Regulation of left ventricular pressure fall

1990 ◽  
Vol 11 (suppl I) ◽  
pp. 124-132 ◽  
Author(s):  
T. C. Gillebert ◽  
D. L. Brutsaert
1987 ◽  
Vol 51 (11) ◽  
pp. 1273-1282 ◽  
Author(s):  
KAZUHIRO KATAYAMA ◽  
TOSHIAKI KUMADA ◽  
MASUNORI MATSUZAKI ◽  
MASAHRU OZAKI ◽  
MASAFUMI YANO ◽  
...  

1982 ◽  
Vol 242 (1) ◽  
pp. H131-H132
Author(s):  
G. Martin ◽  
J. Cosin ◽  
J. V. Gimeno ◽  
A. Ramirez

2002 ◽  
Vol 198 (2) ◽  
pp. 107-118 ◽  
Author(s):  
HIDENARI HOZAWA ◽  
MASAHITO SAKUMA ◽  
MAKOTO NAKAGAWA ◽  
HIDEHIKO ISHIGAKI ◽  
KOHTAROH KOMAKI ◽  
...  

1988 ◽  
Vol 52 (6) ◽  
pp. 518-524 ◽  
Author(s):  
KAZUHIRO KATAYAMA ◽  
TOSHIAKI . KUMADA ◽  
MASUNORI MATSUZAKI ◽  
TAKASHI FUJI ◽  
MICHIHIRO KOHNO ◽  
...  

Heart ◽  
1989 ◽  
Vol 61 (5) ◽  
pp. 426-431 ◽  
Author(s):  
R A Luke ◽  
C E Gillbe ◽  
R S Bonser ◽  
M Paneth ◽  
D Somerset ◽  
...  

1989 ◽  
Vol 256 (1) ◽  
pp. H222-H232 ◽  
Author(s):  
W. Y. Lew ◽  
C. M. Rasmussen

We examined the influence of nonuniformity in regional ventricular function on the rate of left ventricular pressure fall in 10 anesthetized dogs. Ultrasonic segment gauges were implanted in the midwall of the anterior, lateral, and posterior left ventricle. In seven dogs, nonuniformity was produced by infusing isoproterenol (0.4 microgram/ml) into the mid-left anterior descending coronary artery at low flow (0.5 +/- 0.7 ml/min) and high flow (1.5 +/- 1.2 ml/min) rates, for total doses of 0.1 +/- 0.1 and 0.3 +/- 0.2 micrograms, respectively. This produced a dose-dependent increase in anterior segment shortening so that shortening was completed earlier and marked segment lengthening occurred during isovolumic relaxation. Lateral and posterior segments were not directly stimulated. The heart rate, left ventricular end-diastolic pressure, and peak systolic pressure remained constant. However, tau, the time constant of left ventricular pressure fall, increased from 32 +/- 8 to 37 +/- 10 ms with the low dose, and from 35 +/- 6 to 49 +/- 12 ms with the high dose of isoproterenol. Similar results occurred in two dogs when isoproterenol was infused into the proximal, mid, or distal left anterior descending and in three dogs with infusions in the left circumflex coronary artery. We conclude that nonuniformity of regional left ventricular function is an important and independent factor regulating the rate of pressure fall in the intact ejecting left ventricle.


Author(s):  
Stefan F. J. Langer

Background: Hypothermia is well known to elevate the time constant (whatever model is used) of the isochoric left-ventricular pressure fall. Due to different critera in use, it remained unclear whether prolonged diastole in hypothermia is sufficient for complete relaxation. Detecting and quantifying incomplete relaxation may become a valuable tool to prevent diastolic heart failure in hypothermia.Methods: Left-ventricular pressure decays in isolated guinea pig and rat hearts are analysed by 4-parametric regression at different temperatures, at sinus rhythm and electrical stimulation. Residual contraction (F_RC) is introduced and quantified by extrapolating the model's pressure forecast to end-systole, subtracting the asymptote, and normalising.Resultts: Isochoric pressure decay fits the regression model at all temperatures and heart beat frequencies. Residual contraction is virtually absent at normothermia and remains very small (F_RC<3%) down to 31°C. Lower temperatures or pacing induces higher F_RC. Eventually, the pressure curve becomes considerably elevated and looses its concavity.Conclusions: Despite slower pressure fall, ventricular relaxation remains fairly complete at hypothermia; and depends on considerable autoregulation of the individual heart. It is concluded (not proved) that individual emergence of negative lusitropy may indicate imminent heart failure. Asymptotic pressure rises are interpreted at higher ventricular tonus, independent from velocity of relaxation. Gradual increasing time constants may be attributed to a general slowing of bioreactions as temperature falls. Remarkable curve shape changes may be caused by aftercontractions due to elevated Ca++ sensitivity at hypothermia and high Ca++ load by pacing.


1991 ◽  
Vol 261 (3) ◽  
pp. H805-H813 ◽  
Author(s):  
T. C. Gillebert ◽  
W. Y. Lew

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)


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