Beneficial influence of vasoactive intestinal peptide on ventriculovascular coupling in closed-chest dogs

1992 ◽  
Vol 263 (4) ◽  
pp. H1300-H1305
Author(s):  
J. T. Colston ◽  
G. L. Freeman
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Mechanical Energy ◽  
Left Ventricular ◽  
Arterial System ◽  
Stroke Work ◽  
Vascular Effects ◽  
Arterial Elastance ◽  
End Diastolic Volume ◽  
Before And After ◽  
Effective Arterial Elastance

The effect of vasoactive intestinal peptide (VIP) on ventriculovascular coupling in the intact cardiovascular system has not been defined. We studied seven dogs chronically instrumented with left ventricular (LV) pressure manometers and three sets of diameter gauges before and after infusions of 0.02, 0.05, and 0.10 microgram.kg-1.min-1 VIP. The dogs were studied after autonomic blockade, anesthesia, and intubation, with a fixed heart rate of 160 beats/min. Contractility was assessed using LV elastance at end systole (Ees) and the slope of the stroke work-end-diastolic volume relation. The vascular influence of VIP was quantified by determining effective arterial elastance (Ea) under steady-state conditions. The overall effect on ventriculovascular coupling was assessed using the transfer of mechanical energy from LV to the arterial system (TransPVA) quantified as the percentage of pressure-volume area (PVA) expressed as stroke work. LV relaxation was measured using the time constant of LV pressure decay. The results showed that VIP increased contractility (Ees increased to 129, 156, and 181% of control; P < 0.01 for all vs. control) and decreased effective arterial elastance (Ea fell to 84, 68, and 64% of control; P < 0.0155 vs. control for the two higher doses). VIP had no consistent effects on LV relaxation. Thus, in addition to its positive ventricular effects (increased contractility), VIP has beneficial vascular effects (reduced Ea). These properties combine to improve ventriculovascular coupling, such that VIP enhances delivery of mechanical energy from the LV to the circulatory bed.

Left ventricular-arterial coupling in conscious dogs

1991 ◽  
Vol 261 (1) ◽  
pp. H70-H76 ◽  
Author(s):  
W. C. Little ◽  
C. P. Cheng
Keyword(s):  
Stroke Volume ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Arterial System ◽  
Conscious Dogs ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Inotropic State ◽  
End Diastolic Volume ◽  
Wide Range

We investigated the criteria for the coupling of the left ventricle (LV) and the arterial system to maximize LV stroke work (SW) and the transformation of LV pressure-volume area (PVA) to SW. We studied eight conscious dogs that were instrumented to measure LV pressure and determine LV volume from three ultrasonically determined dimensions. The LV end-systolic pressure (PES)-volume (VES) relation was determined by caval occlusion. Its slope (EES) was compared with the arterial elastance (EA) and determined as PES per stroke volume. At rest, with intact reflexes, EES/EA was 0.96 +/- 0.20 EES/EA was varied over a wide range (0.18-2.59) by the infusion of graded doses of phenylephrine and nitroprusside before and during administration of dobutamine. Maximum LV SW, at constant inotropic state and end-diastolic volume (VED), occurred when EES/EA equaled 0.99 +/- 0.15. At constant VED and contractile state, SW was within 20% of its maximum value when EES/EA was between 0.56 and 2.29. The conversion of LV PVA to SW increased as EES/EA increased. The shape of the observed relations of the SW to EES/EA and SW/PVA to EES/EA was similar to that predicted by the theoretical consideration of LV PES-VES and arterial PES-stroke volume relations. We conclude that the LV and arterial system produce maximum SW at constant VED when EES and EA are equal; however, the relation of SW to EES/EA has a broad plateau. Only when EA greatly exceeds EES does the SW fall substantially. However, the conversion of PVA to SW increases as EES/EA increases. These observations support the utility of analyzing LV-arterial coupling in the pressure-volume plane.

Relation of effective arterial elastance to arterial system properties

2002 ◽  
Vol 282 (3) ◽  
pp. H1041-H1046 ◽  
Author(s):  
Patrick Segers ◽  
Nikos Stergiopulos ◽  
Nico Westerhof
Keyword(s):  
Arterial Compliance ◽  
Linear Regression Analysis ◽  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Interaction Model ◽  
Left Ventricular ◽  
Arterial System ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Effective Arterial Elastance

Effective arterial elastance ( E a), defined as the ratio of left ventricular (LV) end-systolic pressure and stroke volume, lumps the steady and pulsatile components of the arterial load in a concise way. Combined with E max, the slope of the LV end-systolic pressure-volume relation, E a/ E max has been used to assess heart-arterial coupling. A mathematical heart-arterial interaction model was used to study the effects of changes in peripheral resistance ( R; 0.6–1.8 mmHg · ml−1 · s) and total arterial compliance (C; 0.5–2.0 ml/mmHg) covering the human pathophysiological range. E a, E a/ E max, LV stroke work, and hydraulic power were calculated for all conditions. Multiple-linear regression analysis revealed a linear relation between E a, R/ T (where T is cycle length), and 1/C: E a= −0.13 + 1.02 R/ T + 0.31/C, indicating that R/ T contributes about three times more to E a than arterial stiffness (1/C). It is demonstrated that different pathophysiological combinations of R and C may lead to the same E a and E a/ E max but can result in differences of 10% in stroke work and 50% in maximal power.

Oxygen-wasting effect of inotropy  in the “virtual work model”

1999 ◽  
Vol 276 (4) ◽  
pp. H1339-H1345 ◽  
Author(s):  
Christian Korvald ◽  
Odd P. Elvenes ◽  
Lars M. Ytrebø ◽  
Dag G. Sørlie ◽  
Truls Myrmel
Keyword(s):  
Virtual Work ◽  
Mechanical Energy ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Stroke Work ◽  
End Diastolic Volume ◽  
Chemomechanical Coupling ◽  
Total Mechanical Energy ◽  
Work Model ◽  
Inotropic Stimulation

In the “virtual work model,” left ventricular total mechanical energy (TME) is linearly related to myocardial oxygen consumption (MV˙o2). This relationship (MV˙o2-TME) is supposedly independent of inotropic stimulation, vascular loading, and heart rate variations. We reexamined the effect of inotropic stimulation (dopamine) on the metabolic to mechanical energy transfer in nine open-chest anesthetized pigs. Left ventricular mechanical energy was calculated using TME (mean ejection pressure × end-diastolic volume + stroke work), TMEW(end-diastolic volume reduced by unstressed ventricular volume), and the pressure-volume area (PVA). A highly linear relationship between MV˙o2and mechanical energy was found for all three indexes during control and dopamine runs ( r = 0.87–0.99). The slopes were unaltered by dopamine. y-Axis intercepts were (control vs. dopamine) as follows (in J ⋅ beat−1⋅ 100 mg−1; means ± SD): TME, 0.36 ± 0.12 vs. 0.61 ± 0.30 ( P< 0.02); TMEW, 0.43 ± 0.16 vs. 0.72 ± 0.32 ( P < 0.02); and PVA, 0.34 ± 0.13 vs. 0.60 ± 0.30 ( P < 0.02). We conclude that the virtual work model is dependent on inotropic stimulation and that new insight into myocardial chemomechanical coupling is not added by this concept.

Effect of vasopressin on left ventricular performance

1993 ◽  
Vol 264 (1) ◽  
pp. H53-H60
Author(s):  
C. P. Cheng ◽  
Y. Igarashi ◽  
H. S. Klopfenstein ◽  
R. J. Applegate ◽  
Z. Shihabi ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Systemic Resistance ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Ventricular Performance ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
End Systolic Volume ◽  
The Right

We assessed the effect of arginine vasopressin (AVP) on left ventricular (LV) performance in eight conscious dogs. Five minutes after AVP infusion (6 microns.kg-1 x min-1 for 2 min) the plasma AVP was elevated from 3.9 +/- 0.9 to 14.7 +/- 4.6 pg/ml (P < 0.05). With all reflexes intact, AVP caused significant increases in LV end-systolic pressure (P) (112 +/- 8 vs. 122 +/- 7 mmHg, P < 0.05) end-systolic volume (V) (30 +/- 5.8 vs. 38 +/- 7.7 ml, P < 0.05), total systemic resistance (6.2 +/- 1.8 vs. 10.6 +/- 4.0 mmHg.dl-1 x min, P < 0.01) and arterial elastance (Ea) (6.8 +/- 3.0 vs. 8.6 +/- 3.9 mmHg/ml, P < 0.05), while the heart rate (110 +/- 6 vs. 82 +/- 10 beats/min, P < 0.05) and stroke volume (16.5 +/- 4.3 vs. 14.2 +/- 3.9 ml, P < 0.05) were decreased. There was no significant change in the coronary sinus blood flow (82 +/- 19 vs. 78 +/- 22 ml/min, P = not significant). AVP decreased the slopes of LV end-systolic P-V relation (10.7 +/- 1.1 vs. 8.1 +/- 1.9 mmHg/ml, P < 0.05), the maximal first derivative of LV pressure (dP/dtmax)-end-diastolic volume (VED) relation (135.2 +/- 18.7 vs. 63.1 +/- 7.7 mmHg.s-1 x ml-1, P < 0.05), and the stroke work-VED relation (81.1 +/- 4.1 vs. 66.7 +/- 2.8 mmHg, P < 0.05) and shifted the relations to the right, indicating a depression of LV performance. A similar increase in Ea produced by methoxamine did not depress LV performance.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Endotoxin impairs cardiac hemodynamics by affecting loading conditions but not by reducing cardiac inotropism

2010 ◽  
Vol 299 (2) ◽  
pp. H492-H501 ◽  
Author(s):  
Li Jianhui ◽  
Nathalie Rosenblatt-Velin ◽  
Noureddine Loukili ◽  
Pal Pacher ◽  
François Feihl ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Myocardial Dysfunction ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Laboratory Animals ◽  
Lv Function ◽  
Stroke Work ◽  
Loading Conditions ◽  
Arterial Elastance ◽  
End Diastolic Volume

Acute myocardial dysfunction is a typical manifestation of septic shock. Experimentally, the administration of endotoxin [lipopolysacharride (LPS)] to laboratory animals is frequently used to study such dysfunction. However, a majority of studies used load-dependent indexes of cardiac function [including ejection fraction (EF) and maximal systolic pressure increment (dP/d tmax)], which do not directly explore cardiac inotropism. Therefore, we evaluated the direct effects of LPS on myocardial contractility, using left ventricular (LV) pressure-volume catheters in mice. Male BALB/c mice received an intraperitoneal injection of E. coli LPS (1, 5, 10, or 20 mg/kg). After 2, 6, or 20 h, cardiac function was analyzed in anesthetized, mechanically ventilated mice. All doses of LPS induced a significant drop in LV stroke volume and a trend toward reduced cardiac output after 6 h. Concomitantly, there was a significant decrease of LV preload (LV end-diastolic volume), with no apparent change in LV afterload (evaluated by effective arterial elastance and systemic vascular resistance). Load-dependent indexes of LV function were markedly reduced at 6 h, including EF, stroke work, and dP/d tmax. In contrast, there was no reduction of load-independent indexes of LV contractility, including end-systolic elastance (ejection phase measure of contractility) and the ratio dP/d tmax/end-diastolic volume (isovolumic phase measure of contractility), the latter showing instead a significant increase after 6 h. All changes were transient, returning to baseline values after 20 h. Therefore, the alterations of cardiac function induced by LPS are entirely due to altered loading conditions, but not to reduced contractility, which may instead be slightly increased.

Abstract P336: Changes in Arterial Pulse Wave Velocity, Effective Arterial Elastance, and Contractility in Hypertension Induced Cardiovascular Disease in Rats: Independent Prognostic Values

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Steve R Roof ◽  
Carlos del Rio
Keyword(s):  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
Pulse Wave ◽  
Left Ventricular ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Diastolic Left Ventricular Dysfunction ◽  
Wide Range ◽  
Effective Arterial Elastance ◽  
Cv Disease

Hypertension is an established comorbidity in cardiovascular (CV) disease. Changes in aortic pulse-wave velocity (PWV) have been shown to predict the longitudinal development of hypertension, its underlying vascular alterations, and associated CV risks. However, as the heart and arterial tree are coupled, it has been shown that the successful monitoring of not only CV disease progression, but of its therapies, requires the evaluation of ventriculo-arterial uncoupling and its determinants. This study aimed to establish the relationships between PWV and changes in the estimated effective arterial elastance (Ea) and/or contractility over a wide-range of hypertension-induced CV pathologies in a controlled rodent model/environment. In a large series (n = 96) of anesthetized (pentobarbital) male Sprague-Dawley rats, PWV (carotid-to-femoral), systolic pressures, contractility (preload recruitable stroke work; PRSW), and Ea were evaluated using echocardiography, invasive hemodynamics, and left ventricular (LV) pressure-volume relationships. Data were collected in healthy animals (n = 37) and those with hypertension-induced chronic systolic/diastolic left-ventricular dysfunction (n = 59) (chronic beta-adrenergic stimulation and/or renoprival). A subset of each group, were also studied under common clinical cardio/vasoactive pharmacological interventions. Disease animals had significantly (P < 0.001) higher systolic pressures (141 ± 4 vs 116 ± 4 mmHg), faster PWV (9.0 ± 0.8 vs 5.1 ± 0.5 m/s), and depressed contractility (PRSW: 39 ± 1 vs. 49 ± 1 mmHg*). Both PWV (7.6 ± 0.7 to 4.3 ± 0.4 m/s) and Ea (95 ± 10 to 63 ± 8 mmHg/mL) decreased in response to vascular therapies in the diseased animals; only PWV was reduced in healthy rats. More interestingly, over all conditions, PWV was a poor predictor of both systolic pressures (R 2 =0.00009) and Ea (R 2 = 0.024). but yet was a moderate predictor of PRSW (R 2 =0.23, P < 0.001), suggesting a contractility-dependent velocity of propagation. Taken together, these data suggest that indices of ventriculo-arterial efficacy, cardiac afterload, and peripheral arterial stiffness while all are affected by CV disease, each cannot be used to predict one another, and all provide independent prognostic information in disease.

scholarly journals Muscle metaboreflex-induced increases in effective arterial elastance: effect of heart failure

2020 ◽  
Vol 319 (1) ◽  
pp. R1-R10 ◽  
Author(s):  
Joseph Mannozzi ◽  
Jasdeep Kaur ◽  
Marty D. Spranger ◽  
Mohamed-Hussein Al-Hassan ◽  
Beruk Lessanework ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Muscle Metaboreflex ◽  
Effective Arterial Elastance

Dynamic exercise elicits robust increases in sympathetic activity in part due to muscle metaboreflex activation (MMA), a pressor response triggered by activation of skeletal muscle afferents. MMA during dynamic exercise increases arterial pressure by increasing cardiac output via increases in heart rate, ventricular contractility, and central blood volume mobilization. In heart failure, ventricular function is compromised, and MMA elicits peripheral vasoconstriction. Ventricular-vascular coupling reflects the efficiency of energy transfer from the left ventricle to the systemic circulation and is calculated as the ratio of effective arterial elastance ( Ea) to left ventricular maximal elastance ( Emax). The effect of MMA on Ea in normal subjects is unknown. Furthermore, whether muscle metaboreflex control of Ea is altered in heart failure has not been investigated. We utilized two previously published methods of evaluating Ea [end-systolic pressure/stroke volume ( EaPV)] and [heart rate × vascular resistance ( EaZ)] during rest, mild treadmill exercise, and MMA (induced via partial reductions in hindlimb blood flow imposed during exercise) in chronically instrumented conscious canines before and after induction of heart failure via rapid ventricular pacing. In healthy animals, MMA elicits significant increases in effective arterial elastance and stroke work that likely maintains ventricular-vascular coupling. In heart failure, Ea is high, and MMA-induced increases are exaggerated, which further exacerbates the already uncoupled ventricular-vascular relationship, which likely contributes to the impaired ability to raise stroke work and cardiac output during exercise in heart failure.

Left ventricular regional work from wall tension-area loop in canine heart

1986 ◽  
Vol 250 (2) ◽  
pp. H151-H158 ◽  
Author(s):  
Y. Goto ◽  
H. Suga ◽  
O. Yamada ◽  
Y. Igarashi ◽  
M. Saito ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Left Ventricular ◽  
Canine Heart ◽  
Stroke Work ◽  
Wall Tension ◽  
Pump System ◽  
End Diastolic Volume ◽  
Regional Area ◽  
Before And After ◽  
Regional Work

To quantitatively evaluate left ventricular (LV) regional work, LV pressure-volume relation and wall tension-regional area (TA) relation were analyzed in the excised cross-circulated left ventricle connected to a volume servo pump system. Wall tension was calculated using Laplace's law for a spherical model, and regional area was determined from orthogonal segment lengths measured with pairs of ultrasonic crystals. Data were obtained by changing LV end-diastolic volume or stroke volume before and after dobutamine infusion and before and after global ischemia. Regional work, assessed from the area within a TA loop during one cardiac cycle, correlated well with simultaneously obtained LV stroke work under all of the above experimental conditions (r = 0.90 +/- 0.09 to 0.97 +/- 0.02), and the linear regression line was not altered by changes in stroke volume, end-diastolic volume, or contractile state. Furthermore, measured regional work (RWm) proved to agree closely with the predicted value (RWp) calculated from LV stroke work and regional area [RWm = 0.91 RWp - 0.69 (mmHg . ml), r = 0.93]. Thus we conclude that TA relation may be useful for quantitative evaluation of regional work of the LV wall.

Effects of increased afterload on left ventricular function in closed-chest dogs

1990 ◽  
Vol 259 (2) ◽  
pp. H619-H625 ◽  
Author(s):  
G. L. Freeman
Keyword(s):  
Mechanical Response ◽  
Systolic Pressure ◽  
Circulatory System ◽  
Left Ventricular ◽  
Stroke Work ◽  
Closed Chest ◽  
End Diastolic Volume ◽  
Before And After ◽  
Pressure Development ◽  
Integrated Response

Mechanical response of the left ventricle (LV) in an intact circulatory system to steady-state increases in afterload may differ from that of an isolated LV, because secondary hemodynamic changes cannot be independently manipulated when the circulation is intact. To evaluate the integrated response of the LV in closed-chest dogs to sustained increases in afterload, six animals chronically instrumented with three orthogonal diameter gauges and LV manometers were studied after autonomic blockade and fentanyl-droperidol anesthesia. End-systolic pressure-volume (PES-VES) and stroke work end-diastolic volume (SW-EDV) relations and the relations between pressure-volume area (PVA, area bounded by PV loop and PES-VES relation) and EDV were quantified. Balloon inflation (BI) in the proximal descending aorta increased LV PES from 100.7 +/- 13.4 to 140.2 +/- 19.3 mmHg (P less than 0.002) and LVEDV from 39.1 +/- 11.3 to 43.3 +/- 12.2 ml (P less than 0.01). The slope of the PES-VES relation was not significantly changed, whereas V100, a volume intercept in the common range of pressures, was reduced from 27.5 +/- 7.3 to 23.7 +/- 6.1 ml (P less than 0.005). PVA-EDV relation was highly linear; its slope was increased after BI. Comparison of beats with matched LVEDV before and after BI showed significant increases in maximum rate of pressure development and PVA; the change in SW after BI was modest and not significant. The efficiency of energy transfer from PVA to SW (TransPVA, SW/PVA X 100) decreased from 52.5 +/- 8.6 to 42.6 +/- 6.3% (P less than 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

Abstract 2162: Mechano-energetic Superiority Of Left Ventricular Apex And Left Ventricular Septal Pacing

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Robert W Mills ◽  
Larry J Mulligan ◽  
Marion Kuiper ◽  
Arne van Hunnik ◽  
Anniek Lampert ◽  
...  
Keyword(s):  
Coronary Flow ◽  
Myocardial Oxygen Consumption ◽  
Mechanical Efficiency ◽  
Left Ventricular ◽  
Stroke Work ◽  
Conductance Catheter ◽  
Arterial Elastance ◽  
Septal Pacing ◽  
Effective Arterial Elastance ◽  
Cost Figure

Objective: Previous studies showed hemodynamic benefits over right ventricular (RV) apex pacing by left ventricular (LV) septal or LV apex pacing. We investigated whether this benefit is also reflected in mechanical efficiency. Methods: After AV-nodal ablation, dogs received 16 weeks of VDD pacing at the RV apex (RVa; n = 8), LV apex (LVa; n = 7) or LV septum (LVs; n = 8; transventricular-septal approach). After chronic pacing, LV stroke work (SW; conductance catheter) was measured, as well as relative myocardial oxygen consumption (MVO 2 , coronary flow velocity and arterial-coronary sinus O 2 difference). Baseline efficiency (SW/MVO 2 ) was assessed during implant site (IS), RVa, LVa, and RVa + LV lateral (BiV) pacing. In order to investigate the effect of pacing site udner different conditions, measurements were performed during baseline and dobutamine infusion +/− partial aortic occlusion. The O 2 cost of generating SW, corrected for end-systolic elastance and effective arterial elastance, was calculated using the Suga model of mechano-energetics. Results: RVa pacing after chronic LV pacing reduced SW/MVO 2 (Figure a ; mean ± SD, *p<0.05 vs. 1) and increased O 2 cost (Figure b ) in combination with a 12% fall in LV dP/dt-max. However, LVa or BiV pacing after chronic RVa pacing did not significantly alter efficiency, despite a 12% increase in LV dP/dt-max. LVa pacing improved efficiency over LVs and collectively over BiV pacing (p<0.05). Conclusions: Acutely, LVa pacing results in the greatest mechanical efficiency. The lack of improvement in efficiency despite increasing contractility when switching from chronic RVa pacing to LV based pacing may indicate contractile remodeling.

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