Effect of afterload resistance on end-systolic pressure-thickness relationship

1988 ◽  
Vol 254 (4) ◽  
pp. H658-H663
Author(s):  
T. Aversano ◽  
W. L. Maughan ◽  
K. Sunagawa ◽  
L. C. Becker
Keyword(s):  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Arterial System ◽  
Wall Thickening ◽  
Significant Shift ◽  
Systolic Performance ◽  
Shortening Deactivation ◽  
The Right ◽  
Systolic Wall Thickening ◽  
Contractile Performance

The influence of afterload resistance on the end-systolic pressure-thickness relationship (ESPTR) was assessed in six isolated canine left ventricles made to eject into a simulated arterial system. An increase of simulated peripheral resistance from 1.5 to 6.0 mmHg.s.ml-1 resulted in a modest but significant shift of the ESPTR upward and to the right, indicating augmented contractile performance. A relationship between the extent of systolic wall thickening and end-systolic performance was also observed: increased wall thickening impairing and decreased wall thickening enhancing end-systolic performance. The dependence of end-systolic performance on wall thickening history in this setting is consistent with shortening deactivation. This phenomenon appears to account at least in part for the observed shift in the ESPTR with altered afterload resistance.

Effect of ischemic zone size on nonischemic zone function

1990 ◽  
Vol 258 (6) ◽  
pp. H1786-H1795 ◽  
Author(s):  
T. Aversano ◽  
P. N. Marino
Keyword(s):  
Systolic Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Wall Thickening ◽  
Acute Ischemia ◽  
Coronary Perfusion ◽  
Zone Size ◽  
Reduced Pressure ◽  
Systolic Performance ◽  
Shortening Deactivation

To study the influence of ischemic zone size on function in nonischemic regions, wall thickening and the end-systolic pressure-thickness (ESPTR) relationship were measured before and during a 90-s coronary occlusion, which produced either a small or large (24 or 35% of left ventricular mass) area of ischemia. With both size ischemic areas, nonischemic zone isovolumic and ejection phase wall thickening increased during occlusion, primarily because of increased preload and, to a lesser extent, a reduced pressure component of afterload. The nonischemic region ESPTR was unchanged from preocclusion control with small ischemic mass. With larger ischemic mass, the nonischemic region ESPTR was shifted downward and to the left, indicating reduced end-systolic performance. The decline in the nonischemic zone ESPTR with large ischemic zone size was not due to reduced blood flow, shortening deactivation, reflex effects, or "tethering" but rather to the associated decline in coronary perfusion pressure. Thus the increase of nonischemic region wall thickening during acute ischemia is due to a change in ventricular loading conditions and not augmentation of contractile performance. Larger ischemic zone size can impair function in nonischemic myocardium by reducing the erectile component of end-systolic performance.

Vascular peripheral resistance and compliance in the lobster Homarus americanus

1997 ◽  
Vol 200 (3) ◽  
pp. 477-485 ◽  
Author(s):  
J Wilkens ◽  
G Davidson ◽  
M Cavey
Keyword(s):  
Striated Muscle ◽  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Body Part ◽  
Homarus Americanus ◽  
Arterial System ◽  
Flow Rates ◽  
Flow Through ◽  
Lateral Walls

The peripheral resistance to flow through each arterial bed (in actuality, the entire pathway from the heart back to the pericardial sinus) and the mechanical properties of the seven arteries leaving the lobster heart are measured and compared. Resistance is inversely proportional to artery radius and, for each pathway, the resistance falls non-linearly as flow rate increases. The resistance of the hepatic arterial system is lower than that predicted on the basis of its radius. Body-part posture and movement may affect the resistance to perfusion of that region. The total vascular resistance placed on the heart when each artery is perfused at a rate typical of in vivo flow rates is approximately 1.93 kPa s ml-1. All vessels exhibit adluminal layers of fibrils and are relatively compliant at pressures at or below heart systolic pressure. Arteries become stiffer at pressures greater than peak systolic pressure and at radii greater than twice the unpressurized radius. The dorsal abdominal artery possesses striated muscle in the lateral walls. This artery remains compliant over the entire range of hemolymph pressures expected in lobsters. These trends are illustrated when the incremental modulus of elasticity is compared among arteries. All arteries should function as Windkessels to damp the pulsatile pressures and flows generated by the heart. The dorsal abdominal artery may also actively regulate its flow.

Myocardial blood flow and function with critical coronary stenosis in exercising dogs

1982 ◽  
Vol 243 (5) ◽  
pp. H698-H707 ◽  
Author(s):  
K. P. Gallagher ◽  
G. Osakada ◽  
M. Matsuzaki ◽  
W. S. Kemper ◽  
J. Ross
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Wall Thickening ◽  
Critical Stenosis ◽  
Vasodilator Reserve ◽  
Primary Determinant ◽  
And Function ◽  
Systolic Wall Thickening ◽  
Coronary Blood Flow Velocity ◽  
Contractile Performance

Critical stenosis of coronary arteries does not alter myocardial blood flow (MBF) at rest, but eliminates hyperemia and corresponds to a degree of arterial narrowing that expends subendocardial vasodilator reserve. Because subepicardial vasodilator reserve remains with critical stenosis at rest, we tested the significance of this reserve in six exercising dogs chronically instrumented to measure MBF (microspheres), regional function (systolic wall thickening with sonomicrometers), and coronary blood flow velocity (CBFV, pulsed Doppler). Critical stenosis produced with a hydraulic occluder limited CBFV and mean MBF to the resting level during treadmill exercise, but MBF was maldistributed. Subendocardial MBF decreased 50% (P less than 0.05) and subepicardial MBF increased 104% (P less than 0.01) compared with resting control conditions, suggesting that a transmural "steal" phenomenon had occurred, with augmented MBF in the subepicardial region at the expense of subendocardial MBF. Systolic wall thickening decreased markedly from 31.5 +/- 6.8 to 9.4 +/- 2.0% (P less than 0.01) during exercise, indicating that use of subepicardial vasodilator reserve with critical stenosis had little sustaining effect on regional contractile performance. Rather, subepicardial vasodilator reserve is potentially deleterious, inasmuch as a steal effect could contribute to reduced subendocardial perfusion, the primary determinant of systolic wall thickening.

Effect of aortic constriction on the functional border zone

1987 ◽  
Vol 252 (4) ◽  
pp. H826-H835 ◽  
Author(s):  
K. P. Gallagher ◽  
X. H. Ning ◽  
R. A. Gerren ◽  
D. H. Drake ◽  
W. R. Dunham
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Coronary Occlusion ◽  
Systolic Pressure ◽  
Border Zone ◽  
Wall Thickening ◽  
Aortic Constriction ◽  
Tissue Samples ◽  
Systolic Wall Thickening ◽  
Functional Border Zone

To evaluate how aortic constriction affects nonischemic myocardium adjacent to the perfusion boundary (the "functional border zone"), we measured systolic wall thickening (dWT) with sonomicrometers in eight anesthetized, open-chest dogs. The locations of the wall thickening measurements relative to the perfusion boundary (PB) were determined with myocardial blood flow (microspheres) maps constructed from multiple, small tissue samples. In nonischemic myocardium more than 10 mm from the PB produced by circumflex coronary occlusion, dWT increased significantly from 2.57 +/- 0.62 (mean +/- SD) to 3.24 +/- 0.73 mm (P less than 0.01). Within 10 mm of the PB, however, dWT did not change significantly (2.48 +/- 0.79 to 2.38 +/- 0.66 mm, NS). When the aorta was mechanically constricted, peak systolic pressure increased approximately 50%. Wall thickening decreased to the same relative degree in nonischemic muscle less than 10 mm and more than 10 mm from the perfusion boundary. By fitting sigmoid curves to the data, we estimated the extent of nonischemic dysfunction. It averaged 26 +/- 6 degrees (6-8 mm of endocardial circumference) during coronary occlusion alone and it was not significantly different (29 +/- 11 degrees) after aortic constriction. Thus elevated afterload affects nonischemic myocardium uniformly and does not increase the size or relative severity of the functional border zone.

Evidence favoring a cardiac mechanism in irreversible hemorrhagic shock

1961 ◽  
Vol 201 (5) ◽  
pp. 893-896 ◽  
Author(s):  
Jack W. Crowell ◽  
Arthur C. Guyton
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Pulmonary Artery ◽  
Hemorrhagic Shock ◽  
Left Atrial ◽  
Peripheral Resistance ◽  
Arterial System ◽  
Operating Parameters ◽  
The Right ◽  
Oxygen Difference

Shock was induced in 55 dogs by removing blood until the arterial pressure had fallen to 30 mm Hg. The pressure was kept at this level for as long as 10 hr by constantly adding additional blood to the reservoir. The hematocrit was kept constant to prevent large variations in the viscosity. Mean pressures of the right and left atrium, the pulmonary artery, and the systemic arterial system were recorded as well as oxygen consumption and A-V oxygen difference. Total peripheral resistance and cardiac output were calculated. That period of time during which the animal passed from a reversible stage of shock to an irreversible stage of shock was studied. It was found that no significant change occurred in oxygen consumption, cardiac output, or peripheral resistance during this transition phase. However, changes did occur in the operating parameters of the heart. The left atrial pressure began rising with the transition from reversible to irreversible shock and continued rising until death of the animal. It is suggested that irreversible hemorrhagic shock is due to acute cardiac failure.

Improved contractile performance of right ventricle in response to increased RV afterload in newborn lamb

2000 ◽  
Vol 278 (1) ◽  
pp. H100-H105 ◽  
Author(s):  
Maartje de Vroomen ◽  
Robbert H. Lopes Cardozo ◽  
Paul Steendijk ◽  
Frank van Bel ◽  
Jan Baan
Keyword(s):  
Right Ventricle ◽  
Systolic Function ◽  
Systolic Pressure ◽  
Balloon Occlusion ◽  
Newborn Lamb ◽  
End Diastolic Volume ◽  
Volume Relation ◽  
The Right ◽  
Homeometric Autoregulation ◽  
Contractile Performance

Pulmonary hypertension results in an increased afterload for the right ventricle (RV). To determine the effects of this increased afterload on RV contractile performance, we examined RV performance before and during 4 h of partial balloon occlusion of the pulmonary artery and again after releasing the occlusion in nine newborn lambs. RV contractile performance was quantified by indexes derived from systolic RV pressure-volume relations obtained by a combined pressure-conductance catheter during inflow reduction. An almost twofold increase of end-systolic RV pressure (from 22 to 38 mmHg) was maintained during 4 h. Cardiac output (CO) (0.74 ± 0.08 l/min) and stroke volume (4.3 ± 0.4 ml) were maintained, whereas end-diastolic volume (7.9 ± 1.3 ml) did not change significantly during this period. RV systolic function improved substantially; the end-systolic pressure-volume relation shifted leftward indicated by a significantly decreased volume intercept (up to 70%), together with a slightly increased slope. In this newborn lamb model, maintenance of CO during increased RV afterload is not obtained by an increased end-diastolic volume (Frank-Starling mechanism). Instead, the RV maintains its output by improving contractile performance through homeometric autoregulation.

Less afterload sensitivity in short-term hibernating than in acutely ischemic and stunned myocardium

2000 ◽  
Vol 279 (3) ◽  
pp. H1106-H1110 ◽  
Author(s):  
Rainer Schulz ◽  
Jochen Rose ◽  
Heiner Post ◽  
Andreas Skyschally ◽  
Gerd Heusch
Keyword(s):  
Contractile Function ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Negative Slope ◽  
Stunned Myocardium ◽  
Hibernating Myocardium ◽  
Wall Thickening ◽  
Short Term ◽  
The Relationship ◽  
Systolic Wall Thickening

Short-term hibernating myocardium is characterized by reduced contractile function during persistent moderate ischemia, the recovery of metabolic parameters, and the absence of necrosis. To study the afterload dependence of regional wall excursion in short-term hibernating myocardium, in 11 enflurane-anesthetized swine the left anterior descending coronary artery was cannulated and hypoperfused for 90 min to reduce anterior systolic wall thickening (WT, sonomicrometry) by 60%. Under control conditions, at 5 and 90 min ischemia the descending thoracic aorta was acutely constricted to increase left ventricular (LV) pressure by 30 mmHg. Under control conditions, increased LV pressure resulted in decreased WT [i.e., a negative slope of the relationship between WT and LV end-systolic pressure: −11.2 ± 4.2 (SD) μm/mmHg]. This slope was further significantly decreased at 5 min ischemia (−26.5 ± 8.8 μm/mmHg) but returned toward control values in short-term hibernating myocardium at 90 min ischemia (−17.2 ± 6.6 μm/mmHg). At 30 min reperfusion, the slope was once more significantly decreased (−27.8 ± 8.1 μm/mmHg). In conclusion, WT in short-term hibernating myocardium is less afterload dependent than in acutely ischemic and reperfused myocardium.

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.

Biventricular systolic function in young lambs subject to chronic systemic right ventricular pressure overload

2001 ◽  
Vol 281 (6) ◽  
pp. H2697-H2704 ◽  
Author(s):  
Boudewijn P. J. Leeuwenburgh ◽  
Willem A. Helbing ◽  
Paul Steendijk ◽  
Paul H. Schoof ◽  
Jan Baan
Keyword(s):  
Systolic Function ◽  
Systolic Pressure ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Biventricular Function ◽  
Pressure Volume Relationship ◽  
Lv Volume ◽  
The Right ◽  
Contractile Performance ◽  
Biventricular Systolic Function

In various clinical situations of congenital heart disease, the right ventricle (RV) is subject to a chronic systemic pressure overload which affects biventricular function and may progress to the development of RV failure. Young lambs (2–3 wk old) underwent adjustable pulmonary artery banding (PAB) at systemic (aortic) level for 8 wk. Biventricular function was determined by using load-independent indexes of global ventricular contractile performance by the end-systolic pressure-volume relationship (ESPVR) using the conductance catheter at baseline and during dobutamine infusion. PAB resulted in a significant fivefold increase in RV end-systolic pressure (12–64 mmHg) and a doubling of the RV-to-left ventricular (LV) wall thickness ratio ( P < 0.01). RV global contractile performance increased significantly, as indicated by an increased slope of the ESPVR. Compared with age-matched control lambs, cardiac output decreased from 2.6 to 1.6 l/min ( P < 0.05) whereas heart rates were equal. In contrast with RV volume, LV volume decreased significantly after PAB ( P < 0.01), whereas the LV-ESPVR slope was unchanged. In the PAB group, the RV, but not the LV, showed a reduced response to dobutamine. We concluded that chronic RV pressure overload for 8 wk results in diminished pump function despite compensatory increased RV global contractile performance.

Calcineurin-induced energy wasting in a transgenic mouse model of heart failure

2008 ◽  
Vol 294 (3) ◽  
pp. H1459-H1466 ◽  
Author(s):  
Ilka Pinz ◽  
Sanford E. Ostroy ◽  
Kirsten Hoyer ◽  
Hanna Osinska ◽  
Jeffrey Robbins ◽  
...  
Keyword(s):  
Heart Failure ◽  
Mouse Model ◽  
Enzyme Activities ◽  
Systolic Pressure ◽  
Atp Synthesis ◽  
Glycolytic Enzyme ◽  
Mouse Heart ◽  
Adrenergic Stimulation ◽  
Systolic Performance ◽  
Contractile Performance

Overexpression of calcineurin (CLN) in the mouse heart induces severe hypertrophy that progresses to heart failure, providing an opportunity to define the relationship between energetics and contractile performance in the severely failing mouse heart. Contractile performance was studied in isolated hearts at different pacing frequencies and during dobutamine challenge. Energetics were assessed by 31P-NMR spectroscopy as ATP and phosphocreatine concentrations ([ATP] and [PCr]) and free energy of ATP hydrolysis (|Δ G∼ATP|). Mitochondrial and glycolytic enzyme activities, myocardial O2 consumption, and myocyte ultrastructure were determined. In transgenic (TG) hearts at all levels of work, indexes of systolic performance were reduced and [ATP] and capacity for ATP synthesis were lower than in non-TG hearts. This is the first report showing that myocardial [ATP] is lower in a TG mouse model of heart failure. [PCr] was also lower, despite an unexpected increase in the total creatine pool. Because Pi concentration remained low, despite lower [ATP] and [PCr], |Δ G∼ATP| was normal; however, chemical energy did not translate to systolic performance. This was most apparent with β-adrenergic stimulation of TG hearts, during which, for similar changes in |Δ G∼ATP|, systolic pressure decreased, rather than increased. Structural abnormalities observed for sarcomeres and mitochondria likely contribute to decreased contractile performance. On the basis of the increases in enzyme activities of proteins important for ATP supply observed after treatment with the CLN inhibitor cyclosporin A, we also conclude that CLN directed inhibition of ATP-producing pathways in non-TG and TG hearts.

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