Loading determinants of isovolumic pressure fall in closed-chest dogs

1991 ◽  
Vol 260 (3) ◽  
pp. H690-H697 ◽  
Author(s):  
J. B. Su ◽  
L. Hittinger ◽  
M. Laplace ◽  
B. Crozatier
Keyword(s):  
Systolic Pressure ◽  
Wall Stress ◽  
Load Level ◽  
Aortic Constriction ◽  
Autonomic Blockade ◽  
Loading Sequence ◽  
Lv Volume ◽  
Control State ◽  
Pressure Fall

The respective roles of load level and loading sequence of the left ventricle (LV) are controversial in the in situ heart. They were analyzed under autonomic blockade and sedation in 17 dogs previously instrumented with a pressure micromanometer and ultrasonic crystals measuring LV diameters and wall thickness for computation of LV volume and stress. The time constant of isovolumic pressure fall (T) and end-systolic pressure (ESP) were calculated during the control state, caval occlusion, aortic constriction obtained by inflation of a hydraulic cuff occluder positioned around the aorta, and during the inflation of an intra-aortic balloon. Caval occlusion significantly decreased both ESP (from 124.0 +/- 6.6 to 88.7 +/- 3.7 mmHg; P less than 0.005) and T (from 29.0 +/- 2.2 to 18.8 +/- 2.4 ms; P less than 0.005), which were linearly correlated (mean r = 0.90 +/- 0.03) and inflation of an intra-aortic balloon increased both ESP (from 107.3 +/- 7.1 to 150.6 +/- 10.4 mmHg; P less than 0.005) and T (from 24.6 +/- 2.1 to 32.7 +/- 2.3 ms; P less than 0.005). Both interventions did not modify the loading sequence (analyzed by the evolution of systolic wall stress vs. time). In contrast, aortic constriction delayed to midsystole the time to which wall stress reached its peak and, for matched ESP with intra-aortic balloon inflation, T was not significantly different from control. We conclude that both the level of afterload and the loading sequence of LV are the determinants of T when contractility is not modified.

Abstract 12880: A Clinical Index of Myocardial Afterload Can Replace Wall Stress Calculations

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Nathaniel Reichek ◽  
Jonathan Weber ◽  
Madhavi Kadiyala ◽  
Marie Grgas ◽  
Tazim Merchant ◽  
...  
Keyword(s):  
Treatment Guidelines ◽  
Systolic Pressure ◽  
Wall Stress ◽  
Stress Index ◽  
Stress Indices ◽  
Lv Volume ◽  
And Gender ◽  
Brachial Systolic Pressure ◽  
Myocardial Level

Introduction: Afterload at the myocardial level is a principal determinant of LV chamber and myocardial wall function, generated by interplay of LV pressure, volume, and mass. Quantitation has relied on wall stress indices which require additional measurements and calculations as well as incorrect assumptions. Unfamiliar to most clinicians, they have largely fallen out of use, but the role of myocardial afterload in contemporary heart failure pathophysiology and therapy merits reevaluation given the roles of EF and myocardial strains in prognostic indices and treatment guidelines. Hypothesis: A simple clinical afterload index using variables fundamental to wall stress indices (systolic pressure(mmHg) * LV volume(ml))/LV mass(g)) or PV/M correlates closely with stress indices and relates similarly to LV EF and myocardial strains. Methods: In 277 normals (54% female, mean age 50.9±12.9 yrs) and small cohorts with dilated non-ischemic cardiomyopathy(35), aortic stenosis(12) and cancer chemotherapy(43), each with matched controls, we used CMR LV volumes, mass and brachial systolic pressure during imaging to compare end-systolic PV/M to stress indices and systolic pressure alone using correlations and correlation standard errors(SEs). Results: There were extremely close correlations (r= 0.97-0.99, all p< 0.001) with minimal SEs between PV/M and Arts and Alters stress indices with similar slopes in all groups and in normal subgroups by age and gender. Negative correlations with EF, global strains and strain rates were also present and extremely similar in all groups. But Mirsky’s stress index and brachial pressure performed less well. Conclusions: A simple clinical afterload index correlates closely with wall stress indices and similarly with LV ejection fraction and strains. It can support efficient reassessment of the role of afterload at the myocardial level in research and potentially, in clinical practice.

Reversible effects of isoproterenol-induced hypertrophy on in situ left ventricular function in rat hearts

2004 ◽  
Vol 287 (1) ◽  
pp. H277-H285 ◽  
Author(s):  
Yutaka Kitagawa ◽  
Daisuke Yamashita ◽  
Haruo Ito ◽  
Miyako Takaki
Keyword(s):  
Cardiac Hypertrophy ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Lv Function ◽  
Osmotic Minipump ◽  
Good Index ◽  
Rat Hearts ◽  
Lv Volume ◽  
Work Capability

The aim of the present study was to evaluate specifically left ventricular (LV) function in rat hearts as they transition from the normal to hypertrophic state and back to normal. Either isoproterenol (1.2 and 2.4 mg·kg−1·day−1 for 3 days; Iso group) or vehicle (saline 24 μl·day−1 for 3 days; Sa group) was infused by subcutaneous implantation of an osmotic minipump. After verifying the development of cardiac hypertrophy, we recorded continuous LV pressure-volume (P-V) loops of in situ ejecting hypertrophied rat hearts. The curved LV end-systolic P-V relation (ESPVR) and systolic P-V area (PVA) were obtained from a series of LV P-V loops in the Sa and Iso groups 1 h or 2 days after the removal of the osmotic minipump. PVA at midrange LV volume (PVAmLVV) was taken as a good index for LV work capability ( 13 , 15 , 20 , 21 ). However, in rat hearts during remodeling, whether PVAmLVV is a good index for LV work capability has not been determined yet. In the present study, in contrast to unchanged end-systolic pressure at midrange LV volume, PVAmLVV was significantly decreased by isoproterenol treatment relative to saline; however, these measurements were the same 2 days after pump removal. Simultaneous treatment with a β1-blocker, metoprolol (24 mg·kg−1·day−1), blocked the formation of cardiac hypertrophy and thus PVAmLVV did not decrease. The reversible changes in PVAmLVV reflect precisely the changes in LV work capability in isoproterenol-induced hypertrophied rat hearts mediated by β1-receptors. These results indicate that the present approach may be an appropriate strategy for evaluating the effects of antihypertrophic and antifibrotic modalities.

Curvilinearity of LV end-systolic pressure-volume and dP/dtmax-end-diastolic volume relations

1993 ◽  
Vol 265 (3) ◽  
pp. H910-H917 ◽  
Author(s):  
T. Noda ◽  
C. P. Cheng ◽  
P. P. De Tombe ◽  
W. C. Little
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Aortic Constriction ◽  
Contractile State ◽  
End Diastolic Volume ◽  
Open Chest ◽  
Geometric Factors ◽  
Lv Volume ◽  
Length Dependent Activation

We investigated the effect of contractile state (CS) on the curvilinearity of the left ventricular (LV) end-systolic pressure-volume (Pes-Ves) and the dP/dtmax-end-diastolic volume (dP/dtmax-Ved) relations in eight anesthetized open-chest dogs. LV volume was determined from three orthogonal diameters measured by sonomicrometry. The Pes-Ves relation and dP/dtmax-Ved relation were assessed during transient vena caval occlusion and aortic constriction, while CS was altered with dobutamine. At all CS, both relations were linear when volumes were decreased by caval occlusion. However, at higher volumes obtained by aortic constriction, the relations became nonlinear. At enhanced CS, the nonlinearity of both the Pes-Ves relation and the dP/dtmax-Ved relation increased. The dP/dtmax-Ved relation began to deviate from linearity at larger volumes, but closer to baseline operating volume, than the Pes-Ves relation. The relation between end-systolic mean circumference stress and wall strain (sigma es-epsilon es) was linear at control CS when the Pes-Ves relation was nonlinear but became nonlinear with enhanced CS. We conclude that both the Pes-Ves relation and the dP/dtmax-Ved relation are nonlinear, saturating at higher volumes. With increased CS, the nonlinearity of both relations increases. This CS-dependent curvilinearity of the Pes-Ves relation is due to both CS-dependent nonlinearity of the sigma es-epsilon es relation (consistent with length-dependent activation) and geometric factors that alter the relation between Pes and sigma es.

scholarly journals Left ventricular volumetric conductance catheter for rats

1996 ◽  
Vol 270 (4) ◽  
pp. H1509-H1514 ◽  
Author(s):  
H. Ito ◽  
M. Takaki ◽  
H. Yamaguchi ◽  
H. Tachibana ◽  
H. Suga
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Conductance Catheter ◽  
Inferior Vena Caval ◽  
Essential Parameter ◽  
Cardiac Pump Function ◽  
Catheter Tip ◽  
Electromagnetic Flow Probe ◽  
Lv Volume

Left ventricular (LV) volume (V) is an essential parameter for assessment of the cardiac pump function. Measurement of LVV in situ by a conductance catheter method has been widely used in dogs and humans but not yet in small experimental animals such as rats. We instituted a miniaturized six-electrode conductance catheter (3-F) for rat LVV measurement and its signal processing apparatus. We compared stroke volumes (SVs) simultaneously measured with this conductance catheter introduced into the LV through the apex and an electromagnetic flow probe placed on the ascending aorta during gradual decreases in LVV by an inferior vena caval occlusion. A high and linear correlation (r = 0.982) was obtained between these differently measured by SVs pooled from six rats. In another group of three rats, LV pressure was simultaneously measured with a 3-F catheter-tip micromanometer introduced into the LV through the apex. We obtained the slope of the end-systolic pressure-volume (P-V) relationship (Emax) by a gradual ascending aortic occlusion. After administration of propranolol, Emax obviously decreased with no change in volume intercept of the P-V relationship. The conductance volumetry proved to be useful in rats.

End-systolic pressure-volume, pressure-length, and stress-strain relations in canine hearts

1985 ◽  
Vol 249 (3) ◽  
pp. H648-H654 ◽  
Author(s):  
S. Kaseda ◽  
H. Tomoike ◽  
I. Ogata ◽  
M. Nakamura
Keyword(s):  
Systolic Pressure ◽  
Wall Stress ◽  
Regional Wall Motion ◽  
Stress Strain ◽  
Contractile State ◽  
Inotropic State ◽  
Inferior Caval Vein ◽  
Strain Relationship ◽  
Pressure Volume Relationship ◽  
Lv Volume

End-systolic pressure-volume relationship (ESPVR) of the in situ heart in the dog was measured during changes in contractile state and was compared with end-systolic pressure-length (ESPLR) or stress-strain relationship (ESSSR). Circumferential segmental length and wall thickness at the equator and external long and short axis diameters of the left ventricle (LV) were determined sonomicrometrically, and LV volume was calculated by an ellipsoidal model. Circumferential wall stress at the equator was calculated by a very thin shell model. Contractile state was enhanced by an intravenous infusion of dobutamine and was suppressed by propranolol. ESPVR, ESPLR, and ESSSR were determined during a reduction of arterial pressure by occluding temporarily the inferior caval vein (IVC). ESPVR, ESPLR, and ESSSR during changes in end-systolic pressure from 108 +/- 3 to 71 +/- 2 mmHg were linear, irrespective of inotropic states (r greater than 0.92). Slopes of these relationships increased similarly in case of dobutamine and were reduced after propranolol, yet the extrapolated X-axis intercept of ESPVR, ESPLR, and ESSSR remained unchanged. Thus the slope of ESPVR is unique to the inotropic state, and both ESPLR and ESSSR are useful as a substitute for ESPVR when there is no regional wall motion abnormality.

Rhythm effects on contractility of the beating isovolumic left ventricle

1960 ◽  
Vol 199 (6) ◽  
pp. 1115-1120 ◽  
Author(s):  
B. Lendrum ◽  
H. Feinberg ◽  
E. Boyd ◽  
L. N. Katz
Keyword(s):  
Heart Rate ◽  
Left Ventricle ◽  
Systolic Pressure ◽  
Ventricular Volume ◽  
Contractile Force ◽  
Postextrasystolic Potentiation ◽  
Pressure Development ◽  
Induced Changes ◽  
Electrical Alternans

Variation in contractile force of the isovolumic contracting left ventricle of the dog was studied in open-chested in situ hearts. The electrocardiogram and intraventricular pressures were recorded at various heart volumes. Spontaneous changes in heart rate and rhythm occurred at all volumes. Isovolumic systolic pressure development (contractile force) varied with rate and rhythm. Contractile force increased with heart rate (treppe) regardless of pacemaker origin. When a premature beat was followed by a compensatory pause, the premature beat showed a decrease and the next beat an increase in contractile force (postextrasystolic potentiation). The magnitude of the changes varied directly with the prematurity of the beat. Mechanical alternans was observed with electrical alternans, despite the absence of significant volume change. Rate-induced changes, postextrasystolic potentiation and mechanical alternans were additive when they occurred simultaneously. For practical purposes, ventricular volume (filling), hence muscle fiber length, remained constant during these rate and rhythm change, therefore could not affect the strength of contraction. Contractile force changes directly attributable to rate and rhythm changes do, therefore, occur in the intact mammalian heart.

NHE-1 participates in isoproterenol-induced downregulation of SERCA2a and development of cardiac remodeling in rat hearts

2011 ◽  
Vol 301 (5) ◽  
pp. H2154-H2160 ◽  
Author(s):  
Munetaka Shibata ◽  
Daisuke Takeshita ◽  
Koji Obata ◽  
Shinichi Mitsuyama ◽  
Haruo Ito ◽  
...  
Keyword(s):  
Body Weight ◽  
Cardiac Hypertrophy ◽  
Cardiac Remodeling ◽  
Mechanical Energy ◽  
Systolic Pressure ◽  
Beneficial Effects ◽  
Rat Hearts ◽  
Total Mechanical Energy ◽  
Male Wistar Rats ◽  
Lv Volume

Impaired Ca2+ handling is one of the main characteristics in heart failure patients. Recently, we reported abnormal expressions of Ca2+-handling proteins in isoproterenol (ISO)-induced hypertrophied rat hearts. On the other hand, Na+/H+ exchanger (NHE)-1 inhibitor has been demonstrated to exert beneficial effects in ischemic-reperfusion injury and in the development of cardiac remodeling. The aims of the present study are to investigate the role of NHE-1 on Ca2+ handling and development of cardiac hypertrophy in ISO-infused rats. Male Wistar rats were randomly divided into vehicle [control (CTL)] and ISO groups without or with pretreatment with a selective NHE-1 inhibitor, BIIB-723. ISO infusion for 1 wk significantly increased the ratios of heart to body weight and left ventricle (LV) to body weight and collagen accumulation. All of these increases were antagonized by coadministration with BIIB-723. The ISO-induced significant increase in LV wall thickness was suppressed significantly ( P < 0.05) by BIIB-723. ISO-induced decreases in cardiac stroke volume and a total mechanical energy per beat index, systolic pressure-volume area at midrange LV volume, were normalized by BIIB-723. The markedly higher expression of NHE-1 protein in the ISO group than that in CTL group was suppressed ( P < 0.05) by BIIB-723. Surprisingly, ISO induced downregulation of the important Ca2+-handling protein sarcoplasmic reticulum Ca2+-ATPase 2a, the expression of which was also normalized by BIIB-723 without changes in phosphorylated phospholamban (PLB)/PLB expression. We conclude that NHE-1 contributes to ISO-induced abnormal Ca2+ handling associated with cardiac hypertrophy. Inhibition of NHE-1 ameliorates cardiac Ca2+-handling impairment and prevents the development of cardiac dysfunction in ISO-infused rats.

Inotropic effects of ejection are myocardial properties

1994 ◽  
Vol 266 (3) ◽  
pp. H1202-H1213 ◽  
Author(s):  
P. P. De Tombe ◽  
W. C. Little
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Negative Effects ◽  
Inotropic Effects ◽  
Contraction Duration ◽  
Loading System ◽  
Positive Effect ◽  
Isolated Rat

Recent studies in isolated and in vivo canine hearts have suggested that the left ventricular end-systolic pressure (LVPes) of ejecting beats is the net result of a balance between positive and negative effects of ejection. At present, it is unknown whether these ejection effects are merely a ventricular chamber property or represent a fundamental myocardial property. Accordingly, we examined the effects of ejection in eight isolated rat cardiac trabeculae at the sarcomere level. We approximated in situ sarcomere shortening patterns using an iterative computer loading system. Six isovolumic contractions were compared with four ejecting contractions. The superfusing solution contained either 0.7 mM Ca2+ or 0.65 mM Sr2+ plus 0.15 mM Ca2+. With Ca2+, simulated LVPes ("LVP"es) of ejecting contractions was significantly lower than isovolumic "LVP"es (-5.3 +/- 5.6%), whereas with Sr2+, ejecting "LVP"es was significantly higher than isovolumic "LVP"es (+4.5 +/- 7.5%). Contraction duration and time to end systole were markedly prolonged in ejecting vs. isovolumic contractions with either Ca2+ or Sr2+. As a consequence, comparison of simulated LVP between ejecting and isovolumic beats throughout the contraction, i.e., at the same simulated LVV and time, revealed only a positive effect of ejection with either Ca2+ (+18.8 +/- 5.5%) or Sr2+ (+23.4 +/-9.3%). We conclude that both positive and negative effects of ejection are basic myocardial properties.

Mechanical and Dimensional Adaptation of Rat Aorta to Hypertension

1994 ◽  
Vol 116 (3) ◽  
pp. 278-283 ◽  
Author(s):  
T. Matsumoto ◽  
K. Hayashi
Keyword(s):  
Blood Pressure ◽  
Elastic Modulus ◽  
Wall Stress ◽  
Dimensional Change ◽  
Biological Tissues ◽  
Rat Aorta ◽  
Mechanical Adaptation ◽  
Male Wistar Rats ◽  
Load Effects

To investigate mechanisms of the mechanical adaptation of soft biological tissues to load, effects of hypertension on the mechanical properties and wall dimensions of thoracic aortas were studied in rats. Goldblatt hypertension was induced in male Wistar rats aged 8 to 9 weeks by constricting their left renal arteries. Two, 4, 8, or 16 weeks after the operation, thoracic aortas were excised and used to determine static pressure-diameter relations and wall dimensions. Wall thickness correlated significantly with the systolic blood pressure before sacrifice, Psys, at each period. The aortic hoop stress became almost constant at all Psys 2 weeks after the operation. On the other hand, the stress calculated for 100 and 200 mmHg correlated negatively with Psys. The incremental elastic modulus of the wall at Psys had a significant correlation with Psys having a positive slope at each period, although the correlation disappeared at 16 weeks after the operation. These results imply that: 1) thickness of the aortic wall increases very rapidly in response to hypertension; 2) wall stress developed by the in-situ blood pressure is kept constant at a normal level irrespective of hypertension; 3) elastic modulus of the wall of the hypertensive rats at the in-situ blood pressure becomes equal to the normal value after relatively long period of time; 4) in response to the alteration of the applied force, dimensional change appears much earlier than the change in the elastic properties.

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