scholarly journals Dynamic left ventricular elastance: a model for integrating cardiac muscle contraction into ventricular pressure-volume relationships

2008 ◽  
Vol 104 (4) ◽  
pp. 958-975 ◽  
Author(s):  
Kenneth B. Campbell ◽  
Amy M. Simpson ◽  
Stuart G. Campbell ◽  
Henk L. Granzier ◽  
Bryan K. Slinker
Keyword(s):  
Muscle Fiber ◽  
Fiber Length ◽  
Phase 1 ◽  
Left Ventricular ◽  
Isolated Rat Heart ◽  
Rate Of Change ◽  
Lv Function ◽  
Elastic Distortion ◽  
Length Changes ◽  
Incremental Step

To integrate myocardial contractile processes into left ventricular (LV) function, a mathematical model was built. Muscle fiber force was set equal to the product of stiffness and elastic distortion of stiffness elements, i.e., force-bearing cross bridges (XB). Stiffness dynamics arose from recruitment of XB according to the kinetics of myofilament activation and fiber-length changes. Elastic distortion dynamics arose from XB cycling and the rate-of-change of fiber length. Muscle fiber stiffness and distortion dynamics were transformed into LV chamber elastance and volumetric distortion dynamics. LV pressure equaled the product of chamber elastance and volumetric distortion, just as muscle-fiber force equaled the product of muscle-fiber stiffness and lineal elastic distortion. Model validation was in terms of its ability to reproduce cycle-time-dependent LV pressure response, ΔP( t), to incremental step-like volume changes, ΔV, in the isolated rat heart. All ΔP( t), regardless of the time in the cycle at which ΔP( t) was elicited, consisted of three phases: phase 1, concurrent with the leading edge of ΔV; phase 2, a brief transient recovery from phase 1; and phase 3, sustained for the duration of systole. Each phase varied with the time in the cycle at which ΔP( t) was elicited. When the model was fit to the data, cooperative activation was required to sustain systole for longer periods than was possible with Ca2+ activation alone. The model successfully reproduced all major features of the measured ΔP( t) responses, and thus serves as a credible indicator of the role of underlying contractile processes in LV function.

Pressure response to quick volume changes in tetanized isolated ferret hearts

1989 ◽  
Vol 257 (1) ◽  
pp. H38-H46 ◽  
Author(s):  
K. B. Campbell ◽  
A. R. Rahimi ◽  
D. L. Bell ◽  
R. D. Kirkpatrick ◽  
J. A. Ringo
Keyword(s):  
Cardiac Muscle ◽  
Muscle Fiber ◽  
Volume Change ◽  
Initial Pressure ◽  
Recovery Phase ◽  
Left Ventricular ◽  
Fast Recovery ◽  
Volume Changes ◽  
Slow Recovery ◽  
Length Changes

Observed pressure responses to quick volume changes in the isolated tetanized heart of ferrets were compared with previously reported tension responses to quick length changes in isolated cardiac muscle. Hearts were isolated from ferrets, perfused with ryanodine solution, and stimulated rapidly (50 ms between stimulations) to produce repeated 4-s intervals of tetanus. During each tetanus interval, volume increments of different amplitudes were rapidly removed and then reinfused into the left ventricular chamber. The pressure responses to these volume changes were evaluated for differences between withdrawals and infusions and for dependence on the amplitude of the volume change. It was found for both withdrawal and infusion that the response could be divided into three phases: 1) an immediate phase coincident with volume change, 2) a fast-recovery phase, and 3) a slow-recovery phase. The amplitude of the immediate phase was linearly dependent on the volume change so that a single regression line fit all the data (withdrawal and infusion). The fast recovery phase was 2.5 times faster for infusion than for withdrawal and generated a rebound effect with the pressure going below the initial pressure in the response to infusion. The pressure never went above the initial pressure in the response to withdrawal. The slow-recovery phases in infusion and withdrawal did not differ. These responses in the isolated heart bear striking similarities to tension responses to quick length changes in isolated constantly activated cardiac muscle. We concluded that muscle fiber dynamics were being faithfully transformed to left ventricular (LV) chamber dynamics without appreciable distortion because of the many intervening factors between the wall muscle fiber and the LV chamber.(ABSTRACT TRUNCATED AT 250 WORDS)

Muscle fiber length: a determinant of left ventricular contraction pattern

1966 ◽  
Vol 211 (2) ◽  
pp. 301-306 ◽  
Author(s):  
VJ Fisher ◽  
RJ Lee ◽  
A Gourin ◽  
H Bolooki ◽  
JH Stuckey ◽  
...  
Keyword(s):  
Muscle Fiber ◽  
Fiber Length ◽  
Left Ventricular ◽  
Ventricular Contraction ◽  
Contraction Pattern

Abstract 3894: Inhibition of iNOS Uncoupling by Tetrahydrobiopterin Confers Cardioprotection through Protein S- Nitrosylation in Streptozotocin-Induced Diabetic Rat

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Toru Okazaki ◽  
Hajime Otani ◽  
Koji Yamashita ◽  
Hiromi Jo ◽  
Kei Yoshioka ◽  
...  
Keyword(s):  
Infarct Size ◽  
Rat Heart ◽  
Ischemia Reperfusion ◽  
Protein S ◽  
Left Ventricular ◽  
Isolated Rat Heart ◽  
Diabetic Rat ◽  
Lv Function ◽  
Oxide Synthase

Although expression of inducible nitric oxide synthase (iNOS) and oxidative stress are increased in diabetic (DM) hearts, the role of iNOS uncoupling in ischemia/reperfusion (IR) injury remains unknown. Because iNOS-derived NO is known to play a crucial role in cardioprotection against IR injury in non-DM hearts, we hypothesized that iNOS uncoupling may compromise tolerance to IR injury in the DM heart by decreasing the bioavailability of NO. The expression and activity of iNOS but not n/eNOS were increased in the streptozotocin-induced DM rat heart. Under Langendorff perfusion, superoxide generation as evaluated by dihydroethidium accumulation in the nucleus was significantly increased in cardiomyocytes of the DM heart, but it was inhibited by treatment with the NOS co-factor tetrahydrobiopterin (BH4; 10 μM) or an iNOS selective inhibitor 1400W (10 μM). BH4 increased NOx, a marker of NO bioavailability, and cGMP in the DM heart. The increase in cGMP by BH4 was abrogated by co-treatment with 1400W or a NO-sensitive guanylyl cyclase inhibitor ODQ (10 μM). BH4 significantly decreased nitrotyrosin formation but increased protein S -nitrosylation in the DM heart. The increase in protein S -nitrosylation by BH4 was abolished by co-treatment with a thiol reducing agent dithiothreitol (DTT; 5 mM). The isolated rat heart was subjected to 30 min global ischemia followed by 120 min reperfusion. Post-ischemic recovery of left ventricular (LV) function and infarct size was comparable between the non-DM and the DM hearts. Pre-ischemic treatment with BH4 significantly improved post-ischemic LV function and reduced infarct size only in the DM heart. Co-treatment with BH4 and 1400W, ODQ, or DTT had no significant effect on post-ischemic LV function and infarct size in the non-DM heart. However, co-treatment with BH4 and 1400W or DTT but not ODQ abolished BH4-induced improvement of post-ischemic LV function and reduction of infarct size in the DM heart. These results suggest that inhibition of iNOS uncoupling by BH4 confers cardioprotection against IR injury in the streptozotocin-induced DM rat heart by increasing the bioavailability of NO and this cardioprotective effect is mediated by protein S -nitrosylation but not cGMP.

scholarly journals Effect of vitamin C and l-NMMA on the inotropic response to dobutamine in patients with heart failure

2005 ◽  
Vol 289 (6) ◽  
pp. H2424-H2428 ◽  
Author(s):  
Susanna Mak ◽  
Christopher B. Overgaard ◽  
Gary E. Newton
Keyword(s):  
Heart Failure ◽  
Vitamin C ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Lv Function ◽  
Inotropic Response ◽  
Positive Rate ◽  
Endogenous Nitric Oxide ◽  
Inotropic Responses ◽  
Positive Effect

The positive effect of vitamin C on left ventricular (LV) inotropic responses to dobutamine, observed in patients with preserved LV function, is lost in heart failure (HF). We tested the hypothesis that in HF, endogenous nitric oxide (NO) opposes the positive effect of vitamin C on adrenergically stimulated contractility by examining the effects of vitamin C on dobutamine responses during NO synthase inhibition. In 11 HF patients, a micromanometer-tipped catheter was inserted into the LV and an infusion catheter was positioned in the left main coronary artery. The peak positive rate of change of LV pressure (LV +dP/d t) was measured in response to intravenous dobutamine (Dob-1). After recontrol, intracoronary NG-monomethyl-l-arginine (l-NMMA) was infused before reinfusion of dobutamine (l-NMMA + Dob-2). Finally, intracoronary vitamin C was infused in addition to intracoronary l-NMMA and dobutamine (l-NMMA + Dob-2 + vitamin C). Intracoronary l-NMMA alone had no effect on LV +dP/d t. After a stable inotropic response to intracoronary l-NMMA and dobutamine was established, the addition of intracoronary vitamin C resulted in a modest but significant increase in LV +dP/d t. The change in LV +dP/d t in response to dobutamine alone was 25 ± 5%, with intracoronary l-NMMA, 27 ± 6%, and with intracoronary l-NMMA plus vitamin C, 37 ± 5% ( P < 0.05 vs. Dob-1 and l-NMMA + Dob-2). These findings demonstrate that an interaction between endogenous NO and redox environment exists and exerts some influence on stimulated contractility in HF.

Mechanism of mitral leaflet excursion

1995 ◽  
Vol 269 (6) ◽  
pp. H2100-H2108 ◽  
Author(s):  
J. M. Dent ◽  
W. D. Spotnitz ◽  
S. P. Nolan ◽  
A. R. Jayaweera ◽  
W. P. Glasheen ◽  
...  
Keyword(s):  
Pressure Gradient ◽  
Systolic Function ◽  
Systolic Dysfunction ◽  
Correlation Coefficients ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Lv Function ◽  
Mitral Leaflet ◽  
Rate Of Increase ◽  
Lv Systolic Function

The factors that influence the extent of mitral leaflet opening (MLO) and closure (MLC) have not been defined. We hypothesized that left ventricular (LV) systolic function determines the rate of increase of the early diastolic left atrial (LA)-LV pressure gradient, which is responsible for the extent of MLO, and also the rate of change of the early systolic LV-LA pressure gradient, which determines the degree of MLC. Accordingly, global LV function was changed by altering left main coronary artery flow with LA pressure held relatively constant. LV end-systolic dimension and peak positive LV rate of pressure development (dP/dt) correlated best with the degrees of MLO and MLC, with average correlation coefficients of 0.88 and 0.68, and 0.86 and 0.72, respectively. Although transsecting the submitral apparatus resulted in flailing of the mitral leaflets during normal LV systolic function, the extents of MLO and MLC during LV systolic dysfunction were still influenced by LV systolic function. It is concluded that LV systolic function determines the extent (both opening and closure) of mitral leaflet excursion.

A114 The muscle fiber length changes in human gastrocnemius while treadmill walking revealed as ultrasonography

2007 ◽  
Vol 2007.18 (0) ◽  
pp. 27-28
Author(s):  
Naoto SASAGAWA ◽  
Tasuku MIYOSHI ◽  
Hiroyuki KOYAMA ◽  
Takashi KOMEDA ◽  
Shin-Ichiro YAMAMOTO
Keyword(s):  
Muscle Fiber ◽  
Fiber Length ◽  
Treadmill Walking ◽  
Length Changes

Sympathetic augmentation of cardiac function in developing hypertension in conscious dogs

1988 ◽  
Vol 255 (6) ◽  
pp. H1525-H1534 ◽  
Author(s):  
R. J. Gelpi ◽  
L. Hittinger ◽  
A. M. Fujii ◽  
V. M. Crocker ◽  
I. Mirsky ◽  
...  
Keyword(s):  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Wall Stress ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Conscious Dogs ◽  
Lv Function ◽  
Adrenergic Blockade ◽  
Mean Velocity ◽  
Major Mechanism

To determine the alterations in left ventricular (LV) function and the mechanisms involved that occur during the development of perinephritic hypertension, dogs were instrumented with a miniature LV pressure transducer, aortic and left atrial catheters, and ultrasonic crystals to measure LV diameter in the short and long axes and wall thickness. At 2 wk after initiation of perinephritic hypertension, increases (P less than 0.05) were observed in LV systolic pressure, LV end-diastolic pressure, both short- and long-axis end-diastolic diameters, calculated LV end-diastolic volume, stroke volume, global average LV systolic wall stress, first derivative of LV pressure (LV dP/dt), and ejection fraction, whereas mean velocity of circumferential fiber shortening (Vcf) and rate of change of LV short-axis diameter (LV dD/dt) rose but not significantly. At three levels of matched preload and afterload induced by the administration of graded doses of phenylephrine, Vcf, LV dD/dt, and LV dP/dt increased in hypertension compared with the same levels of preload and afterload before hypertension. When the loading conditions in the normotensive and hypertensive dogs were matched, either after ganglionic blockade or beta-adrenergic blockade, both isovolumic and ejection-phase indexes of LV function remained similar before and after hypertension. Thus we conclude that 1) LV function in intact, conscious dogs with early hypertension is enhanced, and 2) the major mechanism for the increase in LV function involves the sympathetic nervous system.

scholarly journals In vivo muscle force-length behavior during steady-speed hopping in tammar wallabies.

1998 ◽  
Vol 201 (11) ◽  
pp. 1681-1694 ◽  
Author(s):  
A A Biewener ◽  
D D Konieczynski ◽  
R V Baudinette
Keyword(s):  
Energy Expenditure ◽  
Muscle Fiber ◽  
Fiber Length ◽  
Strain Energy ◽  
Length Change ◽  
Metabolic Energy ◽  
Lateral Gastrocnemius ◽  
Length Changes ◽  
Tendon Force

Moderate to large macropodids can increase their speed while hopping with little or no increase in energy expenditure. This has been interpreted by some workers as resulting from elastic energy savings in their hindlimb tendons. For this to occur, the muscle fibers must transmit force to their tendons with little or no length change. To test whether this is the case, we made in vivo measurements of muscle fiber length change and tendon force in the lateral gastrocnemius (LG) and plantaris (PL) muscles of tammar wallabies Macropus eugenii as they hopped at different speeds on a treadmill. Muscle fiber length changes were less than +/-0.5 mm in the plantaris and +/-2.2 mm in the lateral gastrocnemius, representing less than 2 % of total fiber length in the plantaris and less than 6 % in the lateral gastrocnemius, with respect to resting length. The length changes of the plantaris fibers suggest that this occurred by means of elastic extension of attached cross-bridges. Much of the length change in the lateral gastrocnemius fibers occurred at low force early in the stance phase, with generally isometric behavior at higher forces. Fiber length changes did not vary significantly with increased hopping speed in either muscle (P&gt;0.05), despite a 1. 6-fold increase in muscle-tendon force between speeds of 2.5 and 6.0 m s-1. Length changes of the PL fibers were only 7+/-4 % and of the LG fibers 34+/-12 % (mean +/- S.D., N=170) of the stretch calculated for their tendons, resulting in little net work by either muscle (plantaris 0.01+/-0.03 J; gastrocnemius -0.04+/-0.30 J; mean +/- s.d. ). In contrast, elastic strain energy stored in the tendons increased with increasing speed and averaged 20-fold greater than the shortening work performed by the two muscles. These results show that an increasing amount of strain energy stored within the hindlimb tendons is usefully recovered at faster steady hopping speeds, without being dissipated by increased stretch of the muscles' fibers. This finding supports the view that tendon elastic saving of energy is an important mechanism by which this species is able to hop at faster speeds with little or no increase in metabolic energy expenditure.

Urine Albumin to Creatinine Ratio and Echocardiographic Left Ventricular Structure and Function in Patients with Essential Hypertension

2011 ◽  
Vol 9 (2) ◽  
pp. 90 ◽  
Author(s):  
Rohola Hemmati ◽  
Mojgan Gharipour ◽  
Hasan Shemirani ◽  
Alireza Khosravi ◽  
Elham Khosravi ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Peak Velocity ◽  
Left Ventricular ◽  
Lv Function ◽  
Creatinine Ratio ◽  
Uncomplicated Hypertension ◽  
Urine Albumin ◽  
Lv Dysfunction ◽  
Mitral Annulus Velocity ◽  
Lv Mass

Background:Appearance of microalbuminuria, particularly in patients with hypertension, might be associated with a higher prevalence of left ventricular (LV) dysfunction and geometric abnormalities. This study was undertaken to determine whether high urine albumin to creatinine ratio (UACR) as a sensitive marker for microalbuminuria can be associated with LV hypertrophy (LVH) and systolic and diastolic LV dysfunction.Methods:The study population consisted of 125 consecutive patients with essential uncomplicated hypertension. Urine albumin and creatinine concentration was determined by standard methods. LVH was defined as a LV mass index >100 g/m2 of body surface area in women and >130 g/m2 in men. Echocardiographic LV systolic and diastolic parameters were measured.Results:The prevalence of microalbuminuria in patients with essential hypertension was 5.6 %. UACR was significantly no different in patients with LVH than in patients with normal LV geometry (21.26 ± 31.55 versus 17.80 ± 24.52 mg/mmol). No significant correlation was found between UACR measurement and systolic and diastolic function parameters, including early to late diastolic peak velocity (E/A) ratio (R=-0.192, p=0.038), early diastolic peak velocity to early mitral annulus velocity (E/E') ratio (R=-0.025, p=0.794), LV ejection fraction (R=0.008, p=0.929), and LV mass (R=-0.132, p=0.154). According to the receiver operator characteristic (ROC) curve analysis, UACR measurement was not an acceptable indicator of LVH with areas under the ROC curves 0.514 (95 % confidence interval 0.394–0.634). The optimal cut-off value for UACR for predicting LVH was identified at 9.4, yielding a sensitivity of 51.6 % and a specificity of 48.3 %.Conclusion:In patients with uncomplicated essential hypertension, abnormal systolic and diastolic LV function and geometry cannot be effectively predicted by the appearance of microalbuminuria.

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