In vivo determination of left ventricular wall stress-shortening relationship in normal mice

1997 ◽  
Vol 272 (2) ◽  
pp. H1047-H1052 ◽  
Author(s):  
B. D. Hoit ◽  
Z. U. Khan ◽  
C. M. Pawloski-Dahm ◽  
R. A. Walsh
Keyword(s):  
Mouse Genome ◽  
Phenotypic Expression ◽  
Wall Stress ◽  
Left Ventricular ◽  
Loading Conditions ◽  
Inotropic State ◽  
Before And After ◽  
Fractional Shortening

Although targeted alterations of the mouse genome are used increasingly to identify the mechanisms underlying cardiac function, the methods used to study the phenotypic expression of these alterations in vivo are limited. To derive a relatively noninvasive, load-independent measure of left ventricular (LV) contractility in mice, we cannulated the femoral artery and performed two-dimensional directed M-mode echo studies in 28 anesthetized FVB/N mice, using a 9-MHz transducer. Loading conditions were altered by intraarterial methoxamine (3-12 microg/g), and LV shortening fraction was determined at several steady states, both before and after myocardial contractility was altered by either 4 microg/g intraperitoneal dobutamine (n = 16) or 1-2 microg/g verapamil (n = 12). The relation between LV systolic meridional stress and fractional shortening derived from pooled baseline data was inverse and linear [r = 0.80, slope = -0.19, intercept = 48%, standard error of estimate (SEE) = 5.5%, P < 0.001]. Dobutamine produced a parallel upward shift of the relation (r = 0.87, slope = -0.21, intercept = 61%, SEE = 4.5%, P < 0.001), and verapamil produced a downward shift of the relation (r = 0.48, slope = -0.05, intercept = 24%, SEE = 3.7%, P < 0.05). At matched levels of end-systolic stress, dobutamine increased and verapamil decreased the LV shortening fraction. We conclude that 1) inverse stress-shortening relations can be assessed noninvasively in mice; and 2) these relations are sensitive to alterations in inotropic state, independent of loading conditions.

Cardiac dimensions during extracorporeal membrane oxygenation

2005 ◽  
Vol 15 (4) ◽  
pp. 373-378 ◽  
Author(s):  
Ronald B. Tanke ◽  
Otto Daniëls ◽  
Arno F. van Heijst ◽  
Henk van Lier ◽  
Cees Festen
Keyword(s):  
Left Ventricle ◽  
Extracorporeal Membrane Oxygenation ◽  
Left Ventricular ◽  
Loading Conditions ◽  
Volume Loading ◽  
Membrane Oxygenation ◽  
Arterial Duct ◽  
Before And After ◽  
Fractional Shortening

Our aim was to analyze left ventricular fractional shortening during extracorporeal membrane oxygenation under the influence of changing volume loading conditions induced by a ductal left-to-right shunt. In all patients, the fractional shortening was observed using echocardiography before, during, and after bypass, irrespective of the presence or absence of the ductal left-to-right shunt. During membrane oxygenation, there was a significant decrease in fractional shortening (p less than 0.001), with no difference before and after membrane oxygenation. A greater decrease in fractional shortening was observed in the group with a ductal left-to-right shunt when compared to patients lacking the ductal shunt (p less than 0.006). The diastolic diameter of the left ventricle also increased significantly during the membrane oxygenation in those patients with left-to-right ductal shunting. Moreover, the patients with left-to-right shunting showed a very severe decreased fractional shortening, lower than 10 per cent, with significantly greater frequency (p less than 0.05) during the course of membrane oxygenation. Conclusion: An important decrease in left ventricular fractional shortening is observed during veno-arterial extracorporeal membrane oxygenation. Left-to-right shunting during bypass, as seen in the patients with patency of the arterial duct, increases the loading conditions on the left ventricle, and produces a significant increase in left ventricular diastolic dimensions. Despite the effects of volume loading produced by the ductal shunt during bypass, the decrease in fractional shortening is significantly more pronounced for these patients. Therefore, during membrane oxygenation the volume loading produced by the ductal shunt is unable to prevent a decrease in left ventricular fractional shortening.

Nonsympathetic increased inotropic state early after aortic insufficiency

1982 ◽  
Vol 242 (6) ◽  
pp. H973-H979
Author(s):  
B. Crozatier ◽  
D. Caillet ◽  
J. L. Chevrier ◽  
P. Y. Hatt
Keyword(s):  
Volume Overload ◽  
Wall Stress ◽  
Aortic Insufficiency ◽  
Left Ventricular ◽  
Beta Blockade ◽  
Internal Diameter ◽  
Inotropic State ◽  
Chronic Volume Overload ◽  
Before And After ◽  
Ventricular Response

The very early left ventricular response to chronic volume overload induced by aortic insufficiency (AI) was examined in conscious dogs previously instrumented with a left ventricular micromanometer and ultrasonic crystals measuring internal diameter, segmental length, and parietal wall thickness. Acute volume loading with dextran (AVL) was compared with that 24 and 48 h after AI induced by a perforation of the aortic valve. beta-Blockade was also produced before and after AI. For a similar increase in preload in AVL and after AI, the percent change in systolic shortening of diameters and segments (% delta L) increased from 30.4 to 34.1% after AI (P less than 0.01). For matched calculated wall stress during AVL and AI, % delta L and peak velocity of shortening were significantly increased after AI, and the same results were reproduced after beta-blockade. We conclude that, at the early phase of chronic volume overload before hypertrophy appears, left ventricular hyperfunction is mainly due to a nonsympathetic increased contractility and that, in the conscious dog, the inotropic state appears to be modified by a sustained increased preload.

Midwall LV mechanics in rats with or without renovascular hypertension: effect of different Na+ intakes

1996 ◽  
Vol 270 (2) ◽  
pp. H628-H637 ◽  
Author(s):  
G. De Simone ◽  
R. B. Devereux ◽  
M. Volpe ◽  
M. J. Camargo ◽  
D. C. Wallerson ◽  
...  
Keyword(s):  
Wall Stress ◽  
Left Ventricular ◽  
High Salt ◽  
Lv Function ◽  
Hypertensive Rats ◽  
Indirect Measure ◽  
Inotropic State ◽  
Fractional Shortening ◽  
Chamber Size ◽  
Goldblatt Hypertension

Supranormal left ventricular (LV) function has been reported in one-kidney, one-clip (1K,1C) and two-kidney, one-clip (2K,1C) Goldblatt hypertension. However, this finding might be at least partially due to mismatching endocardial rather than midwall fractional shortening to mean end-systolic stress. Accordingly, relations of echocardiographic endocardial and midwall shortening to circumferential end-systolic stress were calculated in 40 Wistar rats on 0.4% NaCl (r = -0.92, SE of estimate = 4.3% and r = -0.62, SE of estimate = 3.2%, both P < 0.0001). Midwall shortening as a percentage of predicted was related to LV chamber diameter in normal animals (r = 0.56, P < 0.0001). Endocardial and midwall shortening were compared as percentage of the normal values predicted from wall stress in 34 2K,1C and 19 1K,1C on 0.4% Na+ 8-9 wk after surgery. Use of midwall shortening reduced the number of these hypertensive rats with supranormal observed-to-predicted shortening ratio from 28 to 7.5% (P < 0.0001). Salt-deprived and high-salt diets (0.0035 and 4% NaCl, respectively) were given to 16 and 18 additional controls, 9 and 7 2K,1C, and 7 and 7 1K,1C. Salt-deprived sham animals had greater endocardial and midwall shortening (106 +/- 7 and 111 +/- 10% of predicted, both P < 0.002) than sham rats on 0.4% NaCl, whereas 4% NaCl had no effect. Five of sixteen salt-deprived sham rats had supranormal observed-to-predicted midwall shortening ratios for LV chamber size, suggesting an enhanced inotropic state. Salt-deprived and high-salt diets had negligible effects on LV performance in Goldblatt rats. Thus use of midwall shortening reduces the number of renovascular hypertensive rats with apparently increased LV function. Salt deprivation stimulates LV myocardial function in normal rats independent of chamber dimension (i.e., an indirect measure of preload) but does not influence LV performance in Goldblatt hypertension 8 wk after renal artery clipping.

Severe myocardial dysfunction induced by ventricular remodeling in aging rat hearts

1990 ◽  
Vol 259 (4) ◽  
pp. H1086-H1096 ◽  
Author(s):  
J. M. Capasso ◽  
T. Palackal ◽  
G. Olivetti ◽  
P. Anversa
Keyword(s):  
Ventricular Remodeling ◽  
Volume Fraction ◽  
Diastolic Pressure ◽  
Structural Characteristics ◽  
Myocardial Dysfunction ◽  
Pressure Rise ◽  
Wall Stress ◽  
Left Ventricular ◽  
Cross Sectional

To determine if aging engenders alterations in the functional properties of the myocardium and ventricular remodeling, the hemodynamic performance and structural characteristics of the left ventricle of male Fischer 344 rats at 4, 12, 20, and 29 mo of age were studied by quantitative physiology and morphology. In vivo assessment of cardiac pump function showed no change up to 20 mo, whereas left ventricular end-diastolic pressure was increased at 29 mo. Moreover, peak rates of pressure rise and decay, stroke volume, ejection fraction, and cardiac output were depressed at the later age interval, demonstrating the presence of ventricular failure at this time. The measurements of chamber size and wall thickness showed that ventricular end-diastolic and end-systolic volumes progressively increased with age with the greatest change occurring at 20-29 mo. Aging was also accompanied by a marked augmentation in the volume fraction of fibrotic areas in the ventricular myocardium that was due to an increase in their number and cross-sectional area with time. These architectural rearrangements, in combination with the abnormalities in ventricular function, resulted in an elevation in the volume of wall stress throughout the cardiac cycle. Wall stress increased by 64, 44, and 50% from 4 to 12, 12 to 20, and 20 to 29 mo of age. In conclusion, aging leads to a continuous rise in wall stress that is not normalized by ventricular remodeling. These two independent processes appear to be responsible for the onset of heart failure in the senescent rat.

Abstract 1008: A Protective Role for Cardiac Specific Muscle Ring Finger-1 (MuRF1) in Ischemia/Reperfusion Injury In Vivo

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Monte S Willis ◽  
Mauricio Rojas ◽  
Pamela Lockyer ◽  
Thomas G Hampton ◽  
Luge Li ◽  
...  
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Ring Finger ◽  
Left Ventricular ◽  
Ex Situ ◽  
Histological Evaluation ◽  
Area At Risk ◽  
Fractional Shortening

We previously identified a critical role for MuRF1 in suppressing pathologic cardiac hypertrophy. To extend these observations to other pathologic processes, we tested the role of MuRF1 in cardiac ischemia reperfusion (I/R) injury. We challenged MuRF1 transgenic (Tg) mice to I/R injury both ex situ and in vivo. First, we examined isolated MuRF1 Tg and age-matched sibling wild-type (WT) hearts after global ischemia (15 min) followed by reperfusion (20 min) in a Langendorff apparatus. Baseline function of MuRF1 Tg hearts did not significantly differ from WT hearts (mean left ventricular developed pressure (LVDP) 88.5 +/− 18 vs. 82.5 +/− 6.7, respectively; n = 4/group). Mean LVDP of hearts from MuRF1 Tg mice after reperfusion was 76.0 +/− 22.9% of baseline function compared to 27.2 +/− 13.3% in WT hearts (N = 5/group, P< 0.05)). To confirm that MuRF1 is cardioprotective in vivo, we subjected MuRF1 Tg and WT mice to a 30 minute ligation of the left anterior descending coronary artery, followed by 24 hours reperfusion. Mice underwent conscious echocardiography at baseline and after 24 hours; cardiac function was further interrogated by Millar pressure volume catheterization at 24 hours. Additionally, hearts underwent a histological evaluation of area at risk and infarct size. By echocardiography, a ~7% decrease in fractional shortening was identified in MuRF1 Tg mice after 24 hours reperfusion compared to baseline. This was in striking contrast to WT mice, which exhibited ~48% decrease in fractional shortening. Steady state catheterization measurements showed a significantly higher ejection fraction in MuRF1 Tg compared to WT mice after I/R injury (81.6 ± 2.3% vs. 49.0 +/− 4.0%, P < 0.05). Contractility reflected by +dP/dt max was better preserved in MuRF1 Tg compared to WT mice after I/R injury (12,614 +/− 776 vs. 7,448 +/−752, N = 3–12/group, P < 0.05). Histologically, the area of infarct in MuRF1 Tg mice was significantly smaller (10.0 +/− 0.8%) than in WT mice (25.5 +/− 2.5%, N = 4/group, P < 0.05). We demonstrate here for the first time that cardiac MuRF1 expression preserves function after I/R injury in vivo. Since MuRF1 is known to interact with metabolic and structural targets, this model will allow us to identify mechanisms by which MuRF1 modifies cardiac pathophysiology.

Ventricular function in the newborn lamb

1965 ◽  
Vol 208 (5) ◽  
pp. 931-937 ◽  
Author(s):  
S. Evans Downing ◽  
Norman S. Talner ◽  
Thomas H. Gardner
Keyword(s):  
Ventricular Function ◽  
Diastolic Pressure ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Ventricular Mechanics ◽  
Inotropic State ◽  
Ejection Rate ◽  
Norepinephrine Infusion

The present study was initiated with the objective of evaluating in the newborn those aspects of ventricular mechanics which form the basis of the Frank-Starling relation, and which permit a determination of changes in the inotropic state of the heart. Left ventricular function was studied in lambs, 12 hr to 5 days old, utilizing a preparation designed to permit control and measurement of systemic arterial pressure (AP), cardiac output, heart rate (HR), and temperature. Continuous measurements of arterial Po2 and pH were made. These data permitted the construction of ventricular function curves relating stroke volume, mean ejection rate, and stroke work and power to left ventricular end-diastolic pressure, at constant AP and HR. In all preparations the Frank-Starling relation was found to be operative. Norepinephrine infusion, 1–2 µg/kg per min, resulted in a substantial increment of both force and speed parameters, thereby demonstrating the ability of the newborn heart to alter its inotropic state. Severe metabolic acidosis did not inhibit the response of the myocardium to norepinephrine.

scholarly journals Prenatal hypoxia impairs cardiac mitochondrial and ventricular function in guinea pig offspring in a sex-related manner

2018 ◽  
Vol 315 (6) ◽  
pp. R1232-R1241 ◽  
Author(s):  
Loren P. Thompson ◽  
Ling Chen ◽  
Brian M. Polster ◽  
Gerard Pinkas ◽  
Hong Song
Keyword(s):  
Heart Function ◽  
Left Ventricular ◽  
Complex Iv ◽  
In Vivo Measurement ◽  
End Diastolic Volume ◽  
Consumption Rates ◽  
Ventricular Wall Thickness ◽  
And Function ◽  
Fractional Shortening

Adverse intrauterine conditions cause fetal growth restriction and increase the risk of adult cardiovascular disease. We hypothesize that intrauterine hypoxia impairs fetal heart function, is sustained after birth, and manifests as both cardiac and mitochondrial dysfunction in offspring guinea pigs (GPs). Pregnant GPs were exposed to 10.5% O2 (HPX) at 50 days of gestation (full term = 65 days) or normoxia (NMX) for the duration of the pregnancy. Pups were allowed to deliver vaginally and raised in a NMX environment. At 90 days of age, mean arterial pressure (MAP) was measured in anesthetized GPs. NMX and prenatally HPX offspring underwent echocardiographic imaging for in vivo measurement of left ventricular cardiac morphology and function, and O2 consumption rates and complex IV enzyme activity were measured from isolated cardiomyocytes and mitochondria, respectively. Prenatal HPX increased ( P < 0.01) MAP (52.3 ± 1.3 and 58.4 ± 1.1 mmHg in NMX and HPX, respectively) and decreased ( P < 0.05) stroke volume (439.8 ± 54.5 and 289.4 ± 15.8 μl in NMX and HPX, respectively), cardiac output (94.4 ± 11.2 and 67.3 ± 3.8 ml/min in NMX and HPX, respectively), ejection fraction, and fractional shortening in male, but not female, GPs. HPX had no effect on left ventricular wall thickness or end-diastolic volume in either sex. HPX reduced mitochondrial maximal respiration and respiratory reserve capacity and complex IV activity rates in hearts of male, but not female, GPs. Prenatal HPX is a programming stimulus that increases MAP and decreases cardiac and mitochondrial function in male offspring. Sex-related differences in the contractile and mitochondrial responses suggest that female GPs are protected from cardiovascular programming of prenatal HPX.

Estimation of regional left ventricular wall stresses in intact canine hearts

1998 ◽  
Vol 275 (5) ◽  
pp. H1879-H1885 ◽  
Author(s):  
Abe DeAnda ◽  
Masashi Komeda ◽  
Marc R. Moon ◽  
G. Randall Green ◽  
Ann F. Bolger ◽  
...  
Keyword(s):  
High Speed ◽  
Systolic Function ◽  
Univariate Analysis ◽  
Interventricular Septum ◽  
Wall Stress ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Regional Wall ◽  
Inotropic State ◽  
Lv Systolic Function

Left ventricular (LV) wall stress is an important element in the assessment of LV systolic function; however, a reproducible technique to determine instantaneous local or regional wall stress has not been developed. Fourteen dogs underwent placement of twenty-six myocardial markers into the ventricle and septum. One week later, marker images were obtained using high-speed biplane videofluoroscopy under awake, sedated, atrially paced baseline conditions and after inotropic stimulation (calcium). With a model taking into account LV pressure, regional wall thickness, and meridional and circumferential regional radii of curvature, we computed average midwall stress for each of nine LV sites. Regional end-systolic and maximal LV wall stress were heterogeneous and dependent on latitude (increasing from apex to base, P < 0.001) and specific wall (anterior > lateral and posterior wall stresses; P = 0.002). Multivariate ANOVA demonstrated only a trend ( P = 0.056) toward increased LV stress after calcium infusion; subsequent univariate analysis isolated significant increases in end-systolic LV wall stress with increased inotropic state at all sites except the equatorial regions. The model used in this analysis incorporates local geometric factors and provides a reasonable estimate of regional LV wall stress compared with previous studies. LV wall stress is heterogeneous and dependent on the particular LV site of interest. Variation in wall stress may be caused by anatomic differences and/or extrinsic interactions between LV sites, i.e., influences of the papillary muscles and the interventricular septum.

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