Effects of cardiac glycosides on myocardial function and energetics in conscious dogs

1994 ◽  
Vol 267 (5) ◽  
pp. H2042-H2049 ◽  
Author(s):  
J. C. Lucke ◽  
J. R. Elbeery ◽  
T. C. Koutlas ◽  
S. A. Gall ◽  
T. A. D'Amico ◽  
...  
Keyword(s):  
Energy Transfer ◽  
Coronary Sinus ◽  
Systolic Function ◽  
Mechanical Energy ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Stroke Work ◽  
O2 Consumption ◽  
End Diastolic Volume ◽  
Total Mechanical Energy

The physiological effects of intravenous ouabain on left ventricular (LV) systolic function and metabolic-to-mechanical energy transfer were examined in eight conscious dogs. LV pressure and volume were measured using micromanometers and ultrasonic dimension transducers during transient vena caval occlusions under control conditions and after increasing doses of ouabain. Doppler coronary flow and coronary sinus O2 saturations were used to determine arterial-to-coronary sinus O2 content difference and thereby to calculate LV O2 consumption; total mechanical energy was computed as the sum of LV stroke work and the product of end-diastolic volume and LV mean ejection pressure, neglecting LV unstressed cavitary volume. The slope (10(4) erg/ml) of the stroke work vs. end-diastolic volume relationship increased progressively with rising doses of ouabain from 7.0 +/- 1.6 at control to 9.6 +/- 1.7 after ouabain 0.75 mg (P = 0.0002). Regression analysis of LV O2 consumption (mW/cm3) vs. total mechanical energy (mW/cm3) yielded a linear relationship that did not change with 0.75 mg of ouabain (P > 0.4). These data indicate that ouabain possesses a significant positive inotropic effect on the intact left ventricle without a change in energy transfer efficiency or O2 wasting.

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.

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.

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 O2 consumption and pressure-volume area in puppies

1987 ◽  
Vol 253 (4) ◽  
pp. H770-H776 ◽  
Author(s):  
H. Suga ◽  
O. Yamada ◽  
Y. Goto ◽  
Y. Igarashi ◽  
Y. Yasumura ◽  
...  
Keyword(s):  
Mechanical Energy ◽  
Regression Line ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
O2 Consumption ◽  
Ventricular Contraction ◽  
Myocardial Mechanics ◽  
Contractile State ◽  
Total Mechanical Energy ◽  
Heart Size

We studied the relation between O2 consumption (VO2) and systolic pressure-volume (PV) area (PVA) in the left ventricles of eight puppies (2-4 mo old). PVA is the area circumscribed by the end-systolic and end-diastolic PV curves and systolic PV trajectory. We assumed PVA to represent the total mechanical energy generated by ventricular contraction. We produced isovolumic contractions at different volumes in the left ventricles isolated and cross-circulated with adult dogs. VO2 closely correlated with PVA in each of control contractile state, an enhanced contractile state with epinephrine, and a depressed contractile state with propranolol in each heart. The slope of the regression line of VO2 on PVA was not significantly affected by epinephrine and propranolol. The regression line shifted upward with epinephrine and downward with propranolol. These characteristics of the puppy's VO2-PVA relation were comparable to those of the adult dog. These results suggest that similar relations hold between myocardial mechanics and energetics in both the puppy and adult dog despite the differences in the heart size and contractile properties.

O2 consumption of dog heart under decreased coronary perfusion and propranolol

1988 ◽  
Vol 254 (2) ◽  
pp. H292-H303 ◽  
Author(s):  
H. Suga ◽  
Y. Goto ◽  
Y. Yasumura ◽  
T. Nozawa ◽  
S. Futaki ◽  
...  
Keyword(s):  
Mechanical Energy ◽  
Systolic Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
O2 Consumption ◽  
Ventricular Contractility ◽  
Total Mechanical Energy ◽  
The Difference ◽  
Different Response

We compared the effects of decreased coronary perfusion pressure (CP) and propranolol on the relation between left ventricular O2 consumption (VO2) and systolic pressure-volume area (PVA). PVA represents total mechanical energy generated by contraction and is the area under the end-systolic pressure-volume (PV) line and systolic PV trajectory. In excised cross-circulated dog hearts, a decrease in CP from 82 (mean) to 51 mmHg decreased ventricular contractility index Emax (slope of end-systolic PV relation) by 17% (P less than 0.05) and slightly (P less than 0.05 in 3 of 11 hearts) lowered the VO2-PVA relation in a parallel fashion. A further decrease in CP to 32 mmHg decreased Emax by 56% (P less than 0.05) and considerably (P less than 0.05) lowered the VO2-PVA relation by decreasing both the VO2-axis intercept by 26% (P less than 0.05) and the slope by 24% (P less than 0.05) from control. Propranolol decreased Emax by 48% (P less than 0.05) and the VO2-axis intercept by 25% (P less than 0.05) without changing the slope (P greater than 0.05). We attributed the different response of the VO2-PVA relation to the difference of the coronary O2 supply-demand balance between decreased CP and propranolol.

Physiology of cardiac tamponade and paradoxical pulse in conscious dogs

1993 ◽  
Vol 265 (6) ◽  
pp. H1996-H2008 ◽  
Author(s):  
M. A. Savitt ◽  
G. S. Tyson ◽  
J. R. Elbeery ◽  
C. H. Owen ◽  
J. W. Davis ◽  
...  
Keyword(s):  
Cardiac Tamponade ◽  
Interventricular Septum ◽  
Systolic Pressure ◽  
Physiological Mechanism ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Stroke Work ◽  
End Diastolic Volume ◽  
Lv Dysfunction ◽  
Volume Curve

The physiological mechanism of paradoxical pulse in cardiac tamponade remains controversial. In eight conscious dogs with intact pericardia, ultrasonic dimension transducers assessed biventricular geometry and volumes, while micromanometers measured right ventricular (RV), left ventricular (LV), pleural, and pericardial pressures. With normal inspiration, peak LV pressure fell by 7.7 +/- 1.3 mmHg at control and by 20.3 +/- 3.7 mmHg during tamponade (P < 0.001), consistent with the development of paradoxical pulse. At peak inspiration during tamponade, RV filling increased, the interventricular septum shifted leftward, transeptal pressure became negative, and LV septal arc length (l theta) became smaller than its respective unpreloaded value at maximal vena caval occlusion (l(o)). Analysis of stroke work (SW)-end-diastolic volume (EDV) and end-systolic pressure-volume coordinates at peak inspiration during tamponade revealed that end-systolic pressure was 19.1 +/- 10.2 mmHg below the baseline end-systolic pressure-volume curve (P < 0.01), and SW was 24.2 +/- 8.8% below the baseline SW-EDV curve (P < 0.01), indicating transient inspiratory LV dysfunction. It is proposed that inspiratory leftward interventricular septal shifting at low LV EDV during tamponade completely unloads the septum (l theta < l o), eliminates the septal contribution to global LV SW, results in transient inspiratory LV dysfunction, and contributes to the phenomenon of paradoxical pulse.

Mechanical determinants of myocardial oxygen consumption in conscious dogs

1995 ◽  
Vol 269 (2) ◽  
pp. H609-H620 ◽  
Author(s):  
J. R. Elbeery ◽  
J. C. Lucke ◽  
M. P. Feneley ◽  
G. W. Maier ◽  
C. H. Owen ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Myocardial Oxygen Consumption ◽  
Virtual Work ◽  
Mechanical Energy ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Stroke Work ◽  
External Energy ◽  
Work Model

A new practical descriptor of metabolic to mechanical myocardial energy transfer (MET), termed the virtual work model, was evaluated in 32 conscious dogs and in 8 isolated canine hearts. An index of total mechanical energy expenditure (TME) was calculated as the sum of external energy (stroke work) and an internal energy index of heat (left ventricular end-diastolic volume times left ventricular mean ejection pressure). Physiological comparison of TME (x-axis) and myocardial oxygen consumption (MVO2; y-axis) yielded highly linear MET relationships (mean r = 0.93 +/- 0.07), with an average slope of 0.86 +/- 0.39 (SD) and a y-intercept of 9.1 +/- 6.4 mW/ml myocardium. The linear MVO2-TME relationship did not vary under steady-state vs. dynamic vena caval occlusion, increased heart rate, increased afterload, or increased inotropic state with calcium infusion. Compared with five other indexes of myocardial energetics, the virtual work model of MET was the most linear, the most practical in not requiring determination of the end-systolic pressure-volume relationship, and the most accurate predictor of MVO2 under normal and altered hemodynamic conditions.

scholarly journals Prognostic value of NT-proBNP for myocardial recovery in peripartum cardiomyopathy (PPCM)

2021 ◽  
Author(s):  
J. Hoevelmann ◽  
E. Muller ◽  
F. Azibani ◽  
S. Kraus ◽  
J. Cirota ◽  
...  
Keyword(s):  
Prognostic Value ◽  
Systolic Function ◽  
Point Of Care ◽  
Diagnostic Value ◽  
Left Ventricular ◽  
Peripartum Cardiomyopathy ◽  
Lv Function ◽  
Myocardial Recovery ◽  
End Diastolic Volume

Abstract Introduction Peripartum cardiomyopathy (PPCM) is an important cause of pregnancy-associated heart failure worldwide. Although a significant number of women recover their left ventricular (LV) function within 12 months, some remain with persistently reduced systolic function. Methods Knowledge gaps exist on predictors of myocardial recovery in PPCM. N-terminal pro-brain natriuretic peptide (NT-proBNP) is the only clinically established biomarker with diagnostic value in PPCM. We aimed to establish whether NT-proBNP could serve as a predictor of LV recovery in PPCM, as measured by LV end-diastolic volume (LVEDD) and LV ejection fraction (LVEF). Results This study of 35 women with PPCM (mean age 30.0 ± 5.9 years) had a median NT-proBNP of 834.7 pg/ml (IQR 571.2–1840.5) at baseline. Within the first year of follow-up, 51.4% of the cohort recovered their LV dimensions (LVEDD < 55 mm) and systolic function (LVEF > 50%). Women without LV recovery presented with higher NT-proBNP at baseline. Multivariable regression analyses demonstrated that NT-proBNP of ≥ 900 pg/ml at the time of diagnosis was predictive of failure to recover LVEDD (OR 0.22, 95% CI 0.05–0.95, P = 0.043) or LVEF (OR 0.20 [95% CI 0.04–0.89], p = 0.035) at follow-up. Conclusions We have demonstrated that NT-proBNP has a prognostic value in predicting LV recovery of patients with PPCM. Patients with NT-proBNP of ≥ 900 pg/ml were less likely to show any improvement in LVEF or LVEDD. Our findings have implications for clinical practice as patients with higher NT-proBNP might require more aggressive therapy and more intensive follow-up. Point-of-care NT-proBNP for diagnosis and risk stratification warrants further investigation.

alpha-Adrenergic control of oxygen delivery to myocardium during exercise in conscious dogs

1982 ◽  
Vol 242 (5) ◽  
pp. H805-H809 ◽  
Author(s):  
G. R. Heyndrickx ◽  
P. Muylaert ◽  
J. L. Pannier
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Oxygen Delivery ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Adrenergic Blockade ◽  
Adrenergic Control

alpha-Adrenergic control of the oxygen delivery to the myocardium during exercise was investigated in eight conscious dogs instrumented for chronic measurements of coronary blood flow, left ventricular (LV) pressure, aortic blood pressure, and heart rate and sampling of arterial and coronary sinus blood. After alpha-adrenergic receptor blockade a standard exercise load elicited a significantly greater increase in heart rate, rate of change of LV pressure (LV dP/dt), LV dP/dt/P, and coronary blood flow than was elicited in the unblocked state. In contrast to the response pattern during control exercise, there was no significant change in coronary sinus oxygen tension (PO2), myocardial arteriovenous oxygen difference, and myocardial oxygen delivery-to-oxygen consumption ratio. It is concluded that the normal relationship between myocardial oxygen supply and oxygen demand is modified during exercise after alpha-adrenergic blockade, whereby oxygen delivery is better matched to oxygen consumption. These results indicate that the increase in coronary blood flow and oxygen delivery to the myocardium during normal exercise is limited by alpha-adrenergic vasoconstriction.

Cardiac dysfunction in mice lacking cytochrome-c oxidase subunit VIaH

2002 ◽  
Vol 282 (2) ◽  
pp. H726-H733 ◽  
Author(s):  
Nina B. Radford ◽  
Bang Wan ◽  
Angela Richman ◽  
Lidia S. Szczepaniak ◽  
Jia-Ling Li ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Cardiac Dysfunction ◽  
Mechanical Performance ◽  
Left Ventricular ◽  
Mutant Mice ◽  
Stroke Work ◽  
Wild Type ◽  
Oxidase Subunit ◽  
End Diastolic Volume

Cytochrome -c oxidase subunit VIaH (COXVIaH) has been implicated in the modulation of COX activity. A gene-targeting strategy was undertaken to generate mice that lacked COXVIaH to determine its role in regulation of oxidative energy production and mechanical performance in cardiac muscle. Total COX activity was decreased in hearts from mutant mice, which appears to be a consequence of altered assembly of the holoenzyme COX. However, total myocardial ATP was not significantly different in wild-type and mutant mice. Myocardial performance was examined using the isolated working heart preparation. As left atrial filling pressure increased, hearts from mutant mice were unable to generate equivalent stroke work compared with hearts from wild-type mice. Direct measurement of left ventricular end-diastolic volume using magnetic resonance imaging revealed that cardiac dysfunction was a consequence of impaired ventricular filling or diastolic dysfunction. These findings suggest that a genetic deficiency of COXVIaH has a measurable impact on myocardial diastolic performance despite the presence of normal cellular ATP levels.

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