Effects of systolic overload and swim training on cardiac mechanics and biochemistry in rats

1988 ◽  
Vol 64 (4) ◽  
pp. 1466-1471 ◽  
Author(s):  
P. M. Buttrick ◽  
A. Malhotra ◽  
J. Scheuer
Keyword(s):  
Cardiac Mechanics ◽  
Heart Weight ◽  
Stroke Work ◽  
Mechanical Function ◽  
Aortic Constriction ◽  
Contraction Coupling ◽  
Combined Load ◽  
Ventricular Myosin ◽  
Heart Apparatus ◽  
Working Heart

We have previously shown that swim conditioning corrects the depressed mechanical function and myosin adenosinetriphosphatase (ATPase) activities associated with renovascular hypertension (HTN) in the rat. The present study was designed to assess the effects of swim conditioning on another form of systolic overload, subdiaphragmatic suprarenal aortic stenosis. Cardiac mechanics in an isolated working heart apparatus and myosin enzymology were studied in four groups of rats: controls (C), animals with chronic systolic overload secondary to aortic constriction (St), swim-conditioning animals (Sw), and animals exposed to a combined load (St-Sw). Heart weight was increased by 23% in St, 27% in Sw, and 36% in St-Sw. In contrast to HTN, cardiac pump and muscle function were not depressed in St. Sw was associated with improved cardiac output, stroke work, and velocity of circumferential fiber shortening. St-Sw showed improved mechanical cardiac performance relative to both C and St. The percent of ventricular myosin of the V1 type and Ca2+-activated myosin ATPase activity relative to C was unchanged in Sw but was depressed in St and St-Sw. These data demonstrate that the salutory mechanical effects of Sw can be superimposed on the systolic overload of St. However, the dissociation between mechanics and myosin enzymology suggests that factors in excitation-contraction coupling other than myosin isoenzyme shifts are responsible for this finding.

Chronic swimming reverses cardiac dysfunction and myosin abnormalities in hypertensive rats

1986 ◽  
Vol 60 (4) ◽  
pp. 1435-1441 ◽  
Author(s):  
T. F. Schaible ◽  
A. Malhotra ◽  
G. J. Ciambrone ◽  
J. Scheuer
Keyword(s):  
Ejection Fraction ◽  
Atpase Activity ◽  
Renal Hypertension ◽  
Heart Weight ◽  
Stroke Work ◽  
Hypertensive Rats ◽  
Myosin Isoenzyme ◽  
End Point ◽  
Heart Apparatus ◽  
Fractional Shortening

The purpose of this study was to determine whether a chronic swimming program could reverse the decreased cardiac function and altered myosin biochemistry found in hearts of rats with established renal hypertension. Ten wk after the onset of hypertension [midpoint (m)], hearts from normotensive controls (C) and hypertensives (H) were studied in an isolated working heart apparatus, and myosin biochemistry was analyzed. Half of the control and hypertensive animals were then subjected to a 10-wk swimming program (Sw) and their hearts were compared with those from age-matched sedentary rats. Body weight was no different at the midpoint of the study between Cm and Hm or at the end point (e) of the study among Ce, Swe, He, or H-Swe. Swimming had no effect on blood pressure in either normotensive or hypertensive rats. Dry heart weight was increased by 46% in Hm compared with Cm and by 36% in He, 21% in Swe, and 61% in H-Swe when compared with Ce. Hypertension was associated in both the mid- and end-point studies, with decreases in coronary flow, stroke work (both per gram left ventricle), ejection fraction, and midwall fractional shortening. In addition, actin-activated myosin adenosinetriphosphatase (ATPase) activity was decreased in Hm and He associated with an increase in the content of the V3 myosin isoenzyme. Although the coronary deficit was not corrected in H-Swe, stroke work, ejection fraction, and fractional midwall shortening were normalized compared with control hearts. Myosin ATPase activity and the myosin isoenzyme distribution were similarly restored in H-Swe.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Impaired left ventricular mechanical and energetic function in mice after cardiomyocyte-specific excision of Serca2

2014 ◽  
Vol 306 (7) ◽  
pp. H1018-H1024 ◽  
Author(s):  
N. T. Boardman ◽  
J. M. Aronsen ◽  
W. E. Louch ◽  
I. Sjaastad ◽  
F. Willoch ◽  
...  
Keyword(s):  
Ex Vivo ◽  
Left Ventricular ◽  
Lv Function ◽  
Mechanical Function ◽  
Transport Mechanisms ◽  
Working Capacity ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Plasmic Reticulum ◽  
The Relationship

Sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA)2 transports Ca2+ from the cytosol into the sarcoplasmic reticulum of cardiomyocytes and is essential for maintaining myocardial Ca2+ handling and thus the mechanical function of the heart. SERCA2 is a major ATP consumer in excitation-contraction coupling but is regarded to contribute to energetically efficient Ca2+ handling in the cardiomyocyte. Previous studies using cardiomyocyte-specific SERCA2 knockout (KO) mice have demonstrated that decreased SERCA2 activity reduces the Ca2+ transient amplitude and induces compensatory Ca2+ transport mechanisms that may lead to more inefficient Ca2+ transport. In this study, we examined the relationship between left ventricular (LV) function and myocardial O2 consumption (MV̇o2) in ex vivo hearts from SERCA2 KO mice to directly measure how SERCA2 elimination influences mechanical and energetic features of the heart. Ex vivo hearts from SERCA2 KO hearts developed mechanical dysfunction at 4 wk and demonstrated virtually no working capacity at 7 wk. In accordance with the reported reduction in Ca2+ transient amplitude in cardiomyocytes from SERCA2 KO mice, work-independent MV̇o2 was decreased due to a reduced energy cost of excitation-contraction coupling. As these hearts also showed a marked impairment in the efficiency of chemomechanical energy transduction (contractile efficiency, i.e, work-dependent MV̇o2), hearts from SERCA2 KO mice were found to be mechanically inefficient. This ex vivo evaluation of mechanical and energetic function in hearts from SERCA2 KO mice brings together findings from previous experimental and mathematical modeling-based studies and demonstrates that reduced SERCA2 activity not only leads to mechanical dysfunction but also to energetic dysfunction.

THE EFFECT OF DIFFERENT DEGREES OF SUBDIAPHRAGMATIC AORTIC CONSTRICTION ON HEART WEIGHT AND BLOOD PRESSURE OF NORMAL AND HYPOPHYSECTOMIZED RATS

1955 ◽  
Vol 33 (1) ◽  
pp. 985-994 ◽  
Author(s):  
Margaret Beznák
Keyword(s):  
Blood Pressure ◽  
Cardiac Hypertrophy ◽  
Blood Pressure Response ◽  
Pressure Response ◽  
Heart Weight ◽  
Aortic Constriction ◽  
Hypophysectomized Rats ◽  
Intact Rats

The aortae of groups of normal and hypophysectomized rats were constricted with rings of five different sizes (0.93, 0.83, 0. 74, 0.71, and 0.63 mm. diameter). In normal rats constriction caused an increase in heart weight and blood pressure which was the greater the narrower the constriction. If constriction exceeded 0.74 mm., cardiac hypertrophy reached extremely high values, while the blood pressure was lower than in groups with less constriction. The blood pressure response to Adrenalin or Infundin increased in proportion to the degree of constriction down to 0.74 mm.; greater constriction reduced the response. In hypophysectomized rats no degree of aortic constriction produced hypertension or cardiac hypertrophy, yet the increase in blood pressure after Adrenalin or Infundin was as great as in the normal intact rats.

Rat model of exercise-induced cardiac hypertrophy: hemodynamic characterization using left ventricular pressure-volume analysis

2013 ◽  
Vol 305 (1) ◽  
pp. H124-H134 ◽  
Author(s):  
Tamás Radovits ◽  
Attila Oláh ◽  
Árpád Lux ◽  
Balázs Tamás Németh ◽  
László Hidi ◽  
...  
Keyword(s):  
Exercise Training ◽  
Cardiac Hypertrophy ◽  
Rat Model ◽  
Left Ventricular ◽  
Heart Weight ◽  
Stroke Work ◽  
Functional Changes ◽  
Exercise Induced

Long-term exercise training is associated with characteristic structural and functional changes of the myocardium, termed athlete's heart. Several research groups investigated exercise training-induced left ventricular (LV) hypertrophy in animal models; however, only sporadic data exist about detailed hemodynamics. We aimed to provide functional characterization of exercise-induced cardiac hypertrophy in a rat model using the in vivo method of LV pressure-volume (P-V) analysis. After inducing LV hypertrophy by swim training, we assessed LV morphometry by echocardiography and performed LV P-V analysis using a pressure-conductance microcatheter to investigate in vivo cardiac function. Echocardiography showed LV hypertrophy (LV mass index: 2.41 ± 0.09 vs. 2.03 ± 0.08 g/kg, P < 0.01), which was confirmed by heart weight data and histomorphometry. Invasive hemodynamic measurements showed unaltered heart rate, arterial pressure, and LV end-diastolic volume along with decreased LV end-systolic volume, thus increased stroke volume and ejection fraction (73.7 ± 0.8 vs. 64.1 ± 1.5%, P < 0.01) in trained versus untrained control rats. The P-V loop-derived sensitive, load-independent contractility indexes, such as slope of end-systolic P-V relationship or preload recruitable stroke work (77.0 ± 6.8 vs. 54.3 ± 4.8 mmHg, P = 0.01) were found to be significantly increased. The observed improvement of ventriculoarterial coupling (0.37 ± 0.02 vs. 0.65 ± 0.08, P < 0.01), along with increased LV stroke work and mechanical efficiency, reflects improved mechanoenergetics of exercise-induced cardiac hypertrophy. Despite the significant hypertrophy, we observed unaltered LV stiffness (slope of end-diastolic P-V relationship: 0.043 ± 0.007 vs. 0.040 ± 0.006 mmHg/μl) and improved LV active relaxation (τ: 10.1 ± 0.6 vs. 11.9 ± 0.2 ms, P < 0.01). According to our knowledge, this is the first study that provides characterization of functional changes and hemodynamic relations in exercise-induced cardiac hypertrophy.

Effects of free wall ischemia and bundle branch block on systolic ventricular interaction in dog hearts

1994 ◽  
Vol 266 (3) ◽  
pp. H1087-H1094 ◽  
Author(s):  
H. Yaku ◽  
B. K. Slinker ◽  
S. P. Bell ◽  
M. M. LeWinter
Keyword(s):  
Right Ventricular ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Free Wall ◽  
Ventricular Pacing ◽  
Aortic Constriction ◽  
Bundle Branch Block ◽  
Ventricular Interaction ◽  
Right Ventricular Stroke Volume

Systolic direct ventricular interaction is thought to occur via the ventricular septum and the coordinated contraction of common fibers shared by both ventricles. The purpose of the present study was to evaluate the effects of transient free wall ischemia and bundle branch block, which disrupt the coordinated contraction of shared common fibers, on left-to-right systolic ventricular interaction. We produced transient right and left ventricular free wall ischemia by 2-min coronary artery occlusions and bundle branch block by ventricular pacing in nine in situ dog hearts. To eliminate any confounding effect of series interaction, we used an abrupt hemodynamic perturbation (aortic constriction), and we measured systolic interaction gain (IG) as delta right ventricular peak systolic pressure/delta left ventricular peak systolic pressure (IG(peak)) and instantaneous delta right ventricular pressure/delta left ventricular pressure at matched data sampling times (IG(inst)), along with changes in right ventricular stroke volume and stroke work before and on the beat immediately after the aortic constriction. To achieve equivalence of the interventricular septal pressure transmission contribution to ventricular interaction, the delta left ventricular peak systolic pressure produced by the aortic constriction was matched under all experimental conditions [average increase: 64 +/- 19 (SD) mmHg]. Control IG(peak) was 0.12 +/- 0.05, and control IG(inst) was 0.11 +/- 0.05. These values did not change with either free wall ischemia or ventricular pacing, with or without an intact pericardium. The changes in right ventricular stroke volume and stroke work produced by the aortic constriction were not different from zero, during either ischemia or ventricular pacing, with or without an intact pericardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanical function, glycolysis, and ultrastructure of perfused working mouse hearts following thoracic aortic constriction

2011 ◽  
Vol 20 (6) ◽  
pp. 343-351 ◽  
Author(s):  
Michael E. Dunn ◽  
Thomas G. Manfredi ◽  
Arthur C. Cosmas ◽  
Frederick J. Vetter ◽  
Joshua N. King ◽  
...  
Keyword(s):  
Mechanical Function ◽  
Aortic Constriction

CHANGES IN HEART WEIGHT AND BLOOD PRESSURE FOLLOWING AORTIC CONSTRICTION IN RATS

1955 ◽  
Vol 33 (6) ◽  
pp. 995-1002 ◽  
Author(s):  
Margaret Beznák
Keyword(s):  
Blood Pressure ◽  
Heart Weight ◽  
Maximum Height ◽  
Pressure Measurements ◽  
Aortic Constriction ◽  
Large Drop ◽  
Epinephrine Injection ◽  
Femoral Blood ◽  
Cardiac Enlargement ◽  
Stimulation Of

Blood pressure measurements in the carotid and femoral arteries of rats after subdiaphragmatic aortic constriction, taken at times varying from immediately afterwards to five days after, indicate that increased carotid pressure precedes cardiac enlargement in these animals. The large drop in femoral blood pressure within the first few hours after aortic constriction seems to be due—at least partly—to stimulation of the pressoreceptors by the increased aortic–carotid pressure. Hypertrophy of the left ventricle can be demonstrated on the second day after constriction. The maximum height of carotid pressure obtainable after epinephrine injection rises with the time after constriction, while the rise over the preinjection value does not increase.

scholarly journals Left-ventricular shape determines intramyocardial mechanical heterogeneity

2011 ◽  
Vol 301 (6) ◽  
pp. H2351-H2361 ◽  
Author(s):  
Hon Fai Choi ◽  
Frank E. Rademakers ◽  
Piet Claus
Keyword(s):  
Finite Element ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Stroke Work ◽  
Mechanical Function ◽  
Fiber Stress ◽  
Hill Model ◽  
Mechanical Heterogeneity ◽  
Left Ventricular Shape

Left-ventricular remodeling is considered to be an important mechanism of disease progression leading to mechanical dysfunction of the heart. However, the interaction between the physiological changes in the remodeling process and the associated mechanical dysfunction is still poorly understood. Clinically, it has been observed that the left ventricle often undergoes large shape changes, but the importance of left-ventricular shape as a contributing factor to alterations in mechanical function has not been clearly determined. Therefore, the interaction between left-ventricular shape and systolic mechanical function was examined in a computational finite-element study. Hereto, finite-element models were constructed with varying shapes, ranging from an elongated ellipsoid to a sphere. A realistic transmural gradient in fiber orientation was considered. The passive myocardium was described by an incompressible hyperelastic material law with transverse isotropic symmetry. Activation was governed by the eikonal-diffusion equation. Contraction was incorporated using a Hill model. For each shape, simulations were performed in which passive filling was followed by isovolumic contraction and ejection. It was found that the intramyocardial distributions of fiber stress, strain, and stroke work density were shape dependent. Ejection performance was reduced with increasing sphericity, which was regionally related to a reduction in the active fiber stress development, fiber shortening, and stroke work in the midwall and subepicardial region at the midheight level in the left-ventricular wall. Based on these results, we conclude that a significant interaction exists between left-ventricular shape and regional myofiber mechanics, but the importance for left-ventricular remodeling requires further investigation.

Effect of thyroid hormone treatment on responses of the isolated working rat heart

1983 ◽  
Vol 61 (11) ◽  
pp. 1382-1390 ◽  
Author(s):  
M. Lynne Marriott ◽  
John H. McNeill
Keyword(s):  
Thyroid Hormone ◽  
Relaxation Times ◽  
Left Ventricular Pressure ◽  
Hormone Treatment ◽  
Left Ventricular ◽  
Heart Weight ◽  
Pressure Curve ◽  
Contraction Times ◽  
Developed Pressure ◽  
Working Heart

Hearts from rats pretreated either with L-triiodothyronine (T3) or with L-thyroxine (T4) exhibited changed function curve characteristics on the working heart apparatus compared with hearts from vehicle-treated rats. There was no supersensitivity of the hyperthyroid myocardium to the inotropic effect of isoproterenol as estimated by pD2 values. There were significant increases in +dP/dt and −dP/dt in hyperthyroid working hearts over the entire range of the function curve. T3 hearts showed much shorter relaxation times and total contraction times throughout the function curve. T4 hearts showed significantly reduced relaxation times and total contraction times as compared with control at all left atrial filling pressures under 15 cm of water. At high filling pressures T4 heart relaxation times and total contraction times were not different from control, but were however, significantly increased from those of T3 hearts. Area under the left ventricular pressure curve was unchanged by thyroid hormone pretreatment. Heart weight increased about 15% following either T3 or T4 treatment while the increases in (+) or (−) dP/dt and the left ventricular developed pressure (LVDP) were about 20–30%. The increase in cardiac mass certainly played a role in the increased cardiac function. Potency of isoproterenol in hyperthyroid working heart preparations was unchanged from control. The pD2 values, as determined from +dP/dt data, were 8.8 ± 0.15 for T3-treated hearts, 8.25 ± 0.40 for T4-treated hearts, and 8.18 ± 0.12 for euthyroid hearts. While the mechanism(s) for the altered performance of the hyperthyroid working heart are not absolutely known, possible biochemical and physiological changes which may be implicated are discussed.

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