Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CSF and Plasma concentrations of atrial natriuretic peptide (ANP) and cyclic GMP (cGMP), which is regarded as a second messenger of ANP, were measured intermittently during the progress of canine kaolin-induced hydrocephalus. Data were analyzed being divided into three groups, normal, acute (within 2 weeks after intracisternal injection of kaolin suspension) and chronic (from 3 to 4 weeks after injection of kaolin suspension) stages of hydrocephalus. The presence of ventricular dilatation was evaluated by MRI or postmortal dissection. ANP, cGMP in CSF and CSF pressure significantly increased in the acute stage of hydrocephalus. In the chronic stage, ANP in CSF and CSF pressure had no statistical difference with data of the normal stage. Cyclic GMP in CSF kept significantly high value in the chronic stage of hydrocephalus. CSF concentrations of Na, CSF osmolarity, plasma ANP, plasma cGMP, plasma ADH, serum Na and serum osmolarity did not change significantly in the course of hydrocephalus. There was a significant positive correlation between ANP in CSF and CSF pressure. ANP in CSF did not correlate with degree of ventricular dilatation. Cyclic GMP in CSF did not correlate with ANP in CSF, nor with CSF pressure. These data suggest that concentration of ANP in CSF may alter directly or indirectly depending on CSF pressure in kaolin-induced hydrocephalus. And cGMP in CSF was suggested to depend not on ANP in CSF, but on other unknown factors in kaolin-induced hydrocephalus.
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PMID:[Alteration of atrial natriuretic peptide and cyclic GMP in cerebrospinal fluid in canine kaolin-induced hydrocephalus]. 132 21

Plasma concentration of immunoreactive atrial natriuretic peptide (ir-ANP) was investigated in 83 Cavalier King Charles Spaniels with variable severity of mitral regurgitation caused by chronic valvular disease (CVD). Severity of mitral incompetence was assessed by echocardiography. Significant differences in plasma concentrations of ir-ANP were not found between clinically normal dogs (New York Heart Association functional class O), dogs with only cardiac murmur (class I), and dogs with echocardiographic evidence of slight to moderate left atrial and ventricular dilatation (class II). Dogs with severe left atrial and ventricular dilatation and clinical signs of congestion (classes III and IV) were found to have significantly (P < 0.001) increased plasma concentration of ir-ANP. Overall, moderate degree of association was found between plasma concentration of ir-ANP and left atrial and left ventricular diameters (Pearson's r = 0.65, 0.60, respectively, P < 0.001), as well as heart rate (r = 0.47, P < 0.01). However, left atrial enlargement was found to have the predominant effect on plasma ir-ANP concentration. It is concluded that the plasma concentration of ir-ANP did not become markedly increased before decompensation of chronic mitral regurgitation associated with severe enlargement of the left atrium and ventricle in Cavalier King Charles Spaniels.
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PMID:Plasma concentration of atrial natriuretic peptide in relation to severity of mitral regurgitation in Cavalier King Charles Spaniels. 806 20

The success of angiotensin-converting enzyme (ACE) inhibitors in reducing cardiovascular morbidity and mortality rates has led to a reexamination of the role of the renin-angiotensin system in pathophysiology. Ventricular dysfunction leading to congestive cardiac failure is associated with sequential activation of the sympathetic system and increases in plasma atrial natriuretic peptide; however, increases in plasma renin and aldosterone do not occur until very late. The renin-angiotensin system is now regarded as both a circulating and tissue hormonal system. All components of the renin-angiotensin system have been detected in the heart. ACE is localized in discrete areas of the heart, including the cardiac valves, coronary vessels, atria, and myocardium. After experimental myocardial infarction in the rat, although plasma renin and aldosterone levels are not increased, ACE in the myocardium is markedly increased. Treatment with ACE inhibitors suppresses cardiac ACE and is associated with hemodynamic improvement, reversal of the neurohumoral activation, prevention of ventricular dilatation, and remodeling and reduction in mortality rates. These results suggest that the beneficial effects of ACE inhibitors in treating congestive cardiac failure, preventing ventricular remodeling, and regressing left ventricular hypertrophy may involve not only reducing preload and afterload but also suppressing the local cardiac renin-angiotensin system.
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PMID:The cardiac renin-angiotensin system in heart failure. 836 49

The purpose of this study was to compare the angiotensin II type 1 receptor antagonist candesartan cilexitil (candesartan) and the angiotensin-converting enzyme inhibitor cilazapril on cardiac function, assessed by Doppler echocardiography and cardiac gene expression associated with cardiac remodeling, in rats with myocardial infarction. Candesartan or cilazapril was administered after myocardial infarction. At 1 and 4 weeks after myocardial infarction, cardiac function and mRNA expression in noninfarcted myocardium were analyzed. Candesartan and cilazapril equally prevented increases in hypertrophy in noninfarcted myocardium, left ventricular dilatation, and ejection fraction at 4 weeks. The E-wave/A-wave velocity ratio and the rate of E-wave deceleration, measures of diastolic function, increased to 9.2+/-0.6 and 26.3+/-2. 6 m/s2 at 1 week after myocardial infarction. Candesartan and cilazapril, administered at a dose of 1 mg/kg per day, prevented increases in E-wave/A-wave velocity ratio and E-wave deceleration at 1 and 4 weeks. Candesartan and cilazapril significantly suppressed increased mRNA expression of beta-myosin heavy chain, alpha-skeletal actin, and atrial natriuretic peptide in noninfarcted ventricle at 1 and 4 weeks and expression of collagen I and III at 4 weeks to a similar extent. When given at a dose of 10 mg/kg per day, both candesartan and cilazapril prevented cardiac dysfunction and gene expression to the same extent as when given at 1 mg/kg per day. In conclusion, Doppler echocardiography showed that candesartan and cilazapril equally improved systolic and diastolic function and that ventricular remodeling accompanied modulation of cardiac gene expression.
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PMID:Effects of candesartan and cilazapril on rats with myocardial infarction assessed by echocardiography. 1020 31

Sodium/hydrogen exchange (NHE) inhibitors show promise as potential therapeutic agents for the treatment of heart failure, but it is not known whether they can reverse the maladaptive remodeling that results in heart failure. We sought to determine the effect of the NHE-1-specific inhibitor EMD-87580 (EMD) on heart failure produced by myocardial infarction in the rat and to assess whether up to 4 wk of treatment delay results in beneficial effects. Male Sprague-Dawley rats were subjected to coronary artery ligation (or a sham procedure) and followed for up to 3 mo, at which time hypertrophy and hemodynamics were determined. EMD was provided in the diet, and treatment commenced immediately or 2-4 wk after ligation. EMD significantly reduced hemodynamic abnormalities, including the elevation in left ventricular end-diastolic pressure, and diminished the loss of systolic function with all treatment protocols. Left ventricular dilatation and hypertrophy, as assessed by heart weight, cell size, and atrial natriuretic peptide (ANP) expression, were similarly reversed to sham or near-sham levels. In addition, the increased plasma ANP and pro-ANP values were reversed to levels not significantly different from sham. Surprisingly, virtually all beneficial effects were identical with all treatment protocols. These effects were observed in the absence of infarct size reduction or blood pressure-lowering effects. Our results suggest that NHE-1 inhibition attenuates and reverses postinfarction remodeling and heart failure with a treatment delay of up to 4 wk after infarction. The effect is independent of infarct size or afterload reduction, indicating a direct effect on the myocardium.
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PMID:Inhibition and reversal of myocardial infarction-induced hypertrophy and heart failure by NHE-1 inhibition. 1468 66

Osteopontin has been reported to have an important role in cardiac fibrosis. However, little is known about the effects of angiotensin-converting enzyme inhibitor (ACEI) and angiotensin type 1 receptor blockers (ARB) on osteopontin expression in infarcted myocardium. The purpose of this study was to elucidate the effects of an ACEI (perindpril) and an ARB (candesartan cilexitil) on cardiac function as assessed by Doppler echocardiography and cardiac osteopontin expression associated with cardiac remodeling in myocardial infarcted rats. ACEI or ARB was administered after myocardial infarction (MI). At 4 weeks after MI, cardiac function, and mRNAs in non-infarcted myocardium were analyzed. ACEI and ARB equally prevented left ventricular dilatation, reduction of ejection fraction, and the increase in E/A wave velocity ratio and the rate of E wave deceleration by MI. ACEI and ARB significantly suppressed increased mRNA expression of atrial natriuretic peptide, brain natriuretic peptide, osteopontin, and collagen I and III in the non-infarcted ventricle at 4 weeks. Immunohistochemically stained osteopontin was increased in interstitial fibrosis of non-infarcted myocardium. Both ACEI and ARB significantly prevented cardiac fibrosis and osteopontin expression. In conclusion, angiotensin blockade inhibits osteopontin expression in non-infarcted myocardium and prevents cardiac remodeling after MI.
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PMID:Angiotensin blockade inhibits osteopontin expression in non-infarcted myocardium after myocardial infarction. 1599 71

Although various neurohormones at initial measurement confer prognostic value in heart failure and correlate with the left ventricular ejection fraction (EF) and cardiac volumes, the significance of their temporal changes (Delta) remains undetermined. This study examined temporal changes in neurohormones related to cardiac remodeling and prognosis in patients with systolic dysfunction and heart failure receiving therapeutic inhibition of the renin-angiotensin-aldosterone system. Temporal changes in plasma renin, angiotensin-II, aldosterone, epinephrine, norepinephrine, B-type natriuretic peptide (BNP), and N-terminal atrial natriuretic peptide (NT-ANP) in 768 treated patients with heart failure measured at baseline and 17 and 43 weeks after randomization were examined for their relations with concurrent changes in the EF, cardiac volumes, and risk for subsequent adverse clinical outcomes. Increasing BNP (p < 0.0001) and NT-ANP (p = 0.01) over time were associated with a concurrent decreasing EF, increasing end-diastolic volume (EDV), and increasing end-systolic volume (ESV; all p < 0.0001). In multivariable analysis, DeltaBNP and DeltaNT-ANP were independent predictors of DeltaESV and DeltaEDV, whereas DeltaBNP also predicted DeltaEF (all p < 0.0001). Patients who died or experienced heart failure hospitalization had larger antecedent increases in NT-ANP (+293.7 vs -21.5 pmol/ml, p = 0.006) and lesser decreases in norepinephrine (-22.3 vs -48.5 pg/ml, p = 0.04). Increasing NT-ANP (hazard ratio [HR] 3.45, p = 0.009) and norepinephrine (HR 2.04, p = 0.02) over time independently predicted increased risk for subsequent death or heart failure hospitalization. In conclusion, in treated patients with heart failure, increasing NT-ANP and BNP over time predict a decreasing EF and ventricular dilatation, while increasing NT-ANP and norepinephrine independently predict greater mortality and morbidity. Serial measurements of these neurohormones may serve as useful surrogate markers of ventricular remodeling and prognosticators for clinical risk stratification.
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PMID:Usefulness of temporal changes in neurohormones as markers of ventricular remodeling and prognosis in patients with left ventricular systolic dysfunction and heart failure receiving either candesartan or enalapril or both. 1612 99

As indicated in ancient Chinese medical books, Corydalis yanhusuo has therapeutic effects on cardiovascular diseases. The analgesic effect of this plant has been fully elucidated, and l-tetrahydropalmatine has been shown to be the main active principle. The aim of this investigation was to evaluate its protective effects in a rat heart failure model. Rats were subjected to coronary artery ligation, and orally administered with ethanolic extract of Corydalis yanhusuo 50, 100, or 200 mg kg(-1) daily, from the 7th day after surgery. We measured cardiac function, plasma atrial natriuretic peptide (ANP), relative heart and lung weights, infarct size and ventricular dilatation after treatment for 8 weeks. Administration with Corydalis yanhusuo led to a significant reduction in infarct size and improvement in cardiac function as demonstrated by lower left ventricular end diastolic pressure (LVEDP) and elevated +/-dp/dt(max). We also found that Corydalis yanhusuo significantly reduced left ventricular (LV)/body weight ratio, lung/body weight ratio and significantly inhibited neurohormonal activation. Taken together, this study indicated that Corydalis yanhusuo exerted salutary effects on heart failure induced by myocardial infarction in rats.
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PMID:Beneficial effects of the extract from Corydalis yanhusuo in rats with heart failure following myocardial infarction. 1752 35

Idiopathic dilated cardiomyopathy (IDCM) is a primary myocardial disease of unknown cause characterized by ventricular chamber enlargement with impaired contractile function. In familial forms of IDCM, mutations of genes coding for cytoskeletal proteins related to force transmission, such as dystrophin, cardiac actin, desmin, and delta-sarcoglycan, have been identified. Here, we report the data of a retrospective investigation carried out to evaluate the expression of atrial natriuretic peptide (ANP), CD34, troponin T and nestin in the myocardium of patients affected with IDCM. Formalin-fixed and paraffin-embedded consecutive tissue sections from the ventricular wall of 10 human normal hearts (NH) following forensic autopsy and 22 IDCM (living explanted hearts) were studied using primary monoclonal antibodies against ANP, CD34, troponin T and nestin by immunohistochemistry. Myocardial fibers were counted independently by three pathologists. Statistics included analysis of variance, log-rank test for Kaplan-Meier analysis, and kappa assessment for intra- and inter-observer variability. ANP and CD34 were significantly overexpressed in IDCM compared to NH (p<0.05). Conversely, troponin T and nestin expression levels did not show significant variation. Inter-observer kappa statistics showed a value of 0.87 and intra-observer kappa statistics a value of 0.98. Evaluation of the marker distribution in the myocardium of patients with IDCM CD34 expression curve was similar to that of troponin T (p<0.0001), although two groups could be identified. Patients with a difference of more than 20 myocardial fibers in expression of CD34 and troponin T had a somewhat less favorable survival although the difference was not significant. The analysis of cells positive for troponin T resulted in a similar number of cardiac fibers between NH and IDCM. This is in agreement with cardiac enlargement present in IDCM, which is due to ventricular dilatation rather than increased number of myocytes. Moreover, the expression of nestin, a marker of activation of myocardial precursors, did not change either, and this may confirm that there are no hyperplastic phenomena in the IDCM pathogenesis. The increase in ANP-positive cells in IDCM could be a consequence of neurohormonal activation due to a decline in the impaired myocyte contractility. Furthermore, since it was already shown that ANP could be important in the control of vascular remodeling, we postulated that the increase in CD34-positive cells might be functionally correlated with the increase in ANP production. Differential expression of CD34 and troponin T might be used in future studies to evaluate their prognostic value.
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PMID:Atrial natriuretic peptide and CD34 overexpression in human idiopathic dilated cardiomyopathies. 1809 54

The purpose of this study was to investigate the effect of resveratrol, a polyphenol present in grapes and red wine, on ventricular remodeling after myocardial infarction (MI) in rats. After permanent ligation of the left anterior descending artery, surviving rats were randomly allocated to three groups and treated with 1 mg/kg/day resveratrol (R-1 group), 0.1 mg/kg/day resveratrol (R-0.1 group), or vehicles (control group) administered by intraperitoneal injection once daily for four weeks. We examined the effects of resveratrol by echocardiography, hemodynamic studies, histologic examinations, and real-time quantitative polymerase chain reaction. The R-1 group had significantly increased fractional shortening of the left ventricle, ameliorated left ventricular dilatation, reduced left ventricular end-diastolic pressure, and reduced infarct size. In contrast, the R-0.1 group experienced no beneficial effects on myocardial infarction. The R-1 group also had significantly attenuated expression of myocardial atrial natriuretic peptide and transforming growth factor-beta1 mRNAs. This study indicates that resveratrol is a potent cardioprotective agent in MI rats. Its cardioprotective effects may be due to a reduction of atrial natriuretic peptide and transforming growth factor-beta1, which are known to protect the heart from detrimental remodeling.
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PMID:Resveratrol reduces infarct size and improves ventricular function after myocardial ischemia in rats. 1863 59


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