Regional circumferential lengthening patterns in canine left ventricle

1983 ◽  
Vol 245 (5) ◽  
pp. H741-H748 ◽  
Author(s):  
W. Y. Lew ◽  
M. M. LeWinter
Keyword(s):  
Left Ventricle ◽  
Regional Differences ◽  
Inferior Vena ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Elastic Recoil ◽  
Rapid Phase ◽  
Inferior Vena Caval ◽  
Ventricular Filling

We employed sonomicrometers in open-chest dogs to study lengthening of short segments of circumferentially oriented myocardium located at the base, midportion, and apex of the anterior left ventricular free wall. Left ventricular pressure was varied by inferior vena caval occlusion and volume expansion. Diastole was divided into rapid and slow lengthening phases. Rapid lengthening was completed first at the basal site at each of three successive levels of left ventricular diastolic pressure (LVDP). At the base, significant further lengthening occurred during the slow lengthening phase while at the apex virtually all lengthening was completed during the rapid phase. At low LVDPs, peak lengthening rates (dl/dt) were greatest at the apex. As LVDP was increased, regional differences in dl/dt diminished. These results indicate that there is regional variation in the timing of the phases of diastole and in lengthening patterns of the left ventricle. The volume-dependent variation in lengthening rates that we observed is consistent with the concept of regional differences in elastic recoil, which may contribute to active ventricular filling.

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.

Estrogen-induced left ventricular chamber enlargement in ewes

1993 ◽  
Vol 264 (4) ◽  
pp. E490-E496 ◽  
Author(s):  
G. D. Giraud ◽  
M. J. Morton ◽  
L. E. Davis ◽  
M. S. Paul ◽  
K. L. Thornburg
Keyword(s):  
Placebo Group ◽  
Stroke Volume ◽  
Inferior Vena ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Chronic Effect ◽  
Inferior Vena Caval ◽  
Intramuscular Dose ◽  
Left Ventricular Chamber ◽  
Chamber Size

We studied the chronic effect of administration of a single large intramuscular dose of 17 beta-estradiol on left ventricular chamber size and output in the ewe. Fourteen oophorectomized ewes were successfully instrumented and studied, with measurements made of left ventricular, aortic, right and left atrial pressures, left ventricular stroke volume, and left ventricular minor axis dimension. Unanesthetized ewes were studied before and 1, 2, and 3 wk after intramuscular administration of 0.6 mg/kg 17 beta-estradiol (7 ewes) or 1.5 ml sesame oil placebo (7 ewes). Left ventricular end-diastolic pressure-end-diastolic dimension (LVEDP-EDD) and left ventricular end-diastolic pressure-stroke volume (LVEDP-SV) relationships were quantified during graded inferior vena caval occlusion and volume infusion. Left ventricular end-diastolic diameter was larger after estrogen but not after placebo administration. The LVEDP-EDD relationship shifted progressively rightward, indicating left ventricular chamber enlargement in the estrogen group but was unchanged in the placebo group. The plateau limb of the LVEDP-SV relationship in the estrogen group shifted up from a mean stroke volume of 77.1-89.5 ml/beat and did not change in the placebo group. We conclude that administration of a single large intramuscular dose of 17 beta-estradiol resulted in left ventricular chamber enlargement and increased stroke volume in the ewe.

scholarly journals Attenuated sarcomere lengthening of the aged murine left ventricle observed using two-photon fluorescence microscopy

2015 ◽  
Vol 309 (5) ◽  
pp. H918-H925 ◽  
Author(s):  
Michael E. Nance ◽  
Justin T. Whitfield ◽  
Yi Zhu ◽  
Anne K. Gibson ◽  
Laurin M. Hanft ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Force Microscopy ◽  
Two Photon ◽  
Atomic Force ◽  
Heart Preparation ◽  
Two Photon Fluorescence ◽  
Ventricular Filling

The Frank-Starling mechanism, whereby increased diastolic filling leads to increased cardiac output, depends on increasing the sarcomere length ( Ls) of cardiomyocytes. Ventricular stiffness increases with advancing age, yet it remains unclear how such changes in compliance impact sarcomere dynamics in the intact heart. We developed an isolated murine heart preparation to monitor Ls as a function of left ventricular pressure and tested the hypothesis that sarcomere lengthening in response to ventricular filling is impaired with advanced age. Mouse hearts isolated from young (3–6 mo) and aged (24–28 mo) C57BL/6 mice were perfused via the aorta under Ca2+-free conditions with the left ventricle cannulated to control filling pressure. Two-photon imaging of 4-{2-[6-(dioctylamino)-2-naphthalenyl]ethenyl}1-(3-sulfopropyl)-pyridinium fluorescence was used to monitor t-tubule striations and obtain passive Ls between pressures of 0 and 40 mmHg. Ls values (in μm, aged vs. young, respectively) were 2.02 ± 0.04 versus 2.01 ± 0.02 at 0 mmHg, 2.13 ± 0.04 versus 2.23 ± 0.02 at 5 mmHg, 2.21 ± 0.03 versus 2.27 ± 0.03 at 10 mmHg, and 2.28 ± 0.02 versus 2.36 ± 0.01 at 40 mmHg, indicative of impaired sarcomere lengthening in aged hearts. Atomic force microscopy nanoindentation revealed that intact cardiomyocytes enzymatically isolated from aged hearts had increased stiffness compared with those of young hearts (elastic modulus: aged, 41.9 ± 5.8 kPa vs. young, 18.6 ± 3.3 kPa; P = 0.006). Impaired sarcomere lengthening during left ventricular filling may contribute to cardiac dysfunction with advancing age by attenuating the Frank-Starling mechanism and reducing stroke volume.

Influence of systolic pressure profile on rate of left ventricular pressure fall

1991 ◽  
Vol 261 (3) ◽  
pp. H805-H813 ◽  
Author(s):  
T. C. Gillebert ◽  
W. Y. Lew
Keyword(s):  
Left Ventricle ◽  
Regional Differences ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Pressure Profile ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Segment Length ◽  
Experimental Conditions ◽  
Pressure Fall

We examined the influence of the systolic left ventricular pressure (LVP) waveform on the rate of isovolumetric LVP fall, as assessed by the time constant tau. Seven open-chest dogs were instrumented with a micromanometer in the left ventricle, with segment length gauges in the anterior and posterior midwall of the left ventricle, and with a balloon-tipped catheter in the proximal aorta. The intra-aortic balloon was inflated before the onset of ejection (early) or during midejection (late) to produce timed and graded increases in peak LVP of 2-20 mmHg. The rate of LVP fall slowed significantly more with late than with early increases in LVP (tau increased 1.5 +/- 0.5 vs. 0.5 +/- 0.3%/mmHg increase in peak LVP, respectively, P less than 0.001). For a similar increase in peak LVP, there was a progressively greater increase in tau when the timing of balloon inflation was progressively delayed from early to late ejection (in 10-ms increments). The differential effect of early vs. late pressure increases on tau was not related to regional differences in segment length behavior nor to an increase in regional nonuniformity between anterior and posterior sites. We conclude that under the experimental conditions of an intact, ejecting left ventricle, the systolic pressure profile is an important determinant of the rate of pressure fall. The rate of LVP fall slows in direct proportion to the magnitude of increase in systolic pressure. The sensitivity to systolic load increases progressively throughout the ejection period, so that the rate of LVP fall slows significantly more with late than with early pressure increases.(ABSTRACT TRUNCATED AT 250 WORDS)

Independent influence of left atrial pressure on regional peak lengthening rates

1990 ◽  
Vol 259 (2) ◽  
pp. H480-H487 ◽  
Author(s):  
B. D. Hoit ◽  
M. LeWinter ◽  
W. Y. Lew
Keyword(s):  
Left Ventricle ◽  
Pressure Gradient ◽  
Left Atrial ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Wide Range

We examined the influence of left atrial pressure on regional peak lengthening rates in six open-chest dogs. Sonomicrometers were implanted in the midwall of the anterior apex, the midanterior wall, and the posterior wall of the left ventricle. A bolus of blood was injected into the left atrium during ventricular systole by a computer-driven power injector to produce an isolated increase in left atrial pressure without altering the peak rate of left ventricular pressure fall, regional systolic shortening, or end-systolic length. Several left atrial injections of different volumes were performed over a wide range of left ventricular end-diastolic pressure (LVEDP) (from 7 to 22 mmHg). The peak lengthening rate increased in direct proportion to the increase of left atrial pressure. This effect was significantly greater in the apical than midanterior or posterior sites and decreased at all sites at higher LVEDP. Similar size left atrial injections produced greater increases in atrioventricular pressure gradient but smaller increases in left atrial pressure at low compared with high LVEDP. We conclude that left atrial pressure is an independent determinant of regional peak lengthening rates in the intact left ventricle. The influence of left atrial pressure is attenuated at higher LVEDP because of a smaller change in the diastolic pressure gradient, although viscoelastic effects may play a role.

Estimation of Left Ventricular Wall Stiffness by Analysis of Late Diastolic Pressure Components

2011 ◽  
Author(s):  
Casandra L. Niebel ◽  
Kelley C. Stewart ◽  
Takahiro Ohara ◽  
John J. Charonko ◽  
Pavlos P. Vlachos ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Diastolic Dysfunction ◽  
Diastolic Pressure ◽  
Left Ventricular Diastolic Dysfunction ◽  
Left Ventricular ◽  
Ventricular Wall ◽  
Ventricular Relaxation ◽  
Wall Stiffness ◽  
Ventricular Diastolic Dysfunction

Left ventricular diastolic dysfunction (LVDD) is any abnormality in the filling of the left ventricle and is conventionally evaluated by analysis of the relaxation driven phase, or early diastole. LVDD has been shown to be a precursor to heart failure and the diagnosis and treatment for diastolic failure is less understood than for systolic failure. Diastole consists of two filling waves, early and late and is primarily dependent on ventricular relaxation and wall stiffness.

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