Influence of the pericardium on left ventricular diastolic pressure-volume curves in dogs with sustained volume overload

1983 ◽  
Vol 105 (6) ◽  
pp. 995-1001 ◽  
Author(s):  
Valmik Bhargava ◽  
Ralph Shabetai ◽  
John Ross ◽  
Kunio Shirato ◽  
Richard S. Pavelec ◽  
...  
Keyword(s):  
Diastolic Pressure ◽  
Volume Overload ◽  
Left Ventricular

Apoptosis in the left ventricle of chronic volume overload causes endocardial endothelial dysfunction in rats

2002 ◽  
Vol 282 (4) ◽  
pp. H1197-H1205 ◽  
Author(s):  
Michael J. Cox ◽  
Harpreet S. Sood ◽  
Matthew J. Hunt ◽  
Derrick Chandler ◽  
Jeffrey R. Henegar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blot Analysis ◽  
Diastolic Pressure ◽  
Volume Overload ◽  
Left Ventricular ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Heart Weight ◽  
Sprague Dawley ◽  
Lung Weight ◽  
Cardiac Relaxation

The hypothesis is that chronic increases in left ventricular (LV) load induce oxidative stress and latent matrix metalloproteinase (MMP) is activated, allowing the heart to dilate in the absence of endothelial nitric oxide (NO) and thereby reduce filling pressure. To create volume overload, an arteriovenous (A-V) fistula was placed in male Sprague-Dawley rats. To decrease oxidative stress and apoptosis, 0.08 mg/ml nicotinamide (Nic) was administered in drinking water 2 days before surgery. The rats were divided into the following groups: 1) A-V fistula, 2) A-V fistula + Nic, 3) sham operated, 4) sham + Nic, and 5) control (unoperated); n = 6 rats/group. After 4 wk, hemodynamic parameters were measured in anesthetized rats. The heart was removed and weighed, and LV tissue homogeneates were prepared. A-V fistula caused an increase in heart weight, lung weight, and end-diastolic pressure compared with the sham group. The levels of malondialdehyde (MDA; a marker of oxidative stress) was 6.60 ± 0.23 ng/mg protein and NO was 6.87 ± 1.21 nmol/l in the LV of A-V fistula rats by spectrophometry. Nic treatment increased NO to 13.88 ± 2.5 nmol/l and decreased MDA to 3.54 ± 0.34 ng/mg protein ( P= 0.005). Zymographic levels of MMP-2 were increased, as were protein levels of nitrotyrosine and collagen fragments by Western blot analysis. The inhibition of oxidative stress by Nic decreased nitrotyrosine content and MMP activity. The levels of tissue inhibitor of metalloproteinase-4 mRNA were decreased in A-V fistula rats and increased in A-V fistula rats treated with Nic by Northern blot analysis. TdT-mediated dUTP nick-end labeling-positive cells were increased in A-V fistula rats and decreased in fistula rats treated with Nic. Acetylcholine and nitroprusside responses in cardiac rings prepared from the above groups of rats suggest impaired endothelial-dependent cardiac relaxation. Treatment with Nic improves cardiac relaxation. The results suggest that an increase in the oxidative stress and generation of nitrotyrosine are, in part, responsible for the activation of metalloproteinase and decreased endocardial endothelial function in chronic LV volume overload.

scholarly journals Modification of a Volume-Overload Heart Failure Model to Track Myocardial Remodeling and Device-Related Reverse Remodeling

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Egemen Tuzun ◽  
Roger Bick ◽  
Cihan Kadipasaoglu ◽  
Jeffrey L. Conger ◽  
Brian J. Poindexter ◽  
...  
Keyword(s):  
Heart Failure ◽  
Wall Thickness ◽  
Ventricular Remodeling ◽  
Diastolic Pressure ◽  
Volume Overload ◽  
Left Ventricular ◽  
Reverse Remodeling ◽  
Sheep Model ◽  
Dystrophin Expression ◽  
Cellular Markers

Purpose. To provide an ovine model of ventricular remodeling and reverse remodeling by creating congestive heart failure (CHF) and then treating it by implanting a left ventricular assist device (LVAD). Methods. We induced volume-overload heart failure in 2 sheep; 20 weeks later, we implanted an LVAD and assessed recovery 11 weeks thereafter. We examined changes in histologic and hemodynamic data and levels of cellular markers of CHF. Results. After CHF induction, we found increases in LV end-diastolic pressure, LV systolic and diastolic dimensions, wall thickness, left atrial diameter, and atrial natriuretic protein (ANP) and endothelin-1 (ET-1) levels; β-adrenergic receptor (BAR) and dystrophin expression decreased markedly. Biopsies confirmed LV remodeling. After LVAD support, LV systolic and diastolic dimensions, wall thickness, and mass, and ANP and ET-1 levels decreased. Histopathologic and hemodynamic markers improved, and BAR and dystrophin expression normalized. Conclusions. We describe a successful sheep model for ventricular and reverse remodeling.

Left ventricular failure induced by myocardial infarction. I. Myocyte hypertrophy

1985 ◽  
Vol 248 (6) ◽  
pp. H876-H882 ◽  
Author(s):  
P. Anversa ◽  
A. V. Loud ◽  
V. Levicky ◽  
G. Guideri
Keyword(s):  
Myocardial Infarction ◽  
Diastolic Pressure ◽  
Pressure Overload ◽  
Volume Overload ◽  
Left Ventricular Pressure ◽  
Systolic Arterial Pressure ◽  
Left Ventricular ◽  
Cellular Growth ◽  
Left Ventricular Failure ◽  
Ventricular Failure

To determine whether left ventricular failure after acute myocardial infarction is associated with a growth response of the myocytes that tends to compensate for the loss of muscle mass and function, the left coronary artery in rats was ligated near its origin, and the animals were killed 3 days later. Elevated left ventricular end-diastolic pressure and decreased first derivative of left ventricular pressure and systolic arterial pressure indicated significant impairment of ventricular function. Absolute infarct size, determined morphometrically by measurement of the fraction of myocyte nuclei lost, averaged 57%. Hypertrophy of surviving left ventricular myocytes was 28%, involving a 14% increase in cell length and a 6% increase in diameter. Right ventricular myocyte volume per nucleus increased 21% by a 10% enlargement of cellular diameter with no change in length. These results show on a cellular basis that myocardial hypertrophy in the left ventricle is accomplished by cellular shape changes characteristic of a combination of pressure and volume overload hypertrophy, whereas cellular growth in the right ventricle is consistent with pressure overload hypertrophy.

Captopril reduces left ventricular enlargement induced by chronic volume overload

1990 ◽  
Vol 259 (3) ◽  
pp. H796-H803
Author(s):  
R. G. Gay
Keyword(s):  
Pulse Pressure ◽  
Diastolic Pressure ◽  
Ex Vivo ◽  
Volume Overload ◽  
Wall Stress ◽  
Left Ventricular ◽  
Aortic Occlusion ◽  
End Diastolic Volume ◽  
Volume Relation ◽  
Captopril Treatment

The effect of captopril treatment on left ventricular (LV) function, mass, and volume during chronic volume overload induced by production of aortic insufficiency (AI) was studied. AI was caused by mechanical disruption of the aortic valve in 175- to 225-g male Sprague-Dawley rats. At 24 h after surgery, AI and sham-operated rats were divided into control and captopril treatment (2 g/l drinking water) groups. After 2 mo of treatment, hemodynamics were measured in open-chest rats, and the LV pressure-volume relation was determined ex vivo. Compared with sham-operated rats, in the untreated AI rats, aortic pulse pressure was increased nearly 100%, LV end-diastolic pressure was 10 +/- 1 vs 3 +/- 1 mmHg, and LV end-diastolic volume was 1.25 +/- 0.07 vs 0.36 +/- 0.03 ml. LV weight was increased 43% and the LV pressure-volume relation was shifted rightward by AI. LV systolic and diastolic wall stress were increased in rats with AI. Peak LV pressure during aortic occlusion was decreased in AI rats, however, peak wall stress during aortic occlusion was not different compared with sham-operated rats. Captopril treatment decreased aortic pulse pressure and LV systolic pressure. Both LV weight and LV end-diastolic volume measured from the ex vivo pressure-volume relation at LV end-diastolic pressure were increased by 33% in untreated AI rats compared with captopril-treated AI rats. Captopril treatment of AI rats shifted the LV pressure-volume to the left compared with untreated rats. LV pressure and wall stress during aortic occlusion were not changed in captopril-treated AI rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Permanent changes of ventricular contractility and compliance in chronic volume overload

1979 ◽  
Vol 237 (5) ◽  
pp. H575-H583
Author(s):  
W. W. Pinsky ◽  
R. M. Lewis ◽  
C. J. Hartley ◽  
M. L. Entman
Keyword(s):  
Diastolic Pressure ◽  
Vena Cava ◽  
Volume Overload ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Segment Length ◽  
Myocardial Segment ◽  
Ventricular Contractility ◽  
Beta Adrenergic ◽  
Ventricular Compliance

Left ventricular volume overload (LVVO) has been created in 18 dogs by anastomosing a Dacron conduit between the infrarenal abdominal aorta and inferior vena cava. The dogs previously were instrumented so that in the awake state LV pressure, systemic arterial pressure, LV dP/dt, myocardial segment length and excursion, and coronary and renal artery velocities could be monitored. The animals were stressed with separate infusions of alpha-adrenergic and beta-adrenergic agonists. Both at rest and with stress, over a 12-wk period, preejection, ejection, and contractility indices decreased. Left ventricular compliance decreased as exemplified by the increased ratio of end-diastolic pressure to end-diastolic length. The shunt was ablated in 7 dogs, and monitoring in conjuction with alpha- and beta-adrenergic stress foan additional 12 wk demonstrated an initial improvement in the previous indices. However, the amelioration plateaued and values similar to the control state were not attained. This suggests that potentially permanent alterations in ventricular function and compliance have occurred.

scholarly journals Volume overload in hemodialysis: diagnosis, cardiovascular consequences, and management

2020 ◽  
Author(s):  
Charalampos Loutradis ◽  
Pantelis A Sarafidis ◽  
Charles J Ferro ◽  
Carmine Zoccali
Keyword(s):  
Time Window ◽  
Diastolic Pressure ◽  
Current Knowledge ◽  
Volume Overload ◽  
Dry Weight ◽  
Left Ventricular ◽  
Bioimpedance Spectroscopy ◽  
Fluid Removal ◽  
Clinical Criteria ◽  
Long Time

Abstract Volume overload in haemodialysis (HD) patients associates with hypertension and cardiac dysfunction and is a major risk factor for all-cause and cardiovascular mortality in this population. The diagnosis of volume excess and estimation of dry weight is based largely on clinical criteria and has a notoriously poor diagnostic accuracy. The search for accurate and objective methods to evaluate dry weight and to diagnose subclinical volume overload has been intensively pursued over the last 3 decades. Most methods have not been tested in appropriate clinical trials and their usefulness in clinical practice remains uncertain, except for bioimpedance spectroscopy and lung ultrasound (US). Bioimpedance spectroscopy is possibly the most widely used method to subjectively quantify fluid distributions over body compartments and produces reliable and reproducible results. Lung US provides reliable estimates of extravascular water in the lung, a critical parameter of the central circulation that in large part reflects the left ventricular end-diastolic pressure. To maximize cardiovascular tolerance, fluid removal in volume-expanded HD patients should be gradual and distributed over a sufficiently long time window. This review summarizes current knowledge about the diagnosis, prognosis and treatment of volume overload in HD patients.

Volume overload hypertrophy in a closed-chest model of mitral regurgitation

1988 ◽  
Vol 254 (6) ◽  
pp. H1034-H1041 ◽  
Author(s):  
J. P. Kleaveland ◽  
W. G. Kussmaul ◽  
T. Vinciguerra ◽  
R. Diters ◽  
B. A. Carabello
Keyword(s):  
Cardiac Output ◽  
Mitral Regurgitation ◽  
Diastolic Pressure ◽  
Volume Ratio ◽  
Volume Overload ◽  
Canine Model ◽  
Left Ventricular ◽  
Closed Chest ◽  
Cardiac Decompensation ◽  
End Diastolic Volume

Chronic volume overload hypertrophy as seen in mitral regurgitation in humans eventually may cause left ventricular dysfunction. Longitudinal study of the mechanisms leading to such dysfunction is difficult in humans and more easily performed in an animal model. In this study, we describe a canine model of volume overload hypertrophy produced by mitral regurgitation. An arterially placed grasping forceps was used to disrupt mitral chordae or leaflets; thus mitral regurgitation was produced without the need for thoracotomy. Eleven of 22 dogs had severe mitral regurgitation (regurgitant fraction greater than 0.50) and survived for greater than or equal to 3 mo (average 9.2 +/- 6 mo) after the production of mitral regurgitation. At 3 mo, end-diastolic volume increased from 48 +/- 9 to 85 +/- 19 ml, P less than 0.01. Left ventricular mass increased from 71 +/- 13 to 90 +/- 10 g, P less than 0.01. Left ventricular end-diastolic pressure increased from 9 +/- 3 to 19 +/- 6 mmHg, P less than 0.01. Cardiac output decreased from 2.3 +/- 0.61 to 1.80 +/- 0.64 l/min, P less than 0.05. The mass-to-volume ratio decreased from 1.44 +/- 0.17 to 1.09 +/- 0.13, P less than 0.01. We conclude that this closed-chest model of chronic mitral regurgitation produces significant eccentric cardiac hypertrophy. Despite a doubling of end-diastolic volume, there was a fall in cardiac output and a rise in left ventricular end-diastolic pressure, suggesting cardiac decompensation.

scholarly journals Low coronary perfusion pressure is associated with endocardial fibrosis in a rat model of volume overload cardiac hypertrophy

2004 ◽  
Vol 59 (5) ◽  
pp. 228-235 ◽  
Author(s):  
Maria Carolina Guido ◽  
Márcia Kiyomi Koike ◽  
Clovis de Carvalho Frimm
Keyword(s):  
Myocardial Fibrosis ◽  
Perfusion Pressure ◽  
Volume Fraction ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Volume Overload ◽  
Left Ventricular ◽  
Driving Pressure ◽  
Coronary Perfusion ◽  
Aortocaval Fistula

Left ventricular hypertrophy following volume overload is regarded as an example of cardiac remodeling without increased fibrosis accumulation. However, infarction is associated with increased fibrosis within the noninfarcted, hypertrophied myocardium, particularly in the subendocardial regions. It is conceivable to suppose that, as also occurs postinfarction, low coronary driving pressure may also interfere with accumulation of myocardial fibrosis following aortocaval fistula. PURPOSE: To investigate the role of acute hemodynamic changes in subsequent deposition of cardiac fibrosis in response to aortocaval fistula. METHOD: Aortocaval fistula were created in 4 groups of Wistar rats that were followed over 4 and 8 weeks: aortocaval fistula 4 and aortocaval fistula 8 (10 rats each) and their respective controls (sham-operated controls - Sh), Sh4 and Sh8 (8 rats each). Hemodynamic measurements were performed 1 week after surgery. Hypertrophy and fibrosis were quantified by myocyte diameter and collagen volume fraction at the end of follow up. RESULT: Compared with Sh4 and Sh8, pulse pressure, left ventricular end-diastolic pressure, and +dP/dt were higher in aortocaval fistula 4 and aortocaval fistula 8, but -dP/dt was similar. Coronary driving pressure (mm Hg), used as an estimate of perfusion pressure, was lower in aortocaval fistula 8 (52.6 ± 4.1) than in Sh8 (100.8 ± 1.3), but comparable between aortocaval fistula 4 (50.0 ± 8.9) and Sh4 (84.8 ± 2.3). Myocyte diameter was greater in aortocaval fistula 8, whereas interstitial and subendocardial fibrosis were greater in aortocaval fistula 4 and aortocaval fistula 8. Coronary driving pressure correlated inversely and independently with subendocardial fibrosis (r² = .86, P <.001), whereas left ventricular systolic pressure (r² = 0.73, P = .004) and end-diastolic pressure (r² = 0.55, P = 012) correlated positively and independently with interstitial fibrosis. CONCLUSION: Coronary driving pressure falls and ventricular pressures increase early after aortocaval fistula and are associated with subsequent myocardial fibrosis deposition.

Temporal evaluation of left ventricular remodeling and function in rats with chronic volume overload

1996 ◽  
Vol 271 (5) ◽  
pp. H2071-H2078 ◽  
Author(s):  
G. L. Brower ◽  
J. R. Henegar ◽  
J. S. Janicki
Keyword(s):  
Ventricular Remodeling ◽  
Diastolic Pressure ◽  
Systolic Function ◽  
Left Ventricular Remodeling ◽  
Isolated Heart ◽  
Volume Overload ◽  
Left Ventricular ◽  
Control Value ◽  
Chronic Volume Overload ◽  
And Function

The left ventricle (LV) significantly dilates and hypertrophies in response to chronic volume overload. However, the temporal responses in LV mass, volume, and systolic/diastolic function secondary to chronic volume overload induced by an infrarenal arteriovenous (A-V) fistula in rats have not been well characterized. To this end, LV end-diastolic pressure, size, and function (i.e., isovolumetric pressure-volume relationships in the blood-perfused isolated heart) were assessed at 1, 2, 3, 5, and 8 wk post-A-V fistula and compared with age-matched control animals. Progressive hypertrophy (192% at 8 wk), ventricular dilatation (172% at 8 wk), and a decrease in ventricular stiffness (257% at 8 wk) occurred in the fistula groups. LV end-diastolic pressure increased from a control value of 4.2 +/- 3.1 mmHg to a peak value of 15.7 +/- 3.6 mmHg after 3 wk of volume overload. A subsequent decline in LVEDP to 11.0 +/- 6.0 mmHg together with further LV dilation (169%) corresponded to a significant decrease in LV stiffness (222%) at 5 wk post-A-V fistula. Myocardial contractility, as assessed by the isovolumetric pressure-volume relationship, was significantly reduced in all A-V fistula groups; however, the compensatory remodeling induced by 8 wk of chronic biventricular volume overload tended to preserve systolic function.

Sign in / Sign up

Export Citation Format

Share Document