scholarly journals A structure-function analysis of the left ventricle

2016 ◽  
Vol 121 (4) ◽  
pp. 900-909 ◽  
Author(s):  
Edward P. Snelling ◽  
Roger S. Seymour ◽  
J. E. F. Green ◽  
Leith C. R. Meyer ◽  
Andrea Fuller ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Structure Function ◽  
Function Analysis ◽  
Left Ventricular ◽  
Work Rate ◽  
Ovis Aries ◽  
Capra Hircus ◽  
Heavy Exercise ◽  
Tension Development ◽  
Arterial Blood

This study presents a structure-function analysis of the mammalian left ventricle and examines the performance of the cardiac capillary network, mitochondria, and myofibrils at rest and during simulated heavy exercise. Left ventricular external mechanical work rate was calculated from cardiac output and systemic mean arterial blood pressure in resting sheep ( Ovis aries; n = 4) and goats ( Capra hircus; n = 4) under mild sedation, followed by perfusion-fixation of the left ventricle and quantification of the cardiac capillary-tissue geometry and cardiomyocyte ultrastructure. The investigation was then extended to heavy exercise by increasing cardiac work according to published hemodynamics of sheep and goats performing sustained treadmill exercise. Left ventricular work rate averaged 0.017 W/cm3 of tissue at rest and was estimated to increase to ∼0.060 W/cm3 during heavy exercise. According to an oxygen transport model we applied to the left ventricular tissue, we predicted that oxygen consumption increases from 195 nmol O2·s−1·cm−3 of tissue at rest to ∼600 nmol O2·s−1·cm−3 during heavy exercise, which is within 90% of the oxygen demand rate and consistent with work remaining predominantly aerobic. Mitochondria represent 21-22% of cardiomyocyte volume and consume oxygen at a rate of 1,150 nmol O2·s−1·cm−3 of mitochondria at rest and ∼3,600 nmol O2·s−1·cm−3 during heavy exercise, which is within 80% of maximum in vitro rates and consistent with mitochondria operating near their functional limits. Myofibrils represent 65–66% of cardiomyocyte volume, and according to a Laplacian model of the left ventricular chamber, generate peak fiber tensions in the range of 50 to 70 kPa at rest and during heavy exercise, which is less than maximum tension of isolated cardiac tissue (120–140 kPa) and is explained by an apparent reserve capacity for tension development built into the left ventricle.

Vascular and metabolic response to cycle exercise in sedentary humans: effect of age

2003 ◽  
Vol 284 (4) ◽  
pp. H1251-H1259 ◽  
Author(s):  
J. G. Poole ◽  
L. Lawrenson ◽  
J. Kim ◽  
C. Brown ◽  
R. S. Richardson
Keyword(s):  
Metabolic Response ◽  
Cycle Ergometry ◽  
Work Rate ◽  
Heavy Exercise ◽  
Cycle Exercise ◽  
Arterial Blood ◽  
Young Subjects ◽  
Effect Of Age ◽  
Maximal Effort ◽  
Sedentary Subjects

We measured leg blood flow (LBF), drew arterial-venous (A-V) blood samples, and calculated muscle O2 consumption (V˙o 2) during incremental cycle ergometry exercise [15, 30, and 99 W and maximal effort (maximal work rate, WRmax)] in nine sedentary young (20 ± 1 yr) and nine sedentary old (70 ± 2 yr) males. LBF was preserved in the old subjects at 15 and 30 W. However, at 99 W and at WRmax, leg vascular conductance was attenuated because of a reduced LBF (young: 4.1 ± 0.2 l/min and old: 3.1 ± 0.3 l/min) and an elevated mean arterial blood pressure (young: 112 ± 3 mmHg and old: 132 ± 3 mmHg) in the old subjects. Leg A-V O2 difference changed little with increasing WR in the old group but was elevated compared with the young subjects. Muscle maximal V˙o 2 and cycle WRmax were significantly lower in the old subjects (young: 0.8 ± 0.05 l/min and 193 ± 7 W; old: 0.5 ± 0.03 l/min and 117 ± 10 W). The submaximally unchanged and maximally reduced cardiac output associated with aging coupled with its potential maldistiribution are candidates for the limited LBF during moderate to heavy exercise in older sedentary subjects.

Peripheral vascular effects of nitroglycerin in a conscious rat model of heart failure

1982 ◽  
Vol 243 (6) ◽  
pp. H974-H981
Author(s):  
S. F. Flaim
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Diastolic Pressure ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Arterial Blood Flow ◽  
Vascular Effects ◽  
Conscious Rat ◽  
Arterial Blood ◽  
Caudal Artery

The effects of intravenous nitroglycerin (NG; 2, 8, 32 micrograms/kg) on cardiocirculatory dynamics were evaluated in control normal (C) and chronically volume-overloaded [high-output heart failure (aortocaval fistula), HCO] conscious rats. Pressures were recorded in the left ventricle, the caudal artery, and the right atrium. Regional blood flows were determined by radioactive microsphere injection into the left ventricle with reference sampling from the caudal artery. Cardiac output (CO) was 289 ml . min-1 . kg in C and did not change with NG; however, in HCO systemic CO was decreased 31, 23, and 23% by NG from 350 ml . min-1 . kg. In both groups left ventricular end-diastolic pressure was reduced (C, 8.4–5.0; HCO, 19.8–12.7 mmHg); however, central venous pressure was reduced only in C (1.2–0.3 mmHg). During NG primarily at 2 and 8 micrograms/kg, arterial blood flow was lower and vascular resistance was higher in HCO compared with C in the following regions: kidney, ileum, jejunum, skin, heart, spleen, stomach, and testes, whereas no major differences were noted in the cerebellum, cerebrum, liver, or skeletal muscle. Thus acute NG infusion is a more potent regional vasodilator in C than in HCO. It is suggested that this difference is related to a more powerful NG-induced sympathetic reflex activation in the HCO group, which strongly attenuates the direct vasodilator effect of NG that was apparent in C.

Mechanics of Active Contraction in Cardiac Muscle: Part II—Cylindrical Models of the Systolic Left Ventricle

1993 ◽  
Vol 115 (1) ◽  
pp. 82-90 ◽  
Author(s):  
J. M. Guccione ◽  
L. K. Waldman ◽  
A. D. McCulloch
Keyword(s):  
Left Ventricle ◽  
Cardiac Muscle ◽  
Sarcomere Length ◽  
Left Ventricular ◽  
Isometric Tension ◽  
Fiber Stress ◽  
Tension Development ◽  
Deactivation Model ◽  
Biomechanical Engineering ◽  
Asme Journal

Models of contracting ventricular myocardium were used to study the effects of different assumptions concerning active tension development on the distributions of stress and strain in the equatorial region of the intact left ventricle during systole. Three models of cardiac muscle contraction were incorporated in a cylindrical model for passive left ventricular mechanics developed previously [Guccione et al. ASME Journal of Biomechanical Engineering, Vol. 113, pp. 42-55 (1991)]. Systolic sarcomere length and fiber stresses predicted by a general “deactivation” model of cardiac contraction [Guccione and McCulloch, ASME Journal of Biomechanical Engineering, Vol. 115, pp. 72-81 (1993)] were compared with those computed using two less complex models of active fiber stress: In a time-varying “elastance” model, isometric tension development was computed from a function of peak intracellular calcium concentration, time after contraction onset and sarcomere length; a “Hill” model was formulated by scaling this isometric tension using the force-velocity relation derived from the deactivation model. For the same calcium ion concentration, the sarcomeres in the deactivation model shortened approximately 0.1 μm less throughout the wall at end-systole than those in the other models. Thus, muscle fibers in the intact ventricle are subjected to rapid length changes that cause deactivation during the ejection phase of a normal cardiac cycle. The deactivation model predicted rather uniform transmural profiles of fiber stress and cross-fiber stress distributions that were almost identical to those of the radial component. These three components were indistinguishable from the principal stresses. Transmural strain distributions predicted at end-systole by the deactivation model agreed closely with experimental measurements from the anterior free wall of the canine left ventricle.

scholarly journals Effect of Angiotensin II on the Left Ventricular Function in a Near-Term Fetal Sheep with Metabolic Acidemia

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Ganesh Acharya ◽  
James C. Huhta ◽  
Mervi Haapsamo ◽  
Ole-Jakob How ◽  
Tiina Erkinaro ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Left Ventricle ◽  
Venous Pressure ◽  
Tissue Doppler ◽  
Left Ventricular ◽  
Doppler Imaging ◽  
Lv Function ◽  
Fetal Sheep ◽  
Arterial Blood ◽  
Near Term

We tested the hypothesis that, in acute metabolic acidemia, the fetal left ventricle (LV) has the capacity to increase its contractility in response to angiotensin II infusion. Eleven ewes and their fetuses were instrumented at 127–138/145 days of gestation. The effect of angiotensin II on fetal LV function was assessed using intraventricular pressure catheter and tissue Doppler imaging (TDI). Angiotensin II increased fetal arterial blood pressure, whereas pH and pO2decreased. The heart rate and systemic venous pressure were not affected significantly. The LV end-diastolic and end-systolic pressures, as well asdP/dtmax, increased. The TDI-derived LV longitudinal myocardial isovolumic contraction velocity and its acceleration and velocity during early filling were higher than those at baseline. The incidence of absent isovolumic relaxation velocity was greater during angiotensin II infusion. In summary, during acute metabolic acidemia, the fetal left ventricle could increase its contractility in response to inotropic stimulus even in the presence of increased afterload. The diastolic LV function parameters were altered by angiotensin II.

Sympathetic drive to liver and nonhepatic splanchnic tissue during heavy exercise

1997 ◽  
Vol 82 (4) ◽  
pp. 1244-1249 ◽  
Author(s):  
Robert H. Coker ◽  
Mahesh G. Krishna ◽  
D. Brooks Lacy ◽  
Eric J. Allen ◽  
David H. Wasserman
Keyword(s):  
Carotid Artery ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Hepatic Vein ◽  
Work Rate ◽  
Heavy Exercise ◽  
Exercise Protocol ◽  
Basal Rate ◽  
Arterial Blood ◽  
H 20

Coker, Robert H., Mahesh G. Krishna, D. Brooks Lacy, Eric J. Allen, and David H. Wasserman. Sympathetic drive to liver and nonhepatic splanchnic tissue during heavy exercise. J. Appl. Physiol. 82(4): 1244–1249, 1997.—The contribution of sympathetic drive and vascular catecholamine delivery to the splanchnic bed during heavy exercise was studied in dogs that underwent a laparotomy during which flow probes were implanted onto the portal vein and hepatic artery and catheters were inserted into the carotid artery, portal vein, and hepatic vein. At least 16 days after surgery, dogs completed a 20-min heavy exercise protocol (mean work rate of 5.7 ± 1 miles/h, 20 ± 2% grade). Arterial epinephrine (Epi) and norepinephrine (NE) increased by ∼500 and ∼900 pg/ml, respectively, after 20 min of heavy exercise. Because Epi is not released from the splanchnic bed and because Epi fractional extraction (FX) = NE FX, NE uptake by splanchnic tissue can be calculated despite simultaneous release of NE. Basal nonhepatic splanchnic (NHS) FX increased from a basal rate of 0.52 ± 0.09 to a peak of 0.64 ± 0.05 at 10 min of exercise. Hepatic Epi FX increased from a basal rate of 0.68 ± 0.10 to 0.81 ± 0.09 at 20 min of exercise. Even though NHS extraction of Epi reduced portal vein Epi levels by ∼60%, the release of NE from NHS tissue maintained portal vein NE at levels similar to those in arterial blood. NHS NE spillover increased from a basal rate of 5.7 ± 1.4 to 11.7 ± 2.8 ng ⋅ kg−1 ⋅ min−1at 20 min of exercise. Hepatic NE spillover increased from a basal rate of 5.0 ± 1.2 ng ⋅ kg−1 ⋅ min−1to a peak of 14.2 ± 2.8 ng ⋅ kg−1 ⋅ min−1at 15 min of exercise. These results show that 1) approximately two- and threefold increases in NHS and hepatic NE spillover occur during heavy exercise, demonstrating that sympathetic drive to these tissues contributes to the increase in circulating NE; 2) the high catecholamine FX by the NHS tissues results in an Epi level at the liver that is considerably lower than that in the arterial blood; and 3) circulating NE delivery to the liver is sustained despite high catecholamine FX due to simultaneous NHS NE release.

Increased left ventricular pressure attenuates the baroreflex in unanesthetized dogs

1986 ◽  
Vol 251 (1) ◽  
pp. R23-R31 ◽  
Author(s):  
M. J. Holmberg ◽  
I. H. Zucker
Keyword(s):  
Left Ventricle ◽  
Baroreflex Sensitivity ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Pulse Interval ◽  
Adrenergic Blockade ◽  
Baroreflex Control ◽  
Arterial Blood

To determine whether stimulation of left ventricular mechanoreceptors alters the baroreflex control of heart rate (HR), dogs were instrumented with a vascular occluder around the ascending aorta and appropriate instrumentation for the recording of left ventricular pressure (LVP), aortic pressure, left atrial pressure, HR, and left ventricular dP/dt. Baroreflex sensitivity (pulse interval or HR vs. aortic systolic pressure linear-regression slopes to infusions of phenylephrine or nitroprusside) was determined in the conscious state a minimum of 7 days postoperatively. After control responses were determined with both phenylephrine and nitroprusside, the experiment was repeated during inflation of the ascending aortic occluder so as to significantly raise left ventricle systolic pressure from 127.9 +/- 8.4 to 178.5 +/- 11.3 mmHg (P less than 0.01) and left ventricle end-diastolic pressure from 3.5 +/- 0.7 to 8.9 +/- 1.0 mmHg (P less than 0.01). There were no changes in mean arterial blood pressure, pulse pressure, or HR during elevation of LVP. The baroreflex sensitivity was reduced only during the infusion of nitroprusside from a control of 11.03 +/- 1.9 to 4.80 +/- 1.2 ms/mmHg (P less than 0.01) for the pulse interval relationship and from -2.51 +/- 0.53 to -1.14 +/- 0.32 beats . min-1 . mmHg-1 (P less than 0.05) for the HR relationship. Cholinergic blockade with atropine abolished the depression in the baroreflex sensitivity during nitroprusside infusion when LVP was increased. beta 1-Adrenergic blockade with metoprolol did not significantly reduce the baroreflex sensitivity during increased LVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical and Experimental Analysis of 201Thallium Uptake of the Heart

1978 ◽  
Vol 17 (04) ◽  
pp. 142-148
Author(s):  
U. Büll ◽  
S. Bürger ◽  
B. E. Strauer
Keyword(s):  
Oxygen Consumption ◽  
Left Ventricle ◽  
Muscle Mass ◽  
Myocardial Oxygen Consumption ◽  
Animal Experiments ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Ventricular Wall ◽  
Flow Measurements ◽  
Myocardial Flow

Studies were carried out in order to determine the factors influencing myocardial 201T1 uptake. A total of 158 patients was examined with regard to both 201T1 uptake and the assessment of left ventricular and coronary function (e. g. quantitative ventriculography, coronary arteriography, coronary blood flow measurements). Moreover, 42 animal experiments (closed chest cat) were performed. The results demonstrate that:1) 201T1 uptake in the normal and hypertrophied human heart is linearly correlated with the muscle mass of the left ventricle (LVMM);2) 201T1 uptake is enhanced in the inner (subendocardial) layer and is decreased in the outer (subepicardial) layer of the left ventricular wall. The 201T1 uptake of the right ventricle is 40% lower in comparison to the left ventricle;3) the basic correlation between 201T1 uptake and LVMM is influenced by alterations of both myocardial flow and myocardial oxygen consumption; and4) inotropic interventions (isoproterenol, calcium, norepinephrine) as well as coronary dilatation (dipyridamole) may considerably augment 201T1 uptake in accordance with changes in myocardial oxygen consumption and/or myocardial flow.It is concluded that myocardial 201T1 uptake is determined by multiple factors. The major determinants have been shown to include (i) muscle mass, (ii) myocardial flow and (iii) myocardial oxygen consumption. The clinical data obtained from patient groups with normal ventricular function, with coronary artery disease, with left ventricular wall motion abnormalities and with different degree of left ventricular hypertrophy are correlated with quantitated myocardial 201T1 uptake.

The Results of the Use of Angiotensin Receptor Inhibitors and Neprilisin in Secondary Functional Mitral Regurgitation in Outpatient Practice

2020 ◽  
Vol 75 (5) ◽  
pp. 514-522
Author(s):  
Alexey S. Ryazanov ◽  
Konstantin I. Kapitonov ◽  
Mariya V. Makarovskaya ◽  
Alexey A. Kudryavtsev
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Mitral Regurgitation ◽  
Effective Area ◽  
Left Ventricular ◽  
Functional Mitral Regurgitation ◽  
Angiotensin Receptor ◽  
Optimal Drug ◽  
Patients With Heart Failure ◽  
Valsartan Group

Background. Morbidity and mortality in patients with functional mitral regurgitation (FMR) remains high, however, no pharmacological therapy has been proven to be effective.Aimsto study the effect of sacubitrile/valsartan and valsartan on functional mitral regurgitation in chronic heart failure.Methods.This double-blind study randomly assigned sacubitrile/valsartan or valsartan in addition to standard drug therapy for heart failure among 100 patients with heart failure with chronic FMR (secondary to left ventricular (LV) dysfunction). The primary endpoint was a change in the effective area of the regurgitation hole during the 12-month follow-up. Secondary endpoints included changes in the volume of regurgitation, the final systolic volume of the left ventricle, the final diastolic volume of the left ventricle, and the area of incomplete closure of the mitral valves.Results.The decrease in the effective area of the regurgitation hole was significantly more pronounced in the sacubitrile/valsartan group than in the valsartan group (0.070.066against0.030.058sm2; p=0.018)in the treatment efficacy analysis, which included 100patients (100%). The regurgitation volume also significantly decreased in the sacubitrile/valsartan group compared to the valsartan group (mean difference:8.4ml; 95%CI, from 13.2 until 1.9;р=0.21). There were no significant differences between the groups regarding changes in the area ofincomplete closure of the mitral valves and LV volumes, with the exception of the index of the final LV diastolic volume (p=0.07).Conclusion.Among patients with secondary FMR, sacubitril/valsartan reduced MR more than valsartan. Thus, angiotensin receptor inhibitors and neprilysin can be considered for optimal drug treatment of patients with heart failure and FMR.

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