Differences in distensibility between the anterior and posterior walls of the left ventricle in dogs

1991 ◽  
Vol 69 (3) ◽  
pp. 334-340
Author(s):  
Zhao-Nian Zhou ◽  
Sheng-Jing Dong ◽  
Eldon R. Smith ◽  
John V. Tyberg
Keyword(s):  
Left Ventricle ◽  
Length Change ◽  
Posterior Wall ◽  
Anterior Wall ◽  
Left Ventricular ◽  
Transmural Pressure ◽  
Segment Length ◽  
Anesthetized Dogs ◽  
Pericardial Pressure ◽  
The Difference

Nonuniformity of myocardial systolic and diastolic performance in the normal left ventricle has been recognized by a number of investigators. Lack of homogeneity in diastolic properties might be caused by or related to differences in the distensibility of different regions of the left ventricular (LV) wall. Thus, we compared the end-diastolic transmural pressure–strain relations in both the anterior and posterior LV walls in seven anesthetized dogs during two interventions (pulmonary artery constriction and aortic constriction). Transmural pressure was defined as the difference between LV intracavitary pressure and local pericardial pressure. LV pressure was measured using a micromanometer; pericardial pressures over the LV anterior and posterior wails were measured with balloon transducers. Circumferentially oriented pairs of sonomicrometer crystals were implanted in the midwall of the anterior and posterior walls of the LV to measure segment lengths. Strains were calculated as (L – L0)/L0, where L was the instantaneous segment length and L0 was the segment length when transmural pressure was zero. The pattern of end-diastolic transmural pressure–strain relations was similar in ail dogs. The change in strain in the posterior wall was always greater than that in the anterior wall. Opening the pericardium did not affect the difference in distensibility of the anterior and posterior walls. The results suggest that the posterior wall is more compliant than the anterior wall (that is, for a given difference in transmural pressure, the local segment length change of the posterior wall was greater). This seems consistent with other observations, which suggest that the posterior wall might make a greater contribution to diastolic filling.Key words: regional ventricular function, diastolic suction, elastic properties.

Finite strains in anterior and posterior wall of canine left ventricle

1990 ◽  
Vol 259 (5) ◽  
pp. H1409-H1418 ◽  
Author(s):  
F. J. Villarreal ◽  
W. Y. Lew
Keyword(s):  
Left Ventricle ◽  
Circumferential Strain ◽  
Diastolic Pressure ◽  
Posterior Wall ◽  
Anterior Wall ◽  
Left Ventricular ◽  
Principal Strain ◽  
Wide Range ◽  
Anesthetized Dogs ◽  
Principal Strains

Piezoelectric crystals were implanted in the anterior and posterior midwall of the left ventricle in six anesthetized dogs to compare regional two-dimensional finite deformations. Increasing left ventricular end-diastolic pressure (LVEDP) from 3 to 18 mmHg caused a similar expansion in the end-diastolic configuration (similar end-diastolic principal strains), but maximal lengthening was more circumferential in the anterior wall (-18 +/- 13 degrees) and more longitudinal in the posterior wall (-54 +/- 19 degrees). End-diastolic in-plane shears were negative in both regions, consistent with a left-handed diastolic torsion. As LVEDP increased, maximal shortening strains increased similarly (similar end-systolic principal strains), but there was a preferential increase in end-systolic circumferential strain in the anterior wall and preferential increase in longitudinal strain in the posterior wall. End-systolic in-plane shears were small and positive in both regions. The circumferential strain accurately reflected maximal end-diastolic and end-systolic principal strains in the anterior wall at mid and high LVEDP but underestimated the maximal end-diastolic principal strain by 50% and the maximal end-systolic principal strain by 30% in the posterior wall at all LVEDPs. We conclude that the magnitude of end-diastolic and end-systolic strains is similar for anterior and posterior walls over a wide range of LVEDP. However, there are regional differences in the directions of maximal deformation that should be considered when evaluating regional ventricular function.

Influence of ischemic zone size on nonischemic area function in the canine left ventricle

1987 ◽  
Vol 252 (5) ◽  
pp. H990-H997 ◽  
Author(s):  
W. Y. Lew
Keyword(s):  
Left Ventricle ◽  
Ventricular Volume ◽  
Anterior Wall ◽  
Left Ventricular ◽  
Acute Ischemia ◽  
Zone Size ◽  
Large Area ◽  
Area Function ◽  
Anesthetized Dogs ◽  
The Relationship

The relationship between ischemic zone size and nonischemic area function was examined in seven anesthetized dogs. Regional ventricular function was measured with sonomicrometers implanted in the midwall of the anterior apex, posterior base, and posterior apex of the left ventricle. Ventricular volume was varied to three levels, corresponding to left ventricular end-diastolic pressures of 7, 12, and 19 mmHg. A small, moderate, and large area of anterior wall ischemia was produced with sequential occlusions of the distal, mid, and proximal left anterior descending coronary artery, respectively. Each occlusion was maintained for 15-30 min; then ventricular volume was varied to three levels, chosen so that end-diastolic segment lengths in the nonischemic areas were matched to their control (preischemia) values. With acute ischemia, paradoxical lengthening developed in the ischemic zone during isovolumic systole. This was accompanied by an increase in isovolumic shortening in the nonischemic areas. The amount of nonischemic area isovolumic shortening increased with increasing ischemic zone size, suggesting that more nonischemic area shortening was expended in paradoxically stretching the ischemic zone. With moderate and large areas of ischemia, the amount of "wasted" isovolumic shortening by nonischemic areas was greater at low than at high ventricular volumes. It is concluded that the ischemic zone imposes a mechanical disadvantage on nonischemic areas in direct relation to ischemic zone size and is inversely related to the ventricular volume.

Restraining effect of intact pericardium during acute volume loading

1992 ◽  
Vol 262 (6) ◽  
pp. H1725-H1733 ◽  
Author(s):  
R. J. Applegate ◽  
W. E. Johnston ◽  
J. Vinten-Johansen ◽  
H. S. Klopfenstein ◽  
W. C. Little
Keyword(s):  
Left Ventricular ◽  
Transmural Pressure ◽  
Equilibrium Analysis ◽  
Volume Loading ◽  
Fluid Infusion ◽  
Anesthetized Dogs ◽  
Similar Range ◽  
Cardiac Volumes ◽  
The Difference ◽  
Lv Volume

To determine the effect of the intact pericardium on ventricular end-diastolic pressures (EDP) during acute volume loading, we measured left ventricular (LV) and right ventricular (RV) micromanometer pressure and LV volume using a conductance catheter in eight open-chest, anesthetized dogs. A range of LV pressure and volume was obtained by intravascular volume expansion with the pericardium intact and then over a similar range after removal of the pericardium. Pericardial pressure (Pper) was calculated using static equilibrium analysis as the difference between LVEDP with the pericardium present and absent at a constant LV volume. At the beginning of the fluid infusion (LVEDP 7.3 +/- 1.7 mmHg and RVEDP 4.4 +/- 2.6 mmHg, mean +/- SD), Pper was not different from zero (-1.0 +/- 2.3 mmHg, P not significant). The onset of pericardial restraint (Pper greater than or equal to 0 mmHg) occurred when LVEDP was 9.1 +/- 2.9 mmHg and RVEDP was 4.1 +/- 2.9 mmHg. At low cardiac volumes before fluid infusion, RV transmural pressure was positive and significantly greater than the near zero Pper. After the onset of pericardial restraint, however, RVEDP and Pper increased similarly and were related according to Pper = 1.1 (+/- 0.34) RVEDP - 4.2 (+/- 2.6) mmHg, standard deviation 0.6 +/- 0.8 mmHg, r = 0.98 +/- 0.10. These data indicate that the intact pericardium behaves in two functionally distinct ways. At low cardiac volumes, Pper is zero and the pericardium does not affect LV filling. RV transmural pressure is positive and greater than Pper.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of systole-specific pericardial pressure increases on coronary flow

1991 ◽  
Vol 71 (1) ◽  
pp. 104-111 ◽  
Author(s):  
C. Hassapoyannes ◽  
J. F. Harper ◽  
L. M. Stuck ◽  
C. A. Hornung ◽  
F. L. Abel
Keyword(s):  
Cardiac Function ◽  
Coronary Flow ◽  
Atrioventricular Node ◽  
Intrathoracic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Transmural Pressure ◽  
Coronary Sinus Flow ◽  
Anesthetized Dogs ◽  
Pericardial Pressure

It has been postulated that intrathoracic pressure increases may impair cardiac function by decreasing coronary flow. To determine whether altered coronary flow causes or results from change in cardiac function, we used 14 anesthetized dogs in propranolol-induced heart failure following atrioventricular node ablation. After thoracoabdominal binding, the animals were paced and ventilated at the same frequency, and inspiration was synchronized with cardiac systole, resulting in systole-specific pericardial pressure increases (SSPPI). At SSPPI magnitudes of 15 and 30 mmHg, left atrial transmural pressure decreased and cardiac output increased, whereas decreases in left ventricular end-systolic transmural pressure and myocardial O2 consumption were directly related. Concurrent decreases in coronary sinus flow (CSF) and coronary arteriovenous O2 gradient with SSPPI 15 mmHg indicate autoregulation. However, the arteriovenous O2 gradient remained unaltered with SSPPI 30 mmHg, despite further decrease in CSF. Because the absolute diastolic aortic pressure decreased, a limit may exist for increasing SSPPI above which CSF may be directly affected.

Basic determinants of epicardial transudation

1997 ◽  
Vol 273 (3) ◽  
pp. H1408-H1414 ◽  
Author(s):  
R. H. Stewart ◽  
D. A. Rohn ◽  
S. J. Allen ◽  
G. A. Laine
Keyword(s):  
Reflection Coefficient ◽  
Coronary Sinus ◽  
Myocardial Edema ◽  
Hydraulic Conductance ◽  
Linear Increase ◽  
Left Ventricular ◽  
Edema Formation ◽  
Anesthetized Dogs ◽  
The Difference ◽  
Osmotic Reflection Coefficient

Myocardial edema formation, which has been shown to compromise cardiac function, and increased epicardial transudation (pericardial effusion) have been shown to occur after elevation of myocardial venous and lymphatic outflow pressures. The purposes of this study were to estimate the hydraulic conductance and osmotic reflection coefficient for the epicardium and to determine the effect of coronary sinus hypertension and cardiac lymphatic obstruction on epicardial fluid flux (JV,e/Ae). A Plexiglas hemispheric capsule was attached to the left ventricular epicardial surface of anesthetized dogs. JV,e/Ae was determined over 30-min periods for three intracapsular pressures (-5, -15, and -25 mmHg) and two intracapsular solutions exerting colloid osmotic pressures of 7.0 and 2.0 mmHg. Hydraulic conductance was estimated to be 3.7 +/- 0.5 microliters.h-1.cm-2.mmHg-1. An osmotic reflection coefficient of 0.9 was calculated from the difference in JV,e/Ae of 16.5 +/- 8.4 microliters.h-1.cm-2 between the two solutions. Graded coronary sinus hypertension induced a linear increase in JV,e/Ae, which was significantly greater in dogs without cardiac lymphatic occlusion than in those with occlusion.

scholarly journals Ventricular interaction and external constraint account for decreased stroke work during volume loading in CHF

2001 ◽  
Vol 281 (6) ◽  
pp. H2385-H2391 ◽  
Author(s):  
Thomas D. Moore ◽  
Michael P. Frenneaux ◽  
Rozsa Sas ◽  
J. J. Atherton ◽  
Jayne A. Morris-Thurgood ◽  
...  
Keyword(s):  
Diastolic Pressure ◽  
Left Ventricular ◽  
Negative Slope ◽  
Segment Length ◽  
Stroke Work ◽  
Volume Loading ◽  
End Diastolic Volume ◽  
Pulmonary Capillary ◽  
Apparent Decrease ◽  
Pericardial Pressure

The slope of the stroke work (SW)-pulmonary capillary wedge pressure (PCWP) relation may be negative in congestive heart failure (CHF), implying decreased contractility based on the premise that PCWP is simply related to left ventricular (LV) end-diastolic volume. We hypothesized that the negative slope is explained by decreased transmural LV end-diastolic pressure (LVEDP), despite the increased LVEDP, and that contractility remains unchanged. Rapid pacing produced CHF in six dogs. Hemodynamic and dimension changes were then measured under anesthesia during volume manipulation. Volume loading increased pericardial pressure and LVEDP but decreased transmural LVEDP and SW. Right ventricular diameter increased and septum-to-LV free wall diameter decreased. Although the slopes of the SW-LVEDP relations were negative, the SW-transmural LVEDP relations remained positive, indicating unchanged contractility. Similarly, the SW-segment length relations suggested unchanged contractility. Pressure surrounding the LV must be subtracted from LVEDP to calculate transmural LVEDP accurately. When this was done in this model, the apparent decrease in contractility was no longer evident. Despite the increased LVEDP during volume loading, transmural LVEDP and therefore SW decreased and contractility remained unchanged.

scholarly journals Effects of Long-term Nonylphenol Exposure on Myocardial Fibrosis and Cardiac Function in Rats

2021 ◽  
Author(s):  
Chao Liu ◽  
Chengyu Ni ◽  
Weichu Liu ◽  
Xiaolian Yang ◽  
Renyi Zhang ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Myocardial Fibrosis ◽  
Posterior Wall ◽  
Anterior Wall ◽  
Left Ventricular ◽  
Environmental Estrogens ◽  
Control Group ◽  
Cardiac Structure ◽  
Collagen Iii

Abstract Background: Myocardial fibrosis is a critical pathological basis for the poor prognosis of cardiovascular diseases. Studies have found that myocardial fibrosis is closely associated with exposure to environmental estrogens such as nonylphenol (NP), as a representative of environmental estrogens. The aim of this study was to examine the effects of NP chronic exposure on myocardial fibrosis as well as cardiac structure and function. Forty Sprague Dawley rats were randomly divided into four groups (n = 10): control group (C), low NP dose (0.4 mg/kg, L), medium NP dose (4 mg/kg, M), and high NP dose (40 mg/kg, H) groups. The NP dose groups were gavaged with NP for 180 days. Results: The NP level in the heart of the NP groups was significantly higher than those in the control group (F = 43.658, P < 0.001). Serum aspartate aminotransferase (AST), creatine kinase (CK), creatine kinase isozyme (CK-MB), lactate dehydrogenase (LDH) and α-hydroxybutyrate dehydrogenase (α-HBDH) significantly increased in the NP groups compared with the control group (). Histopathological examination of the heart biopsy illustrates that in the medium and high NP groups, the fibrous connective tissue had a disordered and loose gridding shape, muscle fibers had fractured, and muscle fibers were loose with a widened gap. Extensive inflammatory cell infiltration and fibroblast proliferation in the myocardial interstitium were also found. With increasing NP dose, the degree of muscle fiber loosing and disorder became more significant in the NP treatment groups, and the collagen volume fraction (CVF) was higher than that in the control group (P < 0.01). Compared with the control group, the expression of collagen I and collagen III increased significantly in the medium and high NP groups (P < 0.05). The values of the systolic thickness of the left ventricular anterior wall (LVAWs), the diastolic thickness of the left ventricular posterior wall (LVPWd), the systolic thickness of the left ventricular posterior wall (LVPWs), and the left ventricular anterior wall (LVAWd) in the NP groups are were slightly lower than those in of the control group. The values of left ventricular end systolic dimensions (LVIDs) in the NP groups increased compared with the control group. Conclusions: Long-term NP exposure could lead to fibrosis in the rat myocardium, which is characterized by increased expressions of myocardial collagen I and collagen III, as well as elevated cardiac enzymes. In addition, the cardiac structure was affected and changes were observed in the thinner ventricular wall and as an enlarged ventricular cavity.

Regional diastolic mechanics of the left ventricle in the conscious dog

1979 ◽  
Vol 236 (2) ◽  
pp. H323-H330 ◽  
Author(s):  
D. Ling ◽  
J. S. Rankin ◽  
C. H. Edwards ◽  
P. A. McHale ◽  
R. W. Anderson
Keyword(s):  
Left Ventricle ◽  
Pressure Gradient ◽  
Regional Differences ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Transmural Pressure ◽  
Diastolic Filling ◽  
Rapid Phase ◽  
Conscious Dog ◽  
Dynamic Relationship

In eight chronically instrumented conscious dogs, apical and middle left ventricular transverse diameters were measured with pulse-transit ultrasonic dimension transducers. Intracavitary apical and midventricular pressures and intrapleural pressure were measured with micromanometers. Both diameters were normalized as a percent extension from the dimension at zero transmural pressure, determined during a transient vena caval occlusion. During the rapid phase of diastolic filling, there was a 2--5 mmHg pressure gradient from the midventricle to the apex. During late rapid filling, the apical transmural pressure and diameter increased more rapidly and reached diastasis 17 +/- 4 ms earlier than the corresponding midventricular measurements (P less than 0.01). The static diastolic pressure-dimension characteristics at the apical and midventricular levels were not significantly different (P greater than 0.30). The dynamic diastolic pressure-dimension relationship was also similar at the two levels and could be represented by a model incorporating parallel viscous properties. Because of regional differences in pressures and dimensions, however, the dynamic relationship could not be modeled when pressure was compared to the dimension at a different level. Thus, diastolic pressures should be measured at the same level as dimensions when assessing left ventricular diastolic mechanics.

scholarly journals P955 left ventricle cardiac remodeling among lithuanian football versus basketball players

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
A Aldujeli ◽  
J Laukaitiene ◽  
R Unikas
Keyword(s):  
Left Ventricle ◽  
Wall Thickness ◽  
Cardiac Remodeling ◽  
Interventricular Septum ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Relative Wall Thickness ◽  
Football Players ◽  
Basketball Players ◽  
Lv Mass

Abstract Background Regular physical exercise causes a continuous gradual increase of the cardiac left ventricular (LV) mass known as physiological adaptive hypertrophy. The extent of LV remodeling depends on the type, amount, and intensity of the exercise. Purpose The aim of this study was to compare structural changes of the heart among Lithuanian football, basketball players and unathletic controls. Methods A total of 50 Lithuanian males aged between 20-29 years volunteered to participate in the study. Football players (n = 15) playing for local II league football clubs,and Basketball players (n = 15) playing for local minor league basketball teams. All athletes had been regularly engaged in their sport for at least three years. Inactive healthy volunteers (n = 20) of similar age served as controls. Routine transthoracic echocardiographic examinations to measure end-diastolic LV dimensions were performed by cardiology fellow under the supervision of a fully licensed cardiologist. Statistical analyses were performed using the SPSS 20.0 software. The value of p &lt; 0,05 was considered as statistically significant. Results No structural or functional pathologies were evident during the echocardiographic examination in any of the subjects. Absolute interventricular septum (IVS) thickness and LV posterior wall thickness, but not LV diameter, were higher in athletes than in inactive controls (P &lt; 0,001). Indexed LV diameter was higher in football players as compared with non-athlete controls and basketball players (P &lt; 0,05). Left ventricular mass of all athletes were higher as compared with controls (p &lt; 0.001). Relative wall thickness was not increased in football players but was higher in basketball players as compared with controls (p &lt; 0.05). Conclusion Cardiac remodeling in Lithuanian football players resulted in left ventricle eccentric hypertrophy due to the LV dilation, increased LV mass and relatively normal relative wall thickness. However in Lithuanian basketball players we noticed an increase in both relative wall thickness and LV mass resulting in LV concentric hypertrophy. Echocardiographic characteristics Groups n End-diastolic LV diameter(mm) End-diastolic Interventricular septum (mm) End-diastolic LV posterior wall LV mass Football Players 15 56.9 10.8 10.8 242 Basketball players 15 53.6 11.5 11.3 254 Inactive individuals 20 53.2 9.1 9.5 182 P value 0.01 &lt;0.001 &lt;0.001 &lt;0.01 Abstract P955 Figure.

scholarly journals Basic values of M-mode echocardiographic parameters of the left ventricle in outbreed Wistar rats

2012 ◽  
Vol 57 (No. 1) ◽  
pp. 42-52 ◽  
Author(s):  
P. Scheer ◽  
V. Sverakova ◽  
J. Doubek ◽  
K. Janeckova ◽  
I. Uhrikova ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Wistar Rats ◽  
Minimum Weight ◽  
Interventricular Septum ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Regression Equations ◽  
Left Ventricular Dimension ◽  
Echocardiographic Parameters ◽  
Ventricular Dimension

This paper describes the partial results of an echocardiographic study in sixty outbreed Wistar rats. Animals of parity sex ratio were chosen for the experiment. The animals were grown up during the observation period (the minimum weight was 220 g; the maximum weight was 909 g) and were then sequentially anaesthetised (2&ndash;2.5% of isoflurane, 3 l/min O<sub>2</sub>). The second, fourth and fifth examinations were performed under anaesthesia maintained by intramuscular injections with diazepam (2 mg/kg), xylazine (5 mg/kg) and ketamine (35 mg/kg). Transthoracal examination was done using the SonoSite Titan echo system (SonoSite Ltd.) with a microconvex transducer C11 (8&ndash;5 MHz). M-mode (according to the leading-edge method of American Society of Echocardiography) echocardiography data were acquired at the papillary muscle: systolic and diastolic interventricular septum (IVSs, d) and left vetricular posterior wall (LVPWs, d) thickness, systolic and diastolic left ventricular dimension (LVDs, d), aorta (Ao) and left atrium (LA) dimensions. According to standard formulas, the following parameters were obtained: ejection fraction (EF), cardiac output (CO), stroke volume (SV), left ventricle end systolic volume (LVESV), left ventricle end diastolic volume (LVEDV), interventricular septum fractional thickening (IVSFT), left ventricular dimension fraction shortening (LVDFS), and left ventricle posterior wall fraction thickening (LVPWFS). In our study we performed 300 examinations both in male and female Wistar rats of various body weights and calculated regression equations to predict expected normal echocardiographic parameters for rats with arbitrary weights. The rats were examined by an echo scan. The first and third examinations were performed during mono-anaesthesia induced by inhalation of isoflurane. Correlations, with one exception (LVDs), were very close, which means that the results of the calculations based on regression equations are very reliable. &nbsp; &nbsp;

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