Acute effects of methoxamine on left ventricular-arterial coupling in streptozotocin-diabetic rats: a pressure-volume analysis

2000 ◽  
Vol 78 (5) ◽  
pp. 415-422 ◽  
Author(s):  
Ying-I Peng ◽  
Kuo-Chu Chang
Keyword(s):  
Left Ventricle ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Arterial System ◽  
Acute Effects ◽  
Energy Transmission ◽  
Arterial Elastance ◽  
Streptozotocin Diabetic Rats ◽  
Effective Arterial Elastance ◽  
Left Ventricular Arterial Coupling

We determined the acute effects of methoxamine, a specific alpha1-selective adrenoceptor agonist, on the left ventricular-arterial coupling in streptozotocin (STZ)-diabetic rats, using the end-systolic pressure-stroke volume relationships. Rats given STZ 65 mg·kg-1 iv (n = 8) were compared with untreated age-matched controls (n = 8). A high-fidelity pressure sensor and an electromagnetic flow probe measured left ventricular (LV) pressure and ascending aortic flow, respectively. Both LV end-systolic elastance ELV,ES and effective arterial elastance Ea were estimated from the pressure-ejected volume loop. The optimal afterload Qload determined by the ratio of Ea to ELV,ES was used to measure the optimality of energy transmission from the left ventricle to the arterial system. In comparison with controls, diabetic rats had decreased LV end-systolic elastance ELV,ES, at 513 ± 30 vs. 613 ± 29 mmHg·mL-1, decreased effective arterial elastance Ea, at 296 ± 20 vs. 572 ± 48 mmHg·mL-1, and decreased optimal afterload Qload, at 0.938 ± 0.007 vs. 0.985 ± 0.009. Methoxamine administration to STZ-diabetic rats significantly increased LV end-systolic elastance ELV,ES, from 513 ± 30 to 602 ± 38 mmHg·mL-1, and effective arterial elastance Ea, from 296 ± 20 to 371 ± 28 mmHg·mL-1, but did not change optimal afterload Qload. We conclude that diabetes worsens not only the contractile function of the left ventricle, but also the matching condition for the left ventricular-arterial coupling. In STZ-diabetic rats, administration of methoxamine improves the contractile status of the ventricle and arteries, but not the optimality of energy transmission from the left ventricle to the arterial system. Key words: streptozotocin-diabetic rats, left ventricular-arterial coupling, left ventricular end-systolic elastance, effective arterial elastance, optimal afterload.

Effect of exercise on left ventricular-arterial coupling assessed in the pressure-volume plane

1993 ◽  
Vol 264 (5) ◽  
pp. H1629-H1633 ◽  
Author(s):  
W. C. Little ◽  
C. P. Cheng
Keyword(s):  
Left Ventricle ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Arterial System ◽  
Adrenergic Blockade ◽  
Stroke Work ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Lv Volume ◽  
Left Ventricular Arterial Coupling

The left ventricle (LV) and arterial system are nearly optimally coupled to produce stroke work (SW) at rest. However, the effect of exercise on the coupling between the LV and arterial system has not been directly determined. We evaluated 11 dogs who were instrumented to determine LV volume from three diameters. The LV end-systolic pressure (Pes)-volume (Ves) relation was determined by transient caval occlusion at rest and while the animals ran at 5-7 mph on a treadmill. During exercise, the Pes-Ves relation was shifted toward the left and the slope [end-systolic elastance (Ees)] increased from 7.7 +/- 2.8 to 12.7 +/- 4.2 (SD) mmHg/ml (P < 0.05). The arterial end-systolic elastance (Ea), calculated as Pes divided by stroke volume, increased during exercise (8.8 +/- 3.0 to 10.9 +/- 4.7 mmHg/ml, P < 0.05). The ratio of Ees to Ea increased during exercise from 0.89 +/- 0.31 to 1.27 +/- 0.12 (P < 0.05). The portion of the pressure-volume area expressed as SW increased during exercise from 0.63 +/- 0.07 to 0.69 +/- 0.10 (P < 0.05). After adrenergic blockade, the Ees-to-Ea ratio was not significantly altered during exercise (0.90 +/- 0.24 vs. 0.83 +/- 0.15, P = NS). At rest and during exercise, both with intact reflexes and after beta-adrenergic blockade, the ratio of Ees to Ea remained within the range in which SW is > 95% of maximum. We conclude that during exercise, beta-adrenergic stimulation shifts the LV Pes-Ves relation to the left with an increased slope. This more than offsets the increase in Ea.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

scholarly journals Arterial-ventricular coupling: mechanistic insights into cardiovascular performance at rest and during exercise

2008 ◽  
Vol 105 (4) ◽  
pp. 1342-1351 ◽  
Author(s):  
Paul D. Chantler ◽  
Edward G. Lakatta ◽  
Samer S. Najjar
Keyword(s):  
Left Ventricle ◽  
Left Ventricular ◽  
The Body ◽  
Arterial System ◽  
Energetic Efficiency ◽  
Arterial Elastance ◽  
Ventricular Performance ◽  
Men And Women ◽  
Left Ventricular Chamber ◽  
Cardiovascular Performance

Understanding the performance of the left ventricle (LV) requires not only examining the properties of the LV itself, but also investigating the modulating effects of the arterial system on left ventricular performance. The interaction of the LV with the arterial system, termed arterial-ventricular coupling (EA/ELV), is a central determinant of cardiovascular performance and cardiac energetics. EA/ELV can be indexed by the ratio of effective arterial elastance (EA; a measure of the net arterial load exerted on the left ventricle) to left ventricular end-systolic elastance (ELV; a load-independent measure of left ventricular chamber performance). At rest, in healthy individuals, EA/ELV is maintained within a narrow range, which allows the cardiovascular system to optimize energetic efficiency at the expense of mechanical efficacy. During exercise, an acute mismatch between the arterial and ventricular systems occurs, due to a disproportionate increase in ELV (from an average of 4.3 to 13.2, and 4.7 to 15.5 mmHg·ml−1·m−2 in men and women, respectively) vs. EA (from an average of 2.3 to 3.2, and 2.3 to 2.9 mmHg·ml−1·m−2 in men and women, respectively), to ensure that sufficient cardiac performance is achieved to meet the increased energetic requirements of the body. As a result EA/ELV decreases from an average of 0.58 to 0.34, and 0.52 to 0.27 in men and women, respectively. In this review, we provide an overview of the concept of EA/ELV, and examine the effects of age, hypertension, and heart failure on EA/ELV and its components (EA and ELV) in men and women. We discuss these effects both at rest and during exercise and highlight the mechanistic insights that can be derived from studying EA/ELV.

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.

Improvement in cardiac dysfunction in streptozotocin-induced diabetic rats following chronic oral administration of bis(maltolato)oxovanadium(IV)

1993 ◽  
Vol 71 (3-4) ◽  
pp. 270-276 ◽  
Author(s):  
Violet G. Yuen ◽  
Chris Orvig ◽  
Katherine H. Thompson ◽  
John H. McNeill
Keyword(s):  
Blood Glucose ◽  
Heart Function ◽  
Myocardial Dysfunction ◽  
Plasma Lipid ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Diabetic Patients ◽  
Vanadium Complex ◽  
Significant Correction ◽  
Streptozotocin Diabetic Rats

Decreased cardiac function in streptozotocin-diabetic rats has been used as a model of diabetes-induced cardiomyopathy, which is a secondary complication in diabetic patients. The present study was designed to evaluate the therapeutic effect of a new organic vanadium complex, bis(maltolato)oxovanadium(IV), (BMOV), in improving heart function in streptozotocin-diabetic rats. There were four groups of male, Wistar rats: control (C), control treated (CT), diabetic (D), and diabetic treated (DT). Treatment consisted of BMOV, 0.5 mg/mL (1.8 mM) for the first 3 weeks and 0.75 mg/mL (2.4 mM) for the next 22 weeks, in the drinking water of rats allowed ad libitum access to food and water. BMOV lowered blood glucose to < 9 mM in 70% of DT animals without any increase in plasma insulin levels, and mean blood glucose and plasma lipid levels were significantly lower in DT vs. D rats. Tissue vanadium levels were measured in plasma, bone, kidney, liver, muscle, and fat of BMOV-treated rats. Plasma vanadium levels averaged 0.84 ± 0.07 μg/mL (16.8 μM) in CT rats and 0.76 ± 0.05 μg/mL (15.2 μM) in DT animals. The highest vanadium levels at termination of this chronic feeding study were in bone, 18.3 ± 3.0 μg/g (0.37 μmol/g) in CT and 26.4 ± 2.6 μg/g (0.53 μmol/g) in DT rats, with intermediate levels in kidney and liver, and low, but detectable levels in muscle and fat. There were no deaths in either the CT or DT group, and no overt signs of vanadium toxicity were present. Tissue vanadium levels were not correlated with the glucose-lowering effect. Isolated working heart parameters of left ventricular developed pressure (LVDP) and rate of pressure development (+dP/dT, and −dP/dT) indicated that BMOV treatment resulted in significant correction of the heart dysfunction associated with streptozotocin-induced diabetes in rat.Key words: bis(maltolato)oxovanadium(IV), vanadium, diabetes, streptozotocin, myocardial dysfunction.

Desflurane, Sevoflurane, and Isoflurane Impair Canine Left Ventricular-Arterial Coupling and Mechanical Efficiency

1996 ◽  
Vol 85 (2) ◽  
pp. 403-413 ◽  
Author(s):  
Douglas A. Hettrick ◽  
Paul S. Pagel ◽  
David C. Warltier
Keyword(s):  
Arterial Pressure ◽  
Myocardial Contractility ◽  
Minimum Alveolar Concentration ◽  
Systolic Pressure ◽  
Mechanical Efficiency ◽  
Left Ventricular ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Ventricular Afterload ◽  
Left Ventricular Arterial Coupling

Background The effects of desflurane, sevoflurane, and isoflurane on left ventricular-arterial coupling and mechanical efficiency were examined and compared in acutely instrumented dogs. Methods Twenty-four open-chest, barbiturate-anesthetized dogs were instrumented for measurement of aortic and left ventricular (LV) pressure (micromanometer-tipped catheter), dP/dtmax, and LV volume (conductance catheter). Myocardial contractility was assessed with the end-systolic pressure-volume relation (Ees) and preload recruitable stroke work (Msw) generated from a series of LV pressure-volume diagrams. Left ventricular-arterial coupling and mechanical efficiency were determined by the ratio of Ees to effective arterial elastance (Ea; the ratio of end-systolic arterial pressure to stroke volume) and the ratio of stroke work (SW) to pressure-volume area (PVA), respectively. Results Desflurane, sevoflurane, and isoflurane reduced heart rate, mean arterial pressure, and left ventricular systolic pressure. All three anesthetics caused similar decreases in myocardial contractility and left ventricular afterload, as indicated by reductions in Ees, Msw, and dP/dtmax and Ea, respectively. Despite causing simultaneous declines in Ees and Ea, desflurane decreased Ees/Ea (1.02 +/- 0.16 during control to 0.62 +/- 0.14 at 1.2 minimum alveolar concentration) and SW/PVA (0.51 +/- 0.04 during control to 0.43 +/- 0.05 at 1.2 minimum alveolar concentration). Similar results were observed with sevoflurane and isoflurane. Conclusions The present findings indicate that volatile anesthetics preserve optimum left ventricular-arterial coupling and efficiency at low anesthetic concentrations (&lt; 0.9 minimum alveolar concentration); however, mechanical matching of energy transfer from the left ventricle to the arterial circulation degenerates at higher end-tidal concentrations. These detrimental alterations in left ventricular-arterial coupling produced by desflurane, sevoflurane, and isoflurane contribute to reductions in overall cardiac performance observed with these agents in vivo.

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.

Cardiac adaptation of sarcomere dynamics to arterial load: a model of hypertrophy

1992 ◽  
Vol 263 (4) ◽  
pp. H1054-H1063 ◽  
Author(s):  
G. M. Drzewiecki ◽  
E. Karam ◽  
J. K. Li ◽  
A. Noordergraaf
Keyword(s):  
Left Ventricle ◽  
Element Model ◽  
Left Ventricular ◽  
Arterial System ◽  
Optimal Point ◽  
The Past ◽  
Cardiac Adaptation ◽  
Arterial Load ◽  
Myocardial O2 Consumption ◽  
Physiological Hypertrophy

In the past, the dynamics of the left ventricle were studied by its response to altered venous and arterial load for a given heart. This led researchers to propose the concept of an arterioventricular match or optimal point of function. The model of this paper reverses that idea by fixing preload and afterload while computing cardiac function due to altered left ventricular size or shape, resulting from modification of the number of parallel and series sarcounits. A mathematical model of physiological hypertrophy is introduced. Series and parallel arrangements of sarcounits constitute a cylindrical model of the left ventricle. Filling occurs from a venous reservoir with constant pressure through a valve, while ejection takes place into a three-element model of the systemic arterial system through another valve. It is found that the dynamics of the myofibrils can be matched to those of the left ventricle by choosing a ventricular shape that results in a minimum in myocardial O2 consumption (MVO2) for any constant ventricular load. A unique solution for the size of the ventricle results if the rate of MVO2 is specified. The model is able to predict correctly hypertrophy due to hypoxia and due to pressure (concentric) and volume (eccentric) overloads.

scholarly journals A ventricular-vascular coupling model in presence of aortic stenosis

2005 ◽  
Vol 288 (4) ◽  
pp. H1874-H1884 ◽  
Author(s):  
Damien Garcia ◽  
Paul J. C. Barenbrug ◽  
Philippe Pibarot ◽  
André L. A. J. Dekker ◽  
Frederik H. van der Veen ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Left Ventricle ◽  
Aortic Stenosis ◽  
Vascular System ◽  
Severe Aortic Stenosis ◽  
Left Ventricular ◽  
Arterial System ◽  
Coefficient Of Determination ◽  
Ventricular Afterload ◽  
Good Agreement

In patients with aortic stenosis, the left ventricular afterload is determined by the degree of valvular obstruction and the systemic arterial system. We developed an explicit mathematical model formulated with a limited number of independent parameters that describes the interaction among the left ventricle, an aortic stenosis, and the arterial system. This ventricular-valvular-vascular (V3) model consists of the combination of the time-varying elastance model for the left ventricle, the instantaneous transvalvular pressure-flow relationship for the aortic valve, and the three-element windkessel representation of the vascular system. The objective of this study was to validate the V3 model by using pressure-volume loop data obtained in six patients with severe aortic stenosis before and after aortic valve replacement. There was very good agreement between the estimated and the measured left ventricular and aortic pressure waveforms. The total relative error between estimated and measured pressures was on average (standard deviation) 7.5% (SD 2.3) and the equation of the corresponding regression line was y = 0.99 x − 2.36 with a coefficient of determination r2 = 0.98. There was also very good agreement between estimated and measured stroke volumes ( y = 1.03 x + 2.2, r2 = 0.96, SEE = 2.8 ml). Hence, this mathematical V3 model can be used to describe the hemodynamic interaction among the left ventricle, the aortic valve, and the systemic arterial system.

scholarly journals Acute effects of nandrolone decanoate on cardiodynamic parameters in isolated rat heart

2016 ◽  
Vol 94 (10) ◽  
pp. 1048-1057 ◽  
Author(s):  
Tamara R. Nikolic ◽  
Vladimir I. Zivkovic ◽  
Ivan M. Srejovic ◽  
Dragan S. Radovanovic ◽  
Nevena S. Jeremic ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Rat Heart ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Isolated Rat Heart ◽  
Albino Rats ◽  
Coronary Perfusion ◽  
Nandrolone Decanoate ◽  
Acute Effects ◽  
Isolated Rat

Despite worldwide use of anabolic steroids in last decades, there is still contradictory information about their acute influence on myocardium. The aim of this study was to examine the acute effects of nandrolone decanoate (ND) on cardiodynamics and coronary flow in isolated rat heart. The hearts of male Wistar albino rats (n = 48, 12 per group, age 8 weeks, body mass 180–200 g) were excised and perfused according to the Langendorff technique at gradually increased coronary perfusion pressures (40–120 cmH2O). After the control sets of experiments, the hearts in different groups were perfused with different doses of ND (1, 10, or 100 μmol/L separately). Using a sensor placed in the left ventricle, we registered maximum and minimum rate of pressure development in the left ventricle (dP/dtmax and dP/dtmin), systolic and diastolic left ventricular pressure (SLVP and DLVP), and heart rate (HR). Coronary flow (CF) was measured flowmetrically. The results clearly show the depression in cardiac function caused by higher doses of ND. The highest concentration of ND (100 μmol/L) induced the most deleterious impact on the myocardial function and perfusion of the heart (coronary circulation), which could be of clinical significance.

Sign in / Sign up

Export Citation Format

Share Document