Asynchrony and ryanodine modulate load-dependent relaxation in the canine left ventricle

1995 ◽  
Vol 268 (1) ◽  
pp. H17-H24 ◽  
Author(s):  
W. Y. Lew

Load-dependent relaxation was studied in six anesthetized dogs by inflating an intra-aortic balloon to increase peak left ventricular (LV) pressure by 1–20 mmHg within a single cardiac cycle. A series of timed and graded pressure loads was produced by inflating the balloon either during diastole (early loads) or midsystole (midsystolic pressure loads). The rate of LV pressure fall was measured with the time constant (tau). There was a significant increase in tau with 63 midsystolic pressure load [tau increased 1.4 +/- 0.1% (SE)/mmHg increase in peak LV pressure] but not with 67 early pressure loads (-0.5 +/- 0.1%/mmHg). This difference remained with LV pacing-induced asynchrony (tau increased 1.8 +/- 0.1%/mmHg with 54 midsystolic pressure loads compared with -0.2 +/- 0.1%/mmHg with 56 early pressure loads) and after 5 micrograms/kg of intravenous ryanodine (tau increased 1.0 +/- 0.2%/mmHg with 58 midsystolic pressure loads compared with -0.7 +/- 0.1%/mmHg with 59 early pressure loads). When compared with control, asynchrony significantly augmented and ryanodine significantly attenuated the effects of midsystolic pressure loads. In conclusion, asynchrony and ryanodine modulate the extent of load-dependent relaxation in the intact left ventricle.

2018 ◽  
Vol 60 (3) ◽  
pp. 286-292 ◽  
Author(s):  
Laurent Bonnemains ◽  
Anne Sophie Guerard ◽  
Paul Soulié ◽  
Freddy Odille ◽  
Jacques Felblinger

Background The relative modification of the myocardial volume between end-systole and end-diastole ([Formula: see text]) has already been assessed with different methods and falls in a range of 0.9–0.97 (mean value = 0.93). Purpose To estimate [Formula: see text] from the three longitudinal ([Formula: see text], circumferential ([Formula: see text]), and radial ([Formula: see text]) strains of the left ventricle using the formula: [Formula: see text] and to test whether this estimate of [Formula: see text] can be used as a marker of the echocardiography quality. Material and Methods Two hundred manuscripts, including a total of 34,690 patients or healthy volunteers, were identified in the Medline database containing values of [Formula: see text], [Formula: see text], and [Formula: see text] measured from echocardiography. Results The median value of was 0.93, in accordance with the literature, with no significant difference between patients or healthy volunteers ( P = 0.38). The proportion of studies with [Formula: see text] was 79%. When only considering groups of healthy volunteers, the studies failing this test had higher standard deviations for the three individual strains: 0.038 vs. 0.029 ( P = 0.02) for [Formula: see text]; 0.060 vs. 0.034 ( P < 10–6) for [Formula: see text], and 0.243 vs. 0.101 ( P < 10–14) for [Formula: see text]. Conclusion The median ratio of the left ventricular myocardial volumes between end-systole and end-diastole in the investigated studies was [Formula: see text]. The formula [Formula: see text] could be used to detect studies with inaccurate strain measurements.


1991 ◽  
Vol 69 (3) ◽  
pp. 334-340
Author(s):  
Zhao-Nian Zhou ◽  
Sheng-Jing Dong ◽  
Eldon R. Smith ◽  
John V. Tyberg

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.


1959 ◽  
Vol 14 (3) ◽  
pp. 417-420 ◽  
Author(s):  
Philip Samet ◽  
William H. Bernstein ◽  
Robert S. Litwak ◽  
William H. Meyer ◽  
Louis Lemberg

Dissociation of electrical and mechanical asynchronism in the right and left ventricle of the dog has been studied by simultaneous registration of the precordial electrocardiogram and right and left ventricular pressure curves. Observations were made during sinus rhythm and during digitalis-induced ventricular premature beats with widened aberrant QRS complexes. Measurements were made of the time of onset of isometric contraction in the ventricles, relative to each other, and to the onset of the QRS complex. The results indicate that mechanical asynchronism in onset of isometric contraction is not a necessary consequence of the asynchronous electrical depolarization of ventricular premature systoles. Submitted on November 10, 1958


1978 ◽  
Vol 235 (6) ◽  
pp. H701-H706 ◽  
Author(s):  
J. W. Frederiksen ◽  
J. L. Weiss ◽  
M. L. Weisfeldt

1986 ◽  
Vol 20 (9) ◽  
pp. 698-704 ◽  
Author(s):  
R. KETTUNEN ◽  
J. TIMISJARVI ◽  
P. RAMO ◽  
E. KOUVALAINEN ◽  
J. HEIKKILA ◽  
...  

1987 ◽  
Vol 65 (2) ◽  
pp. 172-178 ◽  
Author(s):  
W. Reuben Kaufman ◽  
Bodh I. Jugdutt

To determine whether changes in left ventricular catecholamine content occur during the first 30 to 90 min of acute myocardial infarction, myocardial catecholamine (radioenzymatic assay) over the interval was studied in the dog. In nine pentobarbital-anesthetized opened-chest dogs without coronary ligation, myocardial catecholamine at 2.5 h after pentobarbital (i) consisted mainly of norephinephrine (87% total catecholamine), (ii) showed a base to apex gradient in norephinephrine (1.44 ± 0.10 vs. 1.03 ± 0.10 μg/g, p < 0.05) and dopamine (0.20 ± 0.03 vs. 0.12 ± 0.02 μg/g, p < 0.05) but not epinephrine (0.017 vs. 0.016 μg/g), and (iii) showed no difference in norepinephrine, dopamine, or epinephrine across basal, mid, and apical left ventricular transverse planes spanning the vascular territories of the two coronary arteries. In 18 pentobarbital-anesthetized dogs with coronary ligation, (i) norepinephrine, measured in 14 regions across the mid left ventricle after 90 min ischemia in four dogs, was less in the ischemic center of the occluded bed than normal myocardium (1.01 ± 0.04 vs. 1.29 ± 0.04 μg/g, p < 0.05), and (ii) norepinephrine was unchanged in normal myocardium of 14 dogs at 30, 60, 90 min, and 48 h but decreased in ischemic myocardium by 31% at 60 min (0.89 ± 0.10 vs. 1.29 ± 0.08 μg/g, p < 0.025) and 79% at 48 h (0.27 ± 0.04 vs. 1.26 ± 0.08 μg/g, p < 0.001). Thus, norepinephrine depletion from ischemic but not normal myocardium is detectable by 60 min during acute myocardial infarction.


1987 ◽  
Vol 252 (5) ◽  
pp. H990-H997 ◽  
Author(s):  
W. Y. Lew

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.


1992 ◽  
Vol 262 (4) ◽  
pp. H1256-H1267 ◽  
Author(s):  
J. M. Huyghe ◽  
T. Arts ◽  
D. H. van Campen ◽  
R. S. Reneman

The axisymmetric model described represents myocardial tissue as a spongy anisotropic viscoelastic material. It includes torsion around the axis of symmetry of the ventricle, transmural variation of fiber angle, and redistribution of intracoronary blood in the myocardial wall. In simulations, end-systolic principal strains were equal to 0.45, -0.01, and -0.24 at two-thirds of the wall thickness from the epicardium and 0.26, 0.00, and -0.19 at one-third of the wall thickness from the epicardium. The direction of maximal shortening varied by less than 30 degrees from epicardium to endocardium, whereas fiber direction varied by greater than 100 degrees from epicardium to endocardium. During a normal cardiac cycle peak, equatorial intramyocardial pressure differed by less than 5% from peak intraventricular pressure. When redistribution of intracoronary blood in the ventricular wall was suppressed, peak equatorial intramyocardial pressure was found to exceed peak intraventricular pressure by greater than 30%. Simulated contraction of an unloaded left ventricle (left ventricular pressure = 0 kPa) produced similar magnitude for systolic intramyocardial pressures as the normal cardiac cycle. Transmural systolic fiber stress distribution was very sensitive to the chosen transmural fiber angle distribution.


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.


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