Myocardial mechanical alterations during gradual onset long-term hypertension in rats

1981 ◽  
Vol 241 (3) ◽  
pp. H435-H441 ◽  
Author(s):  
J. M. Capasso ◽  
J. E. Strobeck ◽  
E. H. Sonnenblick
Keyword(s):  
Blood Pressure ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Isometric Tension ◽  
Left Renal Artery ◽  
Ventricular Performance ◽  
Time To Peak ◽  
Gradual Onset ◽  
Significant Depression ◽  
Female Wistar Rats

Although a suddenly produced load leads to depressed myocardial contractility, the effects of a slowly induced physiological overload have not been defined. Therefore, a more gradual pressure overload was produced in female Wistar rats by hypertension due to constriction of the left renal artery. Hypertension (systolic blood pressure greater than or equal to 150 mmHg) developed within 3 wk, and blood pressure continued to increase for the next 5 wk. Heart weights in hypertensive animals were elevated by 34% after the onset of hypertension. Isometric and isotonic contractions from left ventricular papillary muscles were recorded at 5, 10, 20, and 30 wk after the onset of hypertension. Total and actively developed isometric tension at all initial muscle lengths were significantly greater in hypertensive animals throughout the 30-wk period. Time to peak tension and time to half relaxation were significantly prolonged. Force-velocity curves demonstrated a significant depression in velocity of shortening at all relative loads in hypertensive muscles that progressed with the duration of hypertension. These studies suggest that myocardial hypertrophy may impart the ability to maintain ventricular performance in terms of force development while speed of shortening decays.

Comparative evaluation of pressure and time factors in estimating left ventricular performance

1976 ◽  
Vol 40 (2) ◽  
pp. 196-205 ◽  
Author(s):  
F. L. Abel
Keyword(s):  
Diastolic Pressure ◽  
Time Factors ◽  
Left Ventricular ◽  
Isometric Tension ◽  
Rate Of Change ◽  
Ventricular Performance ◽  
Time To Peak ◽  
Fractional Rate ◽  
Inotropic State ◽  
Developed Pressure

Left ventricular and ascending aortic pressures were measured in open chest mongrel dogs under pentobarbital anesthesia. The data were digitized, averaged, and subgrouped by mean systolic aortic pressures (MSAP), end-diastolic pressure (EDP), and heart rate (HR). Seven raw and 32 derived variable from the pressure, as a function of time, wave forms were analyzed in each subgroup in the control state and following the infusion of catecholamines. A plot of control variability versus sensitivity to norepinephrine indicates that time to peak ventricular pressure (PVP time) is a more sensitive indicator of changes in the inotropic state than such other commonly used variables as max dP/dt, integrated isometric tension, and (max dP/dt)/developed pressure. PVP time also showed less variability with HR, EDP, and MSAP. Regression lines were also fit to the data using a second-order model. This permitted evaluation of experimentally varying either HR, EDP, or MSAP while maintaining the other two constant. PVP time was again one of the better variables in terms of sensitivity to HR, EDP, or MSAP. Vmax, fractional rate of change of power, preejection period, and systolic time were also analyzed and compared with PVP time using averaged data.

Right ventricular performance during ischemia: an anatomic and hemodynamic analysis

1977 ◽  
Vol 233 (4) ◽  
pp. H505-H513 ◽  
Author(s):  
H. Brooks ◽  
R. Holland ◽  
J. Al-Sadir
Keyword(s):  
Right Ventricular ◽  
Diastolic Pressure ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Ventricular Performance ◽  
Time To Peak ◽  
Contractile Parameters ◽  
Significant Depression ◽  
Right Ventricular Performance ◽  
The Right

This study in the pig was designed to characterize right ventricular (RV) contractile responses during infarction involving three areas of the heart--anteroseptal, anterolateral, and inferoseptal. Porcine coronary architecture was studied from multicolor vinyl casts. Distribution of blood supply to ventricular myocardium and papillary muscles was defined by intra-arterial dye injection. High-fidelity pressure and flow data were measured simultaneously in both ventricles following ligation of approximately equal lengths of the anterior descending, left circumflex, or posterior descending arteries. In the three groups, weight of myocardium involved by the occluded artery was comparable and there was significant depression of left ventricular performance, more pronounced in the two anterior infarcts. However, in anterolateral infarction, despite the obligatory drop in RV flow, there was no significant alteration in RV end-diastolic pressure (EDP), peak rate of rise of RV pressure (dP/dt), or time-to-peak developed dP/dt. In contrast, with both anteroseptal and inferoseptal infarctions there were significant alterations in all RV contractile parameters, at increased levels of RVEDP, signifying a primary depression in RV contractile state. With inferoseptal infarction, further occlusion of the right coronary near its origin produced a more exaggerated and selective RV contractile abnormality and, in half of the animals, varying degrees of acute tricuspid insufficiency.

Alterations in mechanical properties of rat papillary muscle during maturation

1982 ◽  
Vol 242 (3) ◽  
pp. H359-H364 ◽  
Author(s):  
J. M. Capasso ◽  
R. M. Remily ◽  
E. H. Sonnenblick
Keyword(s):  
Left Ventricular ◽  
Isometric Tension ◽  
Time To Peak ◽  
Peak Rate ◽  
Age Related ◽  
Velocity Of Shortening ◽  
Female Wistar Rats ◽  
Tension Time ◽  
Force Velocity ◽  
Rat Papillary Muscle

Myocardial performance was measured during maturation using isolated left ventricular papillary muscles from female Wistar rats. Muscles were studied isometrically and isotonically, stimulated at 0.1 Hz, perfused with Tyrode solution having an external calcium concentration of 2.4 mM, and maintained at 30 degrees C. Heart and body weight increased rapidly during the first 6 mo and then stabilized. Peak isometric developed tension, time to peak isometric developed tension, and time to half relaxation increased substantially during the 1- to 10-mo period with little change in the peak rate of isometric tension rise and peak rate of isometric tension fall. No difference in resting tension was noted among any groups. Force-velocity curves from muscles from 2-, 6-, and 10-mo-old animals show a significant age-related decrease in the isotonic velocity of shortening by as much as 21% between 2 and 10 mo of age. Thus maturation profoundly affects the contractile state of cardiac muscle, with force of contraction increasing and velocity of shortening decreasing as a function of age in the rat.

Contractile behavior of rat myocardium after reversal of hypertensive hypertrophy

1982 ◽  
Vol 242 (5) ◽  
pp. H882-H889 ◽  
Author(s):  
J. M. Capasso ◽  
J. E. Strobeck ◽  
A. Malhotra ◽  
J. Scheuer ◽  
E. H. Sonnenblick
Keyword(s):  
Myocardial Hypertrophy ◽  
Applied Pressure ◽  
Pressure Overload ◽  
Heart Weight ◽  
Biochemical Alterations ◽  
Time To Peak ◽  
Velocity Of Shortening ◽  
Significant Depression ◽  
Contractile Performance ◽  
Biochemical Abnormalities

The effects of renovascular hypertension and its reversal on the contractile performance of papillary muscles from rats has been examined. Hypertension of 10 wk duration caused a 48% increase in heart weight and significant prolongations of isometric time to peak tension (TPT), time to half relaxation, and time to peak shortening (TPS). A significant depression in the velocity of shortening was observed in the 10-wk group. However, muscles from hypertensive rats were still able to maintain normal levels of peak isometric developed tension and peak shortening; this may be due to the observed prolongation of TPT and TPS, respectively. In addition, calcium-activated actomyosin ATPase activity was depressed in hearts of hypertensive animals. Reversal of hypertension was studied at 20 wk after the onset of hypertension (10 wk of hypertension followed by 10 wk of normotension). Contractile and biochemical alterations observed in hypertensive animals were reversed in rats undergoing this regime. Thus reversal of a gradually applied pressure overload resulted in the regression of mechanical and biochemical abnormalities associated with the pressure overload myocardial hypertrophy.

Role of sarcoplasmic reticulum in loss of load-sensitive relaxation in pressure overload cardiac hypertrophy

1994 ◽  
Vol 266 (1) ◽  
pp. H68-H78 ◽  
Author(s):  
C. R. Cory ◽  
R. W. Grange ◽  
M. E. Houston
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Hypertrophy ◽  
Atpase Activity ◽  
Pressure Overload ◽  
Fold Increase ◽  
Left Ventricular ◽  
Isometric Tension ◽  
Tension Development ◽  
Sequestration Potential

The loss of load-sensitive relaxation observed in the pressure-overloaded heart may reflect a strategy of slowed cytosolic Ca2+ uptake to yield a prolongation of the active state of the muscle and a decrease in cellular energy expenditure. A decrease in the potential of the sarcoplasmic reticulum (SR) to resequester cytosolic Ca2+ during diastole could contribute to this attenuated load sensitivity. To test this hypothesis, both in vitro mechanical function of anterior papillary muscles and the SR Ca2+ sequestration potential of female guinea pig left ventricle were compared in cardiac hypertrophy (Hyp) and sham-operated (Sham) groups. Twenty-one days of pressure overload induced by coarctation of the suprarenal, subdiaphragmatic aorta resulted in a 36% increase in left ventricular mass in the Hyp. Peak isometric tension, the rate of isometric tension development, and the maximal rates of isometric and isotonic relaxation were significantly reduced in Hyp. Load-sensitive relaxation were significantly reduced in Hyp. Load-sensitive relaxation quantified by the ratio of a rapid loading to unloading force step in isotonically contracting papillary muscle was reduced 50% in Hyp muscles. Maximum activity of SR Ca(2+)-adenosinetriphosphatase (ATPase) measured under optimal conditions (37 degrees C; saturating Ca2+) was unaltered, but at low free Ca2+ concentrations (0.65 microM), it was decreased by 43% of the Sham response. Bivariate regression analysis revealed a significant (r = 0.84; P = 0.009) relationship between the decrease in SR Ca(2+)-ATPase activity and the loss of load-sensitive relaxation after aortic coarctation. Stimulation of the SR Ca(2+)-ATPase by the catalytic subunit of adenosine 3',5'-cyclic monophosphate-dependent protein kinase resulted in a 2.6-fold increase for Sham but only a 1.6-fold increase for Hyp. Semiquantitative Western blot radioimmunoassays revealed that the changes in SR Ca(2+)-ATPase activity were not due to decreases in the content of the Ca(2+)-ATPase protein or phospholamban. Our data directly implicate a role for decreased SR function in attenuated load sensitivity. A purposeful downregulation of SR Ca2+ uptake likely results from a qualitative rather than a quantitative change in the ATPase and possibly one of its key regulators, phospholamban.

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.

Excitation-contraction coupling in isolated myocardium from dogs with compensated left ventricular hypertrophy

1994 ◽  
Vol 266 (6) ◽  
pp. H2436-H2442 ◽  
Author(s):  
C. L. Perreault ◽  
R. P. Shannon ◽  
Y. T. Shen ◽  
S. F. Vatner ◽  
J. P. Morgan
Keyword(s):  
Intracellular Calcium ◽  
Pressure Overload ◽  
Phosphodiesterase Inhibitors ◽  
Experimental Models ◽  
Left Ventricular ◽  
Isometric Tension ◽  
Lv Function ◽  
Calcium Modulation ◽  
Contraction Duration ◽  
Calcium Indicator

To examine the relationship between left ventricular (LV) function and intracellular calcium modulation in the presence of myocyte hypertrophy, we compared LV muscles from nine dogs with compensated LV hypertrophy (LVH) induced by chronic aortic banding with 11 controls. Mechanical properties were studied in LV muscles (control, n = 25; LVH, n = 23) stretched to the length at which maximal isometric tension developed at 30 degrees C and stimulated at 0.33 Hz; a subset of LVH muscles was loaded with the intracellular calcium indicator aequorin. In LV myocardium from dogs with compensated LVH, both the contraction duration and calcium transients were prolonged at baseline, and the response to phosphodiesterase inhibitors was impaired in keeping with findings in both human and experimental models of pressure-overload hypertrophy and failure. However, in contrast to findings in the failing myocardium, the positive inotropic response to increasing intracellular calcium was preserved in myocardium from dogs with compensated LVH.

Supernormal Left Ventricular Performance in Young Subjects with Mild Hypertension: An Alerting Response to the Echocardiographic Procedure?

1996 ◽  
Vol 91 (3) ◽  
pp. 275-281 ◽  
Author(s):  
Paolo Palatini ◽  
Pieralberto Visentin ◽  
Gianluigi Nicolosi ◽  
Vincenzo Mione ◽  
Paolo Stritoni ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Systolic Blood Pressure ◽  
Systolic Function ◽  
Blood Pressure Monitoring ◽  
Left Ventricular Systolic Function ◽  
Left Ventricular ◽  
Ventricular Performance ◽  
Young Subjects ◽  
Mild Hypertensive

1. To assess the clinical significance of supernormal left ventricular systolic function in the initial phase of hypertension, 635 never-treated 18–45-year-old borderline to mild hypertensive subjects (477 males, 158 females) were studied. All subjects underwent echocardiography, 24 h ambulatory blood pressure monitoring and 24 h urine collection for catecholamine dosage. 2. Subjects whose left ventricular shortening-stress relationship was above the 95% confidence intervals of 50 normotensive subjects of similar age and sex distribution were defined as having supernormal function. 3. Age, duration of hypertension and left ventricular mass were similar in the hypertensive subjects with normal (85%) and supernormal (15%) ejective performance. Subjects with supernormal function showed higher office systolic blood pressure (P < 0001), office heart rate (P = 0.03) and cardiac index (P < 0001). Conversely, 24 h systolic blood pressure, 24 h heart rate and 24 h catecholamine output did not differ according to left ventricular function. 4. In conclusion, the greater white-coat effect and the normal baseline sympathetic tone exhibited by the patients with increased performance suggest that supernormal left ventricular pump function is only a marker of the alerting reaction elicited by the echocardiographic examination.

scholarly journals The Effects of Aqueous Extract from Nardostachys chinensis Batalin on Blood Pressure and Cardiac Hypertrophy in Two-Kidney One-Clip Hypertensive Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Rayile Aisa ◽  
Zhaoxia Yu ◽  
Xiangyang Zhang ◽  
Dilinuer Maimaitiyiming ◽  
Lipeng Huang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Hypertrophy ◽  
Aqueous Extract ◽  
Caspase 3 ◽  
Left Ventricular ◽  
Left Renal Artery ◽  
Hypertensive Rats ◽  
Left Ventricular Tissue ◽  
Nardostachys Chinensis ◽  
Ventricular Tissue

Aims. The aim of this study was to investigate the effects of the aqueous extract of Nardostachys chinensis Batalin (NCBAE) on blood pressure and cardiac hypertrophy using two-kidney one-clip (2K1C) hypertensive rats. Methods. 2K1C rat models were set up by clipping the left renal artery. Sham-operated rats underwent the same surgical procedure except for renal arterial clipping. 2K1C hypertensive rats were orally given NCBAE at doses of 210, 420, and 630 mg·kg−1·d−1 for 6 weeks. Twelve weeks after surgery, rat SBP and echocardiographic parameters were measured, cardiac histopathology was assessed, serum NO and LDH were detected, and the expression of Bcl-2 and caspase-3 of left ventricular tissue was assessed by western blot. Results. Treatment with NCBAE resulted in a decrease of SBP, LVPWd, LVPWs, IVSd, IVSs, LVW/BW ratio, and cardiomyocyte CSA, an increase of LVEF, and inhibition of 2K1C-induced reduction in serum NO and elevation of LDH compared with 2K1C group. NCBAE intervention also showed a significant increase of Bcl-2 expression and reduction of cleaved caspase-3 level dose-dependently in left ventricular tissue. Conclusion. Our data demonstrate that NCBAE has an antihypertensive property and protective effect on 2K1C-induced cardiac hypertrophy especially at the dose of 630 mg·kg−1·d−1.

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