (83.33%), concentric left ventricular hypertrophy is 16.67%. Restructuring of left ventricular concentric for 15.9% of subjects without left ventricular hypertrophy on echocardiography. Conclusion: There have been changed in left ventricular morphology even in prehypertensive

Abstract 3435: Left Ventricular Hypertrophy is Resistant to Inhibition of Expression of the R403Q Alpha-Myosin Heavy Chain Cardiac Hypertrophy-Inducing Mutant Protein

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Leah Cannon ◽  
Tadeusz Marciniec ◽  
Bryony Mearns ◽  
Robert M Graham ◽  
Diane Fatkin
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Interstitial Fibrosis ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Familial Hypertrophic Cardiomyopathy ◽  
Lv Function ◽  
Dependent Manner ◽  
Cardiovascular Morbidity And Mortality ◽  
Lv Mass

Left ventricular hypertrophy (LVH) develops as a compensatory response to myocardial dysfunction due to diverse causes, but is nonetheless a major risk factor for premature cardiovascular morbidity and mortality. It is thus unclear if regressing LVH is beneficial or may worsen patient outcome. To evaluate the effects of LVH regression, we developed a transgenic mouse model in which the expression of a familial hypertrophic cardiomyopathy (FHC)-inducing mutation (R403Q alpha-MHC) can be regulated in a temporal and dose-dependent manner. In this model, transgene expression can be shut off by feeding with a tetracycline analogue (doxycycline). Serial echocardiography and histology studies were performed in a cohort of mice expressing the FHC mutant (“gene-on”) and in wildtype (WT) littermates. A second cohort of WT and 403/+ mice was randomised to placebo or doxycycline (“gene off”) from 6 (Dox6) or 20 weeks (Dox20) and evaluated at 40 weeks of age. Compared to WT littermates, “gene on” 403/+ mice showed increased LV mass, LV end-diastolic diameter (LVDD) and left atrial diameter (LAD), and reduced fractional shortening (LVFS), with changes evident from 12 weeks of age. LV sections from 403/+ mice showed typical features of FHC: myofibre disarray and interstitial fibrosis. LV mass, LV function and myocardial histology were unchanged in both male and female placebo- vs Dox6 or Dox20 mice at 40 weeks (Table 1 ). Thus, consistent with the major LV thickening in FHC humans occurring in adolescence, overexpression of R403Q for only 6 weeks is sufficient to trigger the complete LVH phenotypic response. Moreover, switching off the genetic trigger for LVH in 403/+ mice at 6 weeks (prior to overt disease manifestation) or 20 weeks (established disease) does not induce regression of LVH or exacerbate contractile dysfunction. Interventions to induce LVH regression may, therefore, need to be directed at downstream factors in hypertrophic pathways. Table 1. Echo data for male WT and 403/+ mice aged 40 weeks

Abstract 6: Comparison Between Ambulatory BP Percentile And Load As Predictors Of Target Organ Damage In Youth

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Gilad Hamdani ◽  
Michael A Ferguson ◽  
Marc B Lande ◽  
Kevin Meyers ◽  
Mark Mitsnefes ◽  
...  
Keyword(s):  
Logistic Regression ◽  
Ventricular Hypertrophy ◽  
Significant Contribution ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Left Ventricular ◽  
Target Organ ◽  
Cut Points ◽  
Lv Mass ◽  
Diagnosis Of Hypertension

Ambulatory BP (ABP) is increasingly used to confirm the diagnosis of hypertension. Pediatric but not adult guidelines consider BP load (% readings above 95 th %ile) in risk-stratification of the ABP phenotype. We compared ABP sex- and height- specific percentile and BP load as predictors of left ventricular hypertrophy (LVH) in youth. We measured casual BP, ABP, anthropometrics, and calculated LV mass by echo as (g)/height (m) 2.7 (LVMI) in 357 adolescents (mean age 15.5 + 1.7 years, 63% white, 59% male). ABPM was performed with the Ontrak device (Spacelabs Inc., Snoqualmie, WA). ABP index was defined as mean ABP/sex- and height-specific 95 th %ile. LVH was defined as LVMI ≥38.6 (pediatric cut-point). Logistic regression was used to assess different ABP measures as predictors of LVH. Sensitivity and specificity of different ABP cut points as predictors of LVH were calculated. Seventy (19.6%) participants had LVH. Systolic 24-hour, wake and sleep ABP indices as well as 24-hour SBP load were all significantly associated with LVH, while wake and sleep SBP load were not. When adjusted for BMI percentile and sex, only the associations between ABP indices and LVH remained statistically significant (table). SBP percentiles also had better balanced sensitivities and specificities in predicting LVH (24-hour 65 th percentile: 63% and 59%; wake 70 th percentile: 54% and 62%; sleep 75 th percentile: 60% and 61%). There was no significant association between diastolic BP measures and LVH. We conclude that there is no significant contribution of BP load in predicting LVH in youth. Systolic ABP percentiles lower than the commonly used 95 th percentile are the best predictors of LVH in this population.

scholarly journals Low-intensity aerobic interval training attenuates pathological left ventricular remodeling and mitochondrial dysfunction in aortic-banded miniature swine

2010 ◽  
Vol 299 (5) ◽  
pp. H1348-H1356 ◽  
Author(s):  
Craig A. Emter ◽  
Christopher P. Baines
Keyword(s):  
Body Weight ◽  
Exercise Training ◽  
Mitochondrial Dysfunction ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Heart Weight ◽  
Lv Function ◽  
Body Weight Ratio ◽  
Miniature Swine ◽  
Low Intensity

Cardiac hypertrophy in response to hypertension or myocardial infarction is a pathological indicator associated with heart failure (HF). A central component of the remodeling process is the loss of cardiomyocytes via cell death pathways regulated by the mitochondrion. Recent evidence has indicated that exercise training can attenuate or reverse pathological remodeling, creating a physiological phenotype. The purpose of this study was to examine left ventricular (LV) function, remodeling, and cardiomyocyte mitochondrial function in aortic-banded (AB) sedentary (HFSED; n = 6), AB exercise-trained (HFTR, n = 5), and control sedentary ( n = 5) male Yucatan miniature swine. LV hypertrophy was present in both AB groups before the start of training, as indicated by increases in LV end-diastolic volume, LV end-systolic volume (LVESV), and LV end-systolic dimension (LVESD). Exercise training (15 wk) prevented further increases in LVESV and LVESD ( P < 0.05). The heart weight-to-body weight ratio, LV + septum-to-body weight ratio, LV + septum-to-right ventricle ratio, and cardiomyocyte cross-sectional area were increased in both AB groups postmortem regardless of training status. Preservation of LV function after exercise training, as indicated by the maintenance of fractional shortening, ejection fraction, and mean wall shortening and increased stroke volume, was associated with an attenuation of the increased LV fibrosis (23%) and collagen (36%) observed in HFSED animals. LV mitochondrial dysfunction, as measured by Ca2+-induced mitochondrial permeability transition, was increased in HFSED ( P < 0.05) but not HFTR animals. In conclusion, low-intensity interval exercise training preserved LV function as exemplified by an attenuation of fibrosis, maintenance of a positive inotropic state, and inhibition of mitochondrial dysfunction, providing further evidence of the therapeutic potential of exercise in a clinical setting.

Diminished effect of cAMP on Ca2+ accumulation in skinned fibers of hypertrophied rat heart

1994 ◽  
Vol 266 (2) ◽  
pp. H749-H756
Author(s):  
F. Tomita ◽  
A. L. Bassett ◽  
R. J. Myerburg ◽  
S. Kimura
Keyword(s):  
Body Weight ◽  
Weight Ratio ◽  
Pressure Overload ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Adrenergic Stimulation ◽  
Body Weight Ratio ◽  
The Right ◽  
Hypertrophied Ventricle ◽  
Concomitant Exposure

Sarcoplasmic reticulum (SR) Ca2+ uptake is reduced in the hypertrophied ventricle. To determine whether events initiated by beta-adrenergic stimulation are involved, we compared the effects of adenosine 3',5'-cyclic monophosphate (cAMP) on SR Ca2+ uptake between normal and pressure-overloaded hypertrophied hearts using saponin-skinned rat left ventricular muscles. Left ventricular pressure overload was induced by partial ligation of the abdominal aorta for 4–6 wk before study. Age-matched normal rats served as controls. Pressure overload increased the left ventricular weight-to-body weight ratio 60.8%. The SR was loaded by exposing the muscles to 10(-6) M Ca2+ solution; SR Ca2+ release was induced by 5 or 25 mM caffeine, and the amount of Ca2+ released from the SR was estimated by the area under the caffeine-induced transient contraction. Concomitant exposure to 10(-4) M cAMP did not influence caffeine-induced Ca2+ release in either normal or hypertrophied fibers. When 10(-4) M cAMP was applied during the Ca(2+)-loading periods, the amount of Ca2+ accumulated by the SR increased in both normal and hypertrophied fibers. However, the extent of increase was significantly smaller in hypertrophied fibers than in normal fibers [10.9 +/- 1.7 and 27.4 +/- 5.3% in 1 min of Ca2+ loading (P < 0.05), 12.2 +/- 3.2 and 24.7 +/- 3.8% in 4 min of Ca2+ loading (P < 0.05), respectively]. cAMP (10(-4) M) shifted the force-pCa relationship to the right similarly in normal and hypertrophied muscles, and there was no difference in the force-pCa relationship between the two groups either with or without cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Reversal of myocardial dysfunction in endotoxin shock with insulin

1978 ◽  
Vol 56 (1) ◽  
pp. 132-138 ◽  
Author(s):  
L. T. Archer ◽  
B. K. Beller ◽  
J. K. Drake ◽  
T. L. Whitsett ◽  
L. B. Hinshaw
Keyword(s):  
Insulin Infusion ◽  
Diastolic Pressure ◽  
Myocardial Dysfunction ◽  
Aortic Pressure ◽  
Endotoxin Shock ◽  
Left Ventricular ◽  
Lactate Uptake ◽  
Blood Glucose Concentrations ◽  
Mean Aortic Pressure ◽  
Canine Myocardium

Recent data reported from this laboratory have documented myocardial functional depression in endotoxin shock. The purpose of the present study was to determine the effects of insulin on the dysfunctioning canine myocardium subjected to lethal endotoxin shock. Experiments were conducted on isolated working left ventricular preparations in which LD90–100 endotoxin was administered prior to, or following, isolation of the heart. Determinations of myocardial performance were conducted under the conditions of controlled mean aortic pressure and cardiac output. Myocardial dysfunction occurred between 2 and 6 h postendotoxin, as evidenced by significantly increased left ventricular end-diastolic pressure, decreased power, and depressed negative dP/dt, although blood glucose concentrations were maintained at control values. Intraatrial infusions of insulin at rates of 6 U/min reversed all signs of myocardial dysfunction. During insulin infusion, heart rates decreased (p < 0.02) and myocardial lactate uptake increased (p < 0.02), while oxygen uptake and coronary blood flow were insignificantly altered.

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