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1.
Chinese Journal of Pediatrics ; (12): 684-687, 2008.
Article in Chinese | WPRIM | ID: wpr-300699

ABSTRACT

<p><b>OBJECTIVE</b>Endocardial fibroelastosis (EFE), a common pediatric cardiovascular disease, often results in chronic heart failure (CHF) and death. Clinical trials have shown that the regimen of combining beta-adrenoreceptor blocker with traditional medicines against CHF can improve left ventricular function and prevent the ventricle from remodeling in patients with CHF. The present study aimed to observe the effect of carvedilol on concentration of plasma brain-type natriuretic peptide (BNP), and safety in children with EFE.</p><p><b>METHODS</b>Twenty-one children with EFE were randomly divided into two groups: (1) treated with traditional regimen (digoxin, prednisone and/or diuretics) (n = 10); (2) treated with carvedilol plus traditional regimen (n = 11). Measurement of plasma concentration of BNP by ELISA, cardiac function by ultrasound were performed before and after 6 months of treatment. The changes in clinical symptom, heart rate, heart function, side effect and maximal tolerance dose after treatment with carvedilol were observed.</p><p><b>RESULTS</b>Plasma concentration of BNP was much higher in the group of patients with EFE [(865 +/- 702) ng/L] than that of control group [(154 +/- 78) ng/L] (P < 0.01), and there was a positive correlation between plasma concentration of BNP and cardiac function classification, and cardiac function grades II, III, and IV corresponded to plasma concentration of BNP (286 +/- 125) ng/L, (437 +/- 386) ng/L, (1673 +/- 859) ng/L respectively in children with EFE. Compared with the group treated with traditional medicines, plasma concentration of BNP [(403 +/- 216) ng/L vs. (219 +/- 87) ng/L] significantly decreased, the clinical symptom was significantly improved, cardio-thoracic ratio (CTR) (0.60 +/- 0.05 vs. 0.54 +/- 0.06) (P < 0.05) and heart rate [(115 +/- 20) bpm vs. (90 +/- 14) bpm] (P < 0.01) decreased, ejection fraction (EF) (46.6% +/- 13.4% vs. 54.5% +/- 12.9%), fractional shortening (21.6% +/- 8.1% vs. 24.1% +/- 7.5%), mean velocity of circumferential fiber shortening [(0.8 +/- 0.5) cir/s vs. (0.9 +/- 0.4) cir/s] were significantly increased (P < 0.01), left ventricular end-systolic dimension [(34.0 +/- 8.6) mm vs. (32.2 +/- 9.1) mm] (P < 0.05), left ventricular mass [(65.9 +/- 34.1) g vs. (65.9 +/- 34.1) g], interventricular septal thickness at end-systole [(6.0 +/- 1.0) mm vs (5.5 +/- 1.1) mm] were notably decreased (P < 0.01) after treatment with carvedilol.</p><p><b>CONCLUSION</b>These data indicated that plasma concentration of BNP significantly increased in children with EFE, carvedilol can decrease plasma concentration of BNP, inhibit the remodeling of ventricle, significantly improve the cardiac function in children with EFE. Carvedilol is effective and safe in treatment of children with EFE.</p>


Subject(s)
Child , Child, Preschool , Female , Humans , Infant , Male , Adrenergic beta-Antagonists , Therapeutic Uses , Carbazoles , Therapeutic Uses , Endocardial Fibroelastosis , Drug Therapy , Natriuretic Peptide, Brain , Blood , Propanolamines , Therapeutic Uses , Treatment Outcome
2.
Chinese Journal of Pediatrics ; (12): 733-737, 2006.
Article in Chinese | WPRIM | ID: wpr-278600

ABSTRACT

<p><b>OBJECTIVES</b>Ventricular remodeling is an important pathologic progress in almost all end stage heart failure (HF), and it is characterized by ventricular thickening and cardiac fibrosis with poor prognosis. The connective tissue growth factor (CTGF), a new growth factor with multi-function, has an important role in fibrosis of tissue and organs. It has been demonstrated that angiotensin-converting enzyme inhibitor (ACEI) can prevent the development of cardiomyocyte from remodeling and improve cardiac function. Researchers try to test the hypothesis that cardiac function improvement attributable to ACEI is associated with inhibiting expression of CTGF in patients with HF. The aim of this study was to observe changes in CTGF expression in cardiomyocyte of young rats with HF and effect of benazepril on CTGF.</p><p><b>METHODS</b>The animal model of HF was established by constriction of abdominal aorta. Five weeks old rats were randomly divided into 3 groups after 6 weeks of operation: (1) HF group without treatment (n = 15); (2) HF group where rats were treated with benazepril (n = 15); (3) sham-operated group (n = 15) where rats were administered benazepril through direct gastric gavage. After 4 weeks of treatment, the high frequency ultrasound was performed. The expression of CTGF was detected by immunohistochemistry and semi-quantative reverse transcription-polymerase chain reaction.</p><p><b>RESULTS</b>Compared with the sham-operated group, left ventricular diastolic dimension (LVEDD), left ventricular systolic dimension (LVESD), interventricular septal thickness at end-diastole (IVSTd), interventricular septal thickness at end-systole (IVSTs), left ventricular posterior wall thickness at end-diastole (LVPWTd), left ventricular posterior wall thickness at end-systole (LVPWTs), left ventricular relative weight (LVRW), and right ventricular relative weight (RVRW) were all increased (P < 0.01), but ejection fraction (EF) and fractional shortening (FS) were decreased (P < 0.01). CTGF positive cells and expression of CTGF mRNA (0.609 +/- 0.065 vs 0.117 +/- 0.011, P < 0.01) were increased in HF group without treatment. LVESD, IVSTd, IVSTs, LVPWTd, LVPWTs, LVRW and RVRW were all decreased (P < 0.01), but FS and EF were increased (P < 0.01) in cases of HF treated with benazepril when compared with HF group without treatment. LVESD, IVSTd, IVSTs, LVPWTd, LVPWTs, LVRW and RVRW were higher (P < 0.01), EF and FS were lower (P < 0.01), CTGF positive cells and expression of CTGF mRNA were higher (P < 0.01) in HF group treated with benazepril than those of sham-operated group.</p><p><b>CONCLUSION</b>The expression of CTGF was increased in the cardiomyocyte of young rats with HF and benazepril could prevent left ventricular from remodeling partly and improve cardiac function by inhibiting the expression of CTGF in cardiomyocyte in cases of HF.</p>


Subject(s)
Animals , Male , Rats , Angiotensin-Converting Enzyme Inhibitors , Pharmacology , Benzazepines , Pharmacology , Connective Tissue Growth Factor , Metabolism , Disease Models, Animal , Heart Failure , Diagnostic Imaging , Drug Therapy , Metabolism , Immunohistochemistry , Myocytes, Cardiac , Metabolism , RNA, Messenger , Rats, Wistar , Reverse Transcriptase Polymerase Chain Reaction , Ultrasonography , Ventricular Dysfunction, Left , Diagnostic Imaging , Drug Therapy , Ventricular Remodeling
3.
Journal of Applied Clinical Pediatrics ; (24)2006.
Article in Chinese | WPRIM | ID: wpr-639279

ABSTRACT

Objective To observe the clinical effect and security of carvedilol on children with endocardial fibroelastosis(EFE).Methods Eighteen children with EFE treatment with carvedilol.The improvement of clinical symptom,heart rate,heart function,side effect and maximal tolerance dose after treatment with carvedilol were observed.Results The clinical symptom was obviously improved;eiection fraction(EF),fractional shortening(FS),mean velocity of circumferential fiber(Mvcf)were significantly increased,left ventricular end-systolic dimension(LVDS),left ventricular mass(LVmass),interventricular septal thickness(IVSs)were notably decreased after treatment with carvedilol.Conclusions The data indicates that carvedilol can significantly reduce left ventricular diastolic dimension(LVDD),IVSs,and LVmass,inhibit the remodeling of ventricle,significantly elevate the heart function of EFE.So carvedilol is benefit and security on children with EFE.

4.
Chinese Journal of Pediatrics ; (12): 603-607, 2005.
Article in Chinese | WPRIM | ID: wpr-312110

ABSTRACT

<p><b>OBJECTIVE</b>The release of intracellular stores of Ca(2+) occurs virtually in all types of cells by a means of amplifying external signals that modulate intracellular signaling events. In cardiac myocytes, type 2 ryanodine receptor (RyR(2)) is activated during excitation-contraction (E-C) coupling by Ca(2+)-induced Ca(2+) release (CICR) triggered by Ca(2+) influx across the sarcolemma. The hyperadrenergic state of heart failure results in leaky RyR(2) channels attributable to PKA hyperphosphorylation and depletion of the stabilizing FK506 binding protein, FKBP12.6. Dysregulation of sarcoplasmic reticulum (SR) Ca(2+) release via RyR(2) could contribute to defects in Ca(2+) signaling in failing hearts. Researchers tested the hypothesis that improved cardiac muscle function attributable to beta-AR blockade is associated with restoration of normal RyR(2) channel function in patients with heart failure. The authors aimed to observe change of RyR in junior mouse with HF and the effect of beta-adrenoreceptor blocker on RyR in HF in this experiment.</p><p><b>METHODS</b>The animal model of congestive heart failure was established by constriction of abdominal aorta. Five weeks old mice were randomly divided into 3 groups: (1) HF group without treatment (n = 20); (2) HF group treated with carvedilol (n = 20); (3) Sham-operated group (n = 20). Carvedilol was administered through direct gastric gavage. After 4 weeks of treatment the high frequency ultrasound was performed. Myocardial SR was fractionated with velocity centrifugation. The time courses of Ca(2+) uptake and leak were determined by fluorescent spectrophotometr.</p><p><b>RESULTS</b>Compared with the sham-operated group, left ventricular diastolic dimension (LVEDD) (P < 0.05), left ventricular systolic dimension (LVESD), interventricular septal thickness at end-diastole (IVSTd), interventricular septal thickness at end-systole (IVSTs), left ventricular posterior wall thickness at end-diastole (LVPWTd), and left ventricular posterior wall thickness at end-systole (LVPWTs) were all significantly increased (P < 0.01). Ejection fraction (EF) and fractional shortening (FS) were decreased (P < 0.01) in HF group without treatment. LVEDD (P < 0.05), LVESD, IVSTd, IVSTs, LVPWTd and LVPWTs were all prominently decresed (P < 0.01). EF and FS were increased (P < 0.01) in cases of HF treated with carvedilol when compared with HF group without treatment. After adding thapsigargin to the buffer including SR of three groups, there were fewer Ca(2+) leak in sham-operated group and HF group treated with carvedilol than that of HF group without treatment (P < 0.01), while after adding FK506 and thapsigargin together to the buffer including SR of three groups, there were marked Ca(2+) leak in sham-operated group and HF group treated with carvedilol (P < 0.01). However, there was no additional increase in Ca(2+) leak in HF group compared with that of the group where only thapsigargin was added (P > 0.05).</p><p><b>CONCLUSION</b>There is more cardiac Ca(2+) leak in HF. Carvedilol can inhibite Ca(2+) leak by restoring the contactation of FKBP12.6 back to RyR in HF to improve cardiac function and prevent left ventricle from remodeling.</p>


Subject(s)
Animals , Rats , Adrenergic beta-Antagonists , Pharmacology , Animals, Newborn , Calcium , Metabolism , Calcium Signaling , Calcium-Transporting ATPases , Carbazoles , Pharmacology , Disease Models, Animal , Heart Failure , Diagnostic Imaging , Drug Therapy , Metabolism , Myocardial Contraction , Myocytes, Cardiac , Metabolism , Propanolamines , Pharmacology , Rats, Wistar , Ryanodine Receptor Calcium Release Channel , Metabolism , Sarcoplasmic Reticulum , Metabolism , Spectrometry, Fluorescence , Thapsigargin , Pharmacology , Ultrasonography
5.
Journal of Applied Clinical Pediatrics ; (24)2004.
Article in Chinese | WPRIM | ID: wpr-638774

ABSTRACT

Objective To investigate the clinical characteristics of incomplete Kawasaki disease(KD).Methods Clinical data includi-ng test results,therapeutic methods were analyzed retrospectively in 579 patients with Kawasaki disease.They were divided into classic KD and incomplete KD and made a compared analysis.Results There were no significant differences in gender,age,symptom and laboratory examination between classic and incomplete KD.But the rate of coronary artery lesions was higher in incomplete KD(18.4%) than that of classic KD(11%).Conclusion The rate of coronary artery lesions was higher in incomplete KD,and it should be paid more attention to earlier diagnosis and earlier treatment.

6.
Chinese Journal of Pediatrics ; (12): 219-222, 2003.
Article in Chinese | WPRIM | ID: wpr-280534

ABSTRACT

<p><b>OBJECTIVE</b>Diet is an important factor influencing blood pressure and, increases in dietary carbohydrate intake can raise blood pressure in adult rats. A previous study showed that the blood pressure of the rats fed with high-carbohydrate was 5-20 mmHg higher than that of control rats. While the mechanism involved is not clear. This study aimed to investigate the effects of high-sucrose intake on blood pressure of young Wistar rats and the role that sympathetic nerve system in the process.</p><p><b>METHODS</b>Male neonatal Wistar rats were performed sympathectomy operation with 6-hydroxydopamine (6-OHDA) and then divided into four groups: (1) 0.1% VitC saline-common diet group (VN), (2) 0.1% VitC saline-high sucrose (VS), (3) 6-OHDA-common diet group (OHN) and (4) 6-OHDA-high sucrose (OHS) after three week. The data on the body weight (BW), systolic blood pressure (SBP) and heart rate (HR) were recorded. Then the level of blood glucose, serum insulin and angiotensin II (AngII) were measured and the functional studies of the thoracic aorta was performed.</p><p><b>RESULTS</b>The VS group exhibited higher SBP than the OHS group from the 6th week (113.7 +/- 4.2 mmHg vs. 104.0 +/- 5.8 mmHg, P < 0.01) and the VN group from the 7th week (117.6 +/- 6.3 mmHg vs. 109.6 +/- 4.6 mmHg, P < 0.01), while the SBP of the VN group was similar to those of the OHN group and the OHS group (P > 0.05). No significant differences in blood glucose, serum insulin and insulin sensitive index (ISI) were found among the four groups. The thoracic aorta segments of the VS group had higher contractive response to AngII (P < 0.01) and NE (P < 0.05) than the VN group, but the relaxations to acetylcholine (ACh) and nitroglycerine (NTG) showed no difference among the four groups (P > 0.05).</p><p><b>CONCLUSION</b>The high-sucrose diet might elevate the blood pressure in young Wistar rats and the sympathetic system may play an important role in this process.</p>


Subject(s)
Animals , Male , Rats , Angiotensin II , Blood , Animal Feed , Blood Glucose , Metabolism , Blood Pressure , Physiology , Body Weight , Dietary Sucrose , Insulin , Blood , Oxidopamine , Blood , Rats, Wistar , Sympathectomy
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