Adrenomedullin in experimental congestive heart failure: cardiorenal activation

1997 ◽  
Vol 273 (4) ◽  
pp. R1392-R1399 ◽  
Author(s):  
Michihisa Jougasaki ◽  
Tracy L. Stevens ◽  
Daniel D. Borgeson ◽  
Andreas Luchner ◽  
Margaret M. Redfield ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Diastolic Pressure ◽  
Collecting Duct ◽  
Renal Tissue ◽  
Left Ventricular ◽  
Collecting Duct Cells ◽  
Medullary Collecting Duct ◽  
Rapid Ventricular Pacing ◽  
And Function

Adrenomedullin (ADM) is a new member of a family of vasodilating and natriuretic peptides that plays an important role in cardiorenal regulation. This study was designed to establish the plasma, urinary, cardiac, and renal tissue concentrations and immunohistochemical localizations of ADM in normal dogs and dogs with experimental congestive heart failure (CHF) produced by rapid ventricular pacing. Plasma ADM concentration was 5.6 ± 0.4 pg/ml in normal dogs and significantly increased to 14.5 ± 2.5 pg/ml in CHF dogs ( P < 0.05). Ventricular and renal tissue ADM were significantly increased in CHF dogs compared with normals. Immunohistochemical examination revealed positive ADM immunostaining within the myocytes, and ventricular ADM immunoreactivity was significantly more intense in CHF dogs than in normals. ADM immunoreactivity was also observed in the glomerulus, distal tubules, and medullary collecting duct cells in the kidney, and the intensities of ADM immunoreactivity in these sites were increased in CHF dogs compared with normals. In addition, ventricular ADM was a powerful marker for left ventricular mass, and circulating ADM correlated positively with left ventricular end-diastolic pressure and inversely with cardiac output and ejection fraction. Despite an increase in renal tissue ADM, urinary ADM did not increase in CHF dogs. The current study demonstrates that plasma concentration of ADM is increased in experimental CHF and that ventricular and renal ADM is activated in the progression of CHF. Tissue and circulating ADM also are markers for the alterations in myocardial structure and function. This study supports a potential role for ADM in the neurohumoral activation in experimental CHF.

scholarly journals Changes of renal AQP2, ENaC, and NHE3 in experimentally induced heart failure: response to angiotensin II AT1 receptor blockade

2009 ◽  
Vol 297 (6) ◽  
pp. F1678-F1688 ◽  
Author(s):  
Sophie C. Lütken ◽  
Soo Wan Kim ◽  
Thomas Jonassen ◽  
David Marples ◽  
Mark A. Knepper ◽  
...  
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Diastolic Pressure ◽  
Collecting Duct ◽  
Left Ventricular ◽  
Outer Medulla ◽  
Outer Stripe ◽  
Medullary Collecting Duct ◽  
Type 3

Heart failure (HF) was induced by ligation of the left anterior descending artery (LAD). Left ventricular end-diastolic pressure (LVEDP) >25 mmHg (at day 23 after LAD ligation) was the inclusion criterion. The rats were divided into three groups: sham-operated (Sham, n = 23, LVEDP: 5.6 ± 0.6 mmHg), HF ( n = 14, LVEDP: 29.4 ± 1.4 mmHg), and candesartan (1 mg·kg−1·day−1 sc)-treated HF (HF + Can, n = 9, LVEDP: 29.2 ± 1.2 mmHg). After 7 days (i.e., 29 days after LAD ligation) semiquantitative immunoblotting revealed increased abundance of inner medulla aquaporin-2 (AQP2) and AQP2 phosphorylated at Ser256 (p-AQP2) in HF. There was also markedly enhanced apical targeting of AQP2 and p-AQP2 in inner medullary collecting duct (IMCD) in HF compared with Sham rats, shown by immunocytochemistry. Candesartan treatment significantly reversed the increases in both AQP2 and p-AQP2 expression and targeting. In contrast, there were only modest changes in other collecting duct segments. Semiquantitative immunoblots revealed increased expression of type 3 Na+/H+ exchanger (NHE3) and Na+-K+-2Cl− cotransporter (NKCC2) in kidneys from HF compared with Sham rats: both effects were reversed or prevented by candesartan treatment. The protein abundance of α-epithelial sodium channel (α-ENaC) was increased while β-ENaC and γ-ENaC expression was decreased in the cortex and outer stripe of the outer medulla in HF compared with Sham rats, which was partially reversed by candesartan treatment. These findings strongly support an important role of angiotensin II in the pathophysiology of renal water and sodium retention associated with HF.

Inhibition of NO production increases myocardial blood flow and oxygen consumption in congestive heart failure

2002 ◽  
Vol 282 (6) ◽  
pp. H2278-H2283 ◽  
Author(s):  
Jay H. Traverse ◽  
Yingjie Chen ◽  
Mingxiao Hou ◽  
Robert J. Bache
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
No Production ◽  
Before And After ◽  
Rapid Ventricular Pacing

Coronary blood flow (CBF) and myocardial oxygen consumption (MV˙o 2) are reduced in dogs with pacing-induced congestive heart failure (CHF), which suggests that energy metabolism is downregulated. Because nitric oxide (NO) can inhibit mitochondrial respiration, we examined the effects of NO inhibition on CBF and MV˙o 2 in dogs with CHF. CBF and MV˙o 2 were measured at rest and during treadmill exercise in 10 dogs with CHF produced by rapid ventricular pacing before and after inhibition of NO production with N G-nitro-l-arginine (l-NNA, 10 mg/kg iv). The development of CHF was accompanied by decreases in aortic and left ventricular (LV) systolic pressure and an increase in LV end-diastolic pressure (25 ± 2 mmHg). l-NNA increased MV˙o 2 at rest (from 3.07 ± 0.61 to 4.15 ± 0.80 ml/min) and during exercise; this was accompanied by an increase in CBF at rest (from 31 ± 2 to 40 ± 4 ml/min) and during exercise (both P < 0.05). Althoughl-NNA significantly increased LV systolic pressure, similar increases in pressure produced by phenylephrine did not increase MV˙o 2. The findings suggest that NO exerts tonic inhibition on respiration in the failing heart.

Congestive heart failure in rats is associated with increased collecting duct vasopressin sensitivity and vasopressin type 2 receptor reexternalization

2013 ◽  
Vol 305 (11) ◽  
pp. F1547-F1554 ◽  
Author(s):  
Lone Brønd ◽  
Katrine M. Müllertz ◽  
Malene Torp ◽  
Jonas Nielsen ◽  
Martin Græbe ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Diastolic Pressure ◽  
Collecting Duct ◽  
Water Channel ◽  
Left Ventricular ◽  
Receptor Internalization ◽  
Surface Binding ◽  
Binding Studies

A number of studies have shown that rats with congestive heart failure (CHF) have increased protein levels of the vasopressin (AVP)-regulated water channel aquaporin-2 (AQP2) even during conditions with unchanged circulating levels of AVP, suggesting an increase in the sensitivity of the AVP type 2 (V2) receptor in experimental CHF. The present study was aimed at investigating AVP signaling in rats with moderate CHF (left ventricular end diastolic pressure >10 mmHg; normal plasma AVP levels) induced by ligation of the left anterior descending coronary artery. Sham-operated rats were used as controls. Western blotting analyses revealed an increased abundance of AQP2 in renal cortex (+33 ± 9% of sham; P < 0.05) and in inner medulla (IM) (+54 ± 15% of sham; P < 0.05) in CHF rats compared with sham-operated controls. Dose-response studies on isolated collecting ducts (CDs) showed an increased accumulation of cAMP in response to AVP in CHF rats compared with controls. V2 receptor surface-binding studies in isolated IMCDs showed a marked and comparable AVP-induced V2 receptor internalization in response to AVP in both CHF and control rats. As expected V2 receptor surface binding remained low after AVP challenge in control rats. In contrast to this, V2 receptor surface binding returned to pre-AVP levels within 30 min in the CHF rats, indicating an obtained recycling ability of the V2 receptor in CHF. Together the results indicate the presence of an increased AVP sensitivity in the CDs from CHF rats, associated with an acquired recycling ability of the V2 receptor.

Rapid ventricular pacing in pigs: an experimental model of congestive heart failure

1990 ◽  
Vol 258 (5) ◽  
pp. H1603-H1605 ◽  
Author(s):  
E. Chow ◽  
J. C. Woodard ◽  
D. J. Farrar
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Diastolic Pressure ◽  
Weight Ratio ◽  
Total Body Weight ◽  
Realistic Model ◽  
Left Ventricular ◽  
Heart Weight ◽  
Ventricular Pacing ◽  
Rapid Ventricular Pacing

To develop an improved animal model of congestive heart failure, 11 female farm pigs (wt, 42-46 kg) underwent rapid ventricular pacing at 230 beats/min for 7 days with a modified Medtronic unipolar pacemaker connected to an apical pacing lead. After 7 days the pacemaker was turned off, anesthesia induced, the chest opened, and cardiac hemodynamic and dimensional studies were performed. Results were subsequently compared with data from 12 control pigs that received no pacing. Two pigs died before measurements could be determined. Cardiac output in the paced animals (0.061 +/- 0.018 l.min-1.kg-1) was significantly less (P less than 0.05) than in control pigs (0.085 +/- 0.016 l.min-1.kg-1), when compared at the same resting heart rate. Left ventricular (LV) end-diastolic pressure (23.2 +/- 7.7 vs. 8.6 +/- 3.6 mmHg, P less than 0.01) and right ventricular (RV) end-diastolic pressure (9.0 +/- 3.1 vs. 4.4 +/- 1.7 mmHg, P less than 0.01) were significantly greater in the paced pigs. Significant increases in both septal-lateral LV end-diastolic dimension (60.3 +/- 3.9 vs. 52.1 +/- 7.2 mm, P less than 0.01) and RV end-diastolic dimension (47.2 +/- 5.7 vs. 40.8 +/- 4.7 mm, P less than 0.05) indicated biventricular dilation in the paced pigs. They also exhibited a significantly greater heart weight-to-total body weight ratio and clinical evidence of congestive heart failure, with hepatomegaly and ascites. These results demonstrate that 1 wk of rapid ventricular pacing at 230 beats/min produces a realistic model of congestive heart failure in the pig.

Congestive Heart Failure in Copper-Deficient Mice

2003 ◽  
Vol 228 (7) ◽  
pp. 811-817 ◽  
Author(s):  
Laila Elsherif ◽  
Raymond V. Ortines ◽  
Jack T. Saari ◽  
Y. James Kang
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Left Ventricle ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Experimental Models ◽  
Left Ventricular ◽  
Mouse Heart ◽  
Total Period

Copper Deficiency (CuD) leads to hypertrophic cardiomyopathy in various experimental models. The morphological, electrophysiological, and molecular aspects of this hypertrophy have been under investigation for a long time. However the transition from compensated hypertrophy to decompensated heart failure has not been investigated in the study of CuD. We set out to investigate the contractile and hemodynamic parameters of the CuD mouse heart and to determine whether heart failure follows hypertrophy in the CuD heart. Dams of FVB mice were fed CuD or copper-adequate (CuA) diet starting from the third day post delivery and the weanling pups were fed the same diet for a total period of 5 weeks (pre- and postweanling). At week 4, the functional parameters of the heart were analyzed using a surgical technique for catheterizing the left ventricle. A significant decrease in left ventricle systolic pressure was observed with no significant change in heart rate, and more importantly contractility as measured by the maximal rate of left ventricular pressure rise (+dP/dt) and decline (−dP/dt) were significantly depressed in the CuD mice. However, left ventricle end diastolic pressure was elevated, and relaxation was impaired in the CuD animals; the duration of relaxation was prolonged. In addition to significant changes in the basal level of cardiac function, CuD hearts had a blunted response to the stimulation of the β-adrenergic agonist isoproterenol. Furthermore, morphological analysis revealed increased collagen accumulation in the CuD hearts along with lipid deposition. This study shows that CuD leads to systolic and diastolic dysfunction in association with histopathological changes, which are indices commonly used to diagnose congestive heart failure.

Expectoration of bronchial casts in association with Ramipril treatment

2019 ◽  
Vol 29 (12) ◽  
pp. 1565-1566
Author(s):  
Kim Sarah Plümacher ◽  
Thomas Paul ◽  
Matthias Sigler
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Diastolic Pressure ◽  
Acute Myocarditis ◽  
Parvovirus B19 ◽  
Virus Genome ◽  
Left Ventricular ◽  
Myocardial Biopsy ◽  
Bronchial Cast ◽  
Bronchial Casts

AbstractWe report of a 26-year-old female patient who was referred to our centre with congestive heart failure (CHF). Acute myocarditis with a high Parvovirus B19 virus load was diagnosed by myocardial biopsy. CHF improved after start of ramipril 5 mg/d, metoprolol, diuretics, immunoglobins, and a 24-hour infusion of levosimendan. Soon after initiation of medical therapy, the patient started to expectorate bronchial casts with varying frequencies (three times per week to five times daily). Thorough pneumological workup, including histology of the casts, microbiology, and a CT scan of the lungs, did not reveal any cause for bronchial cast formation. Inhalative corticoids were started without any benefit. Two years later, cardiac catheterisation demonstrated normalised left ventricular function. LV end-diastolic pressure, however, was still elevated at 14 mmHg. Endomyocardial biopsies at this time were negative for virus genome. Finally, we changed afterload reduction therapy from ramipril to candesartan. Within 24 hours, expectoration of bronchial casts terminated. Four weeks later, re-exposition to ramipril prompted immediate re-appearance of cast formation, which again stopped with switching back to candesartan. Finally, we were to prove that treatment with ramipril resulted in bronchial cast formation in this patient.

Echocardiographic Left Ventricular End-Diastolic Pressure Volume Loop Estimate Predicts Survival in Congestive Heart Failure

2013 ◽  
Vol 19 (4) ◽  
pp. 251-259 ◽  
Author(s):  
Daniel M. Spevack ◽  
Justin Karl ◽  
Neeraja Yedlapati ◽  
Ythan Goldberg ◽  
Mario J. Garcia
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Diastolic Pressure ◽  
Left Ventricular

Redistribution and abnormal activity of phospholipase A2 isoenzymes in postinfarct congestive heart failure

2001 ◽  
Vol 280 (3) ◽  
pp. C573-C580 ◽  
Author(s):  
Jane McHowat ◽  
Paramjit S. Tappia ◽  
Song-Yan Liu ◽  
Raetreal McCrory ◽  
Vincenzo Panagia
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Phospholipase D ◽  
Diastolic Pressure ◽  
Contractile Function ◽  
Immunoblot Analysis ◽  
Left Ventricular ◽  
Hemodynamic Assessment ◽  
Intracellular Ca ◽  
Contractile Performance

Cardiac sarcolemmal (SL) cis-unsaturated fatty acid sensitive phospholipase D ( cis-UFA PLD) is modulated by SL Ca2+-independent phospholipase A2(iPLA2) activity via intramembrane release of cis-UFA. As PLD-derived phosphatidic acid influences intracellular Ca2+ concentration and contractile performance of the cardiomyocyte, changes in iPLA2 activity may contribute to abnormal function of the failing heart. We examined PLA2 immunoprotein expression and activity in the SL and cytosol from noninfarcted left ventricular (LV) tissue of rats in an overt stage of congestive heart failure (CHF). Hemodynamic assessment of CHF animals showed an increase of the LV end-diastolic pressure with loss of contractile function. In normal hearts, immunoblot analysis revealed the presence of cytosolic PLA2 (cPLA2) and secretory PLA2 (sPLA2) in the cytosol, with cPLA2 and iPLA2 in the SL. Intracellular PLA2 activity was predominantly Ca2+independent, with minimal sPLA2 activity. CHF increased cPLA2 immunoprotein and PLA2 activity in the cytosol and decreased SL iPLA2 and cPLA2immunoprotein and SL PLA2 activity. sPLA2activity and abundance decreased in the cytosol and increased in SL in CHF. The results show that intrinsic to the pathophysiology of post-myocardial infarction CHF are abnormalities of SL PLA2isoenzymes, suggesting that PLA2-mediated bioprocesses are altered in CHF.

Echocardiographic criteria for detection of postinfarction congestive heart failure in rats

2000 ◽  
Vol 89 (4) ◽  
pp. 1445-1454 ◽  
Author(s):  
Ivar Sjaastad ◽  
Ole M. Sejersted ◽  
Arnfinn Ilebekk ◽  
Reidar Bjørnerheim
Keyword(s):  
Heart Failure ◽  
Cluster Analysis ◽  
Congestive Heart Failure ◽  
Myocardial Function ◽  
Diastolic Pressure ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Frame Rate ◽  
Shortening Velocity ◽  
High Frame Rate

We evaluated postinfarction myocardial function in rats and determined echocardiographic criteria for congestive heart failure (CHF) using high performance echocardiography. Extensive myocardial infarction (MI) was induced in rats by left coronary occlusion. Sham-operated animals served as controls. Five weeks later, high-frame rate (∼200 Hz), fully digitized, shallow-focus (10–25 mm), two-dimensional, M-mode and Doppler echocardiography was performed. A J-tree cluster analysis was performed using parameters indicative of CHF. Reproducibility was examined. The cluster analysis joined the animals into one Sham and two MI clusters. One of the MI clusters had clinical characteristics of CHF and elevated left ventricular end diastolic pressure. Among the echocardiographic variables, only posterior wall shortening velocity separated the failing and nonfailing MI clusters. We conclude that, by high frame rate echocardiography, it is possible to obtain high- quality recordings in rats. It is feasible to distinguish MI rats with CHF due to myocardial dysfunction from those without failure and to perform longitudinal studies on myocardial function.

Sign in / Sign up

Export Citation Format

Share Document