Comparison between End-Systolic Pressure-Volume and End-Systolic Wall Stress in Determining Left Ventricular Contractility with Increased Afterload

Cardiology ◽  
1992 ◽  
Vol 81 (1) ◽  
pp. 69-74 ◽  
Author(s):  
David Ben-Sira ◽  
Michael Sagiv ◽  
Gallila Werber ◽  
Ehud Goldhammer
Keyword(s):  
Systolic Pressure ◽  
Wall Stress ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Left Ventricular Contractility ◽  
Systolic Wall Stress

Histamine decreases left ventricular contractility in normal human subjects

1992 ◽  
Vol 73 (6) ◽  
pp. 2530-2537 ◽  
Author(s):  
D. J. Cooper ◽  
C. R. Thompson ◽  
K. R. Walley ◽  
R. P. Gillis ◽  
P. E. Wolinski-Walley ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Human Subjects ◽  
Systolic Pressure ◽  
Wall Stress ◽  
Receptor Activation ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Left Ventricular Contractility ◽  
H1 Receptor ◽  
Wide Range

To determine whether histamine alters human left ventricular contractility we measured heart rate, calibrated carotid arterial pressure, and left ventricular dimensions (echocardiogram) in nine healthy volunteers. We assessed baseline contractility using the end-systolic pressure-dimension relationship and the end-systolic meridional wall stress-rate-corrected velocity of circumferential fiber shortening relationship determined over a wide range of afterloads using phenylephrine and nitroprusside infusions. We then infused histamine for 3–5 min at a dose predetermined to decrease mean arterial pressure by 20%, both before and after H1 receptor antagonist pretreatment (diphenhydramine 50 mg i.v.). Histamine decreased end-systolic pressure but, unlike an equally hypotensive infusion of nitroprusside, did not decrease end-systolic dimension or increase fractional shortening. Histamine also decreased velocity of circumferential fiber shortening at the same end-systolic meridional wall stress as controls (P < 0.05). These effects of histamine were inhibited by H1 antagonist pretreatment. We conclude that the dominant effect of histamine on the human heart is to decrease left ventricular contractility and that this decrease in contractility is dependent, at least partially, on H1-receptor activation.

Effect of 7.2% Hypertonic Saline/6% Hetastarch on Left Ventricular Contractility in Anesthetized Humans

1995 ◽  
Vol 82 (6) ◽  
pp. 1389-1395. ◽  
Author(s):  
Axel W. Goertz ◽  
Tobias Mehl ◽  
Karl H. Lindner ◽  
Michael G. Rockemann ◽  
Uwe Schirmer ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Hypertonic Saline ◽  
Positive Inotropic Effect ◽  
Wall Stress ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Left Ventricular Contractility ◽  
Inotropic Action ◽  
Positive Inotropic Action ◽  
Systolic Wall Stress

Background Although a positive inotropic effect of hypertonic saline has been demonstrated in isolated cardiac tissue as well as in animal preparations, no information exists about a possible positive inotropic action of hypertonic saline in humans. The aim of this investigation was to determine whether a clinically relevant positive inotropic effect can be demonstrated in humans. Methods Twenty-six patients without cardiovascular disease were randomized to receive 4 ml/kg of either 7.2% hypertonic saline/6% hetastarch or 6% hetastarch (control) at a rate of 1 ml.kg-1.min-1 while under general endotracheal anesthesia. Transesophageal echocardiography was used to evaluate left ventricular function. Arterial pressure, heart rate, and left ventricular end-systolic and end-diastolic diameter, area, and wall thickness were measured immediately before and after administration of either solution. Fractional area change, end-systolic wall stress, and the area under the end-systolic pressure-length relationship curve (ESPLRarea) were calculated. ESPLRarea was used to assess left ventricular contractility. Results Administration of hypertonic saline/hetastarch resulted in a significant decrease of mean arterial pressure and end-systolic wall stress from 77 +/- 14 (mean +/- SD) to 64 +/- 17 mmHg (P &lt; 0.01) and from 52 +/- 14 to 32 +/- 11 10(3) dyne/cm2 (P &gt; 0.01), respectively. End-diastolic area and fractional area change increased from 16.5 +/- 2.9 to 21.7 +/- 3.3 cm2 (P &lt; 0.01) and from 0.53 +/- 0.07 to 0.70 +/- 0.06 (P &lt; 0.01), respectively, whereas there was only a minor change of ESPLRarea from 38 +/- 13 to 44 +/- 13 mmHg.cm (P &lt; 0.05). Conclusions The apparent improvement of left ventricular systolic function in response to hypertonic saline/hetastarch is caused mainly by the combined effect of increased left ventricular preload and reduced left ventricular afterload. A possible positive inotropic action of hypertonic saline/hetastarch is not likely to be clinically relevant.

Effects of acute changes in load and inotropic state on the exponential rate of fiber shortening and other indices of myocardial contractility in the anesthetized intact dog

1987 ◽  
Vol 65 (1) ◽  
pp. 46-53 ◽  
Author(s):  
José Suarez de Lezo ◽  
Pierre Casey ◽  
Anita Casey ◽  
José Luis Carrasco ◽  
José M. Arizon ◽  
...  
Keyword(s):  
Myocardial Contractility ◽  
Wall Stress ◽  
Left Ventricular ◽  
Systemic Resistance ◽  
Exponential Rate ◽  
Ventricular Contractility ◽  
Left Ventricular Contractility ◽  
Inotropic State ◽  
Circumferential Wall Stress ◽  
Inotropic Intervention

The effects of an acute increase in preload, afterload, and inotropic state on several indices of left ventricular contractility were studied in 20 anesthetized intact dogs. The behaviour of the exponential rate of fiber shortening (ERFS), a newly described index, which is based on the instantaneous fiber length – time relationship through ejection, was compared with other classical ejection and isovolumic indices of left ventricular contractility. Acute volume overload by dextran 40 infusion produced a significant increase in preload as reflected by a 103% (p < 0.01) increase in left ventricular end-diastolic pressure and a 121% (p < 0.001) increase in end-diastolic circumferential wall stress. There was also a smaller but significant increase (p < 0.05) of heart rate (30%) and of peak systolic circumferential wall stress (24%). None of the left ventricular contractility indices showed any significant change. Acute pressure overload, produced mechanically by an aortic balloon, increased the afterload significantly as reflected by a 33% (p < 0.05) rise of end-systolic circumferential wall stress and a 43% (p < 0.001) increase in systemic resistance. Stroke volume decreased significantly by 23% (p < 0.05). All ejection indices, including ERFS, were significantly diminished by 30 – 37%; all isovolumic indices showed no significant changes. Positive inotropic intervention was induced by dopamine infusion, which caused a significant 28% (p < 0.05) increase in cardiac output. End-diastolic and end-systolic circumferential wall stress were significantly diminished. All indices of left ventricular contractility increased significantly and ERFS showed the quantitatively greatest change. This study suggests that ERFS is an ejection index of myocardial contractility, which is quite sensitive to inotropic intervention, independent of preload but sensitive to afterload.

Sympathetic stimulation alters left ventricular relaxation and chamber size

1993 ◽  
Vol 264 (1) ◽  
pp. R1-R7 ◽  
Author(s):  
I. G. Burwash ◽  
D. E. Morgan ◽  
C. J. Koilpillai ◽  
G. L. Blackmore ◽  
D. E. Johnstone ◽  
...  
Keyword(s):  
Stellate Ganglion ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Wall Stress ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Ventricular Contractility ◽  
Cross Sectional ◽  
Stress Changes ◽  
Neuronal Stimulation

Alterations in left ventricular (LV) contractility, relaxation, and chamber dimensions induced by efferent sympathetic nerve stimulation were investigated in nine anesthetized open-chest dogs in sinus rhythm. Supramaximal stimulation of acutely decentralized left stellate ganglia augmented heart rate, LV systolic pressure, and rate of LV pressure rise (maximum +dP/dt, 1,809 +/- 191 to 6,304 +/- 725 mmHg/s) and fall (maximum -dP/dt, -2,392 +/- 230 to -4,458 +/- 482 mmHg/s). It also reduced the time constant of isovolumic relaxation, tau (36.5 +/- 4.8 to 14.9 +/- 1.1 ms). Simultaneous two-dimensional echocardiography recorded reductions in end-diastolic and end-systolic LV cross-sectional chamber areas (23 and 31%, respectively), an increase in area ejection fraction (32%), and increases in end-diastolic and end-systolic wall thicknesses (14 and 13%, respectively). End-systolic and end-diastolic wall stresses were unchanged by stellate ganglion stimulation (98 +/- 12 to 95 +/- 9 dyn x 10(3)/cm2; 6.4 +/- 2.4 to 2.4 +/- 0.3 dyn x 10(3)/cm2, respectively). Atrial pacing to similar heart rates did not alter monitored indexes of contractility. Dobutamine and isoproterenol induced changes similar to those resulting from sympathetic neuronal stimulation. These data indicate that when the efferent sympathetic nervous system increases left ventricular contractility and relaxation, concomitant reductions in systolic and diastolic dimensions of that chamber occur that are associated with increasing wall thickness such that LV wall stress changes are minimized.

Different effects of histamine H1 and H2 stimulation on left ventricular contractility in pigs

1995 ◽  
Vol 269 (3) ◽  
pp. H959-H964
Author(s):  
D. J. Cooper ◽  
R. R. Schellenberg ◽  
K. R. Walley
Keyword(s):  
Contractile Function ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Hill Coefficient ◽  
Maximum Effect ◽  
Low Doses ◽  
Ventricular Contractility ◽  
Left Ventricular Contractility ◽  
Receptor Stimulation ◽  
H2 Antagonist

Histamine decreases ventricular contractility in some settings but increases it in others. To better understand these apparently discrepant results, we measured hemodynamics and left ventricular pressure (Millar catheter) and volume (ultrasonic crystals) in atrially paced, alpha- and beta-antagonist-treated pigs. Histamine was infused (0.5-10 micrograms.kg-1.min-1) before and after H2-antagonist (ranitidine) pretreatment. Changes in left ventricular contractile function were measured as shift of the end-systolic pressure-volume relationship (delta ESPVR) at a pressure of 100 mmHg. We found that at low doses (0.5 and 1 micrograms.kg-1.min-1), histamine significantly decreased delta ESPVR (-1.1 +/- 1.4 ml, P < 0.05) after H2-antagonist pretreatment. At doses above 1 micrograms.kg-1.min-1, histamine increased contractility in a dose-response fashion [maximum effect: 5.1 +/- 3.3 ml, dose resulting in 50% effect (ED50): 0.75 +/- 1.79 micrograms.kg-1.min-1] that was best described using a Hill coefficient of 2. Ranitidine increased the ED50 by approximately one order of magnitude (0.75 +/- 1.79 to 9.50 +/- 2.60 micrograms.kg-1.min-1, P < 0.05). We conclude that in vivo, at higher doses, histamine increases left ventricular contractility via H2-receptor stimulation, whereas at low doses histamine decreases left ventricular contractility, probably via H1-receptor stimulation.

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