Pharmacologic Inhibition of Mast Cell Degranulation Prevents Left Ventricular Remodeling Induced by Chronic Volume Overload in Rats

2005 ◽  
Vol 11 (7) ◽  
pp. 548-556 ◽  
Author(s):  
Gregory L. Brower ◽  
Joseph S. Janicki
Keyword(s):  
Mast Cell ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Volume Overload ◽  
Left Ventricular ◽  
Mast Cell Degranulation ◽  
Chronic Volume Overload ◽  
Pharmacologic Inhibition

Response of cardiac mast cells to atrial natriuretic peptide

2007 ◽  
Vol 293 (2) ◽  
pp. H1216-H1222 ◽  
Author(s):  
David B. Murray ◽  
Jason D. Gardner ◽  
Scott P. Levick ◽  
Gregory L. Brower ◽  
Loren G. Morgan ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Ventricular Remodeling ◽  
Volume Overload ◽  
Mast Cell Degranulation ◽  
Aortocaval Fistula ◽  
Chronic Volume Overload ◽  
Atrial Natriuretic

Previously, our laboratory demonstrated that cardiac mast cell degranulation induces adverse ventricular remodeling in response to chronic volume overload. The purpose of this study was to investigate whether atrial natriuretic peptide (ANP), which is known to be elevated in chronic volume overload, causes cardiac mast cell degranulation. Relative to control, ANP induced significant histamine release from peritoneal mast cells, whereas isolated cardiac mast cells were not responsive. Infusion of ANP (225 pg/ml) into blood-perfused isolated rat hearts produced minimal activation of cardiac mast cells, similar to that seen in the control group. ANP also did not increase matrix metalloproteinase-2 activity, reduce collagen volume fraction, or alter diastolic or systolic cardiac function compared with saline-treated controls. In a subsequent study to evaluate the effects of natriuretic peptide receptor antagonism on volume overload-induced ventricular remodeling, anantin was administered to rats with an aortocaval fistula. Comparable increases of myocardial MMP-2 activity in treated and untreated rats with an aortocaval fistula were associated with equivalent decreases in ventricular collagen ( P < 0.05 vs. sham-operated controls). Cardiac functional parameters and left ventricular hypertrophy were unaffected by anantin. We conclude that ANP is not a cardiac mast cell secretagogue and is not responsible for the cardiac mast cell-mediated adverse ventricular remodeling in response to volume overload.

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.

scholarly journals Pleiotropic effects of neutrophils on myocyte apoptosis and left ventricular remodeling during early volume overload

2009 ◽  
Vol 47 (5) ◽  
pp. 634-645 ◽  
Author(s):  
Mikhail A. Kolpakov ◽  
Rachid Seqqat ◽  
Khadija Rafiq ◽  
Hang Xi ◽  
Kennneth B. Margulies ◽  
...  
Keyword(s):  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Volume Overload ◽  
Left Ventricular ◽  
Pleiotropic Effects ◽  
Myocyte Apoptosis

scholarly journals Time-dependent remodeling of transmural architecture underlying abnormal ventricular geometry in chronic volume overload heart failure

2004 ◽  
Vol 287 (5) ◽  
pp. H1994-H2002 ◽  
Author(s):  
Hiroshi Ashikaga ◽  
Jeffrey H. Omens ◽  
James W. Covell
Keyword(s):  
Wall Thickness ◽  
Ventricular Remodeling ◽  
Volume Overload ◽  
Wall Stress ◽  
Anterior Wall ◽  
Left Ventricular ◽  
Ventricular Geometry ◽  
Final Study ◽  
Chronic Volume Overload ◽  
Apical Site

To test the hypothesis that the abnormal ventricular geometry in failing hearts may be accounted for by regionally selective remodeling of myocardial laminae or sheets, we investigated remodeling of the transmural architecture in chronic volume overload induced by an aortocaval shunt. We determined three-dimensional finite deformation at apical and basal sites in left ventricular anterior wall of six dogs with the use of biplane cineradiography of implanted markers. Myocardial strains at end diastole were measured at a failing state referred to control to describe remodeling of myofibers and sheet structures over time. After 9 ± 2 wk (means ± SE) of volume overload, the myocardial volume within the marker sets increased by >20%. At 2 wk, the basal site had myofiber elongation (0.099 ± 0.030; P < 0.05), whereas the apical site did not [ P = not significant (NS)]. Sheet shear at the basal site increased progressively toward the final study (0.040 ± 0.003 at 2 wk and 0.054 ± 0.021 at final; both P < 0.05), which contributed to a significant increase in wall thickness at the final study (0.181 ± 0.047; P < 0.05), whereas the apical site did not ( P = NS). We conclude that the remodeling of the transmural architecture is regionally heterogeneous in chronic volume overload. The early differences in fiber elongation seem most likely due to a regional gradient in diastolic wall stress, whereas the late differences in wall thickness are most likely related to regional differences in the laminar architecture of the wall. These results suggest that the temporal progression of ventricular remodeling may be anatomically designed at the level of regional laminar architecture.

Effects of dietary phytoestrogens on cardiac remodeling secondary to chronic volume overload in female rats

2005 ◽  
Vol 99 (4) ◽  
pp. 1378-1383 ◽  
Author(s):  
Jason D. Gardner ◽  
Gregory L. Brower ◽  
Joseph S. Janicki
Keyword(s):  
Cardiac Function ◽  
Ventricular Remodeling ◽  
Isolated Heart ◽  
Systolic Pressure ◽  
Volume Overload ◽  
Left Ventricular ◽  
Female Rats ◽  
Ventricular Contractility ◽  
Ventricular Compliance ◽  
Chronic Volume Overload

Previously, we demonstrated that intact female rats fed a standard rodent diet containing soybean products exhibit essentially no adverse left ventricular (LV) remodeling in response to aortocaval fistula-induced chronic volume overload. We hypothesized that phytoestrogenic compounds in the diet contributed to the female cardioprotection. To test this hypothesis, four groups of female rats were studied: sham-operated (Sham) and fistula (Fist) rats fed a diet with [P(+)] or without [P(−)] phytoestrogens. Eight weeks postfistula, systolic and diastolic cardiac function was assessed by using a blood-perfused, isolated heart preparation. High-phytoestrogen diet had no effect on body, heart, and lung weights, or cardiac function in Sham rats. Fistula groups developed LV hypertrophy, which was not reduced by dietary phytoestrogens [1,184 ± 229 mg Fist-P(−) and 1,079 ± 199 mg Fist-P(+) vs. 620 ± 47 mg for combined Sham groups, P < 0.05]. Unstressed LV volume increased in Fist-P(−) rats (428 ± 16 vs. 300 ± 14 μl Sham, P < 0.0001), but it was not different from Sham for Fist-P(+) animals (286 ± 17 μl). Fist-P(−) rats developed increased ventricular compliance (5.3 ± 0.8 vs. 2.3 ± 0.3 μl/mmHg Sham, P < 0.01), whereas Fist-P(+) rats had no change in compliance (2.8 ± 0.4 μl/mmHg). Intrinsic ventricular contractility was maintained in the Fist-P(+) rats, but it was reduced ( P < 0.001) in the Fist-P(−) rats [systolic pressure-volume slope: 1.04 ± 0.03, 0.60 ± 0.06, and 0.99 ± 0.08 mmHg/μl, for Fist-P(+), Fist-P(−), and Sham, respectively]. These data indicate that dietary phytoestrogens contribute significantly to female cardioprotection against volume overload-induced adverse ventricular remodeling and that studies evaluating gender differences in cardiovascular remodeling must consider the influence of dietary phytoestrogens.

scholarly journals Right versus left ventricular remodeling in heart failure due to chronic volume overload: pressure-volume and proteome analysis

2021 ◽  
Author(s):  
Tereza Havlenova ◽  
Petra Skaroupkova ◽  
Matus Miklovic ◽  
Matej Behounek ◽  
Martin Chmel ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Systolic Dysfunction ◽  
Volume Overload ◽  
Left Ventricular ◽  
Cytoskeletal Proteins ◽  
Sham Operation ◽  
Stroke Work ◽  
Specific Regulation

Abstract Mechanisms of right ventricular (RV) dysfunction in heart failure (HF) are poorly understood. RV response to volume overload (VO), a common contributing factor to HF, is rarely studied. The goal was to identify interventricular differences in response to chronic VO. Rats underwent aorto-caval fistula (ACF)/sham operation to induce VO. After 24 weeks, RV and left ventricular (LV) functions, gene expression and proteomics were studied. ACF led to biventricular dilatation, systolic dysfunction and hypertrophy affecting relatively more RV. Increased RV afterload contributed to larger RV stroke work increment compared to LV. Both ACF ventricles displayed upregulation of genes of myocardial stress and metabolism. Most proteins reacted to VO in a similar direction in both ventricles, yet the expression changes were more pronounced in RV. The most upregulated were extracellular matrix (POSTN, NRAP, TGM2, CKAP4), cell adhesion (NCAM, NRAP, XIRP2) and cytoskeletal proteins (FHL1, CSRP3) and enzymes of carbohydrate (PKM) or norepinephrine (MAOA) metabolism. Downregulated were MYH6 and FAO enzymes. Therefore, when exposed to identical VO, both ventricles display similar upregulation of stress and metabolic markers. RV reacts to ACF relatively more than LV due to concomitant pulmonary hypertension. No evidence supports RV chamber-specific regulation of protein expression in response to VO.

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