Effect of Atractylodes macrocephala extract on chronic heart failure in rats

Purpose: To investigate the effect of Atractylodes macrocephala extract (AME) on oxidative stress and hemodynamics in chronic congestive heart failure (CHF) rats. Methods: After Sprague Dawley (SD) rats were successfully establised into CHF, they were randomly divided into normal control group, negative control group, captopril group, as well as 1.4, 2.8 and 5.6 g/kg of AME groups, and treated with drugs for 4 weeks. Hemodynamic function, whole heart weight index, blood creatinine kinase (CK), superoxide dismutase (SOD), malondialdehyde (MDA), nitric oxide (NO), nitric oxide synthase (NOS) were measured. Results: Compared with the normal control group, arterial systolic pressure (SBP)(83.12 ± 16.21 mmHg), diastolic pressure (DBP, (75.16 ± 20.18 mmHg), mean arterial pressure (MAP 76.32 ± 13.43 mmHg), heart rate (HR 353.25 ± 36.34 beats/min), left ventricular systolic peak (LVSP 101.24 ± 16.13 mmHg), and left ventricular pressure change rate (dp/dt max) significantly decreased (p < 0.05), while left ventricular end diastolic pressure (LVEDP (22.13 ± 1.57 mmHg), whole heart weight index (2.74 ± 0.16 mg/g), blood CK (0.93 ± 0.14 U/mL), MDA (19.13 ± 2.26 nmol/mL), NO (34.21 ± 3.16 umol/L), and NOS (42.13 ± 3.24 U/mL) increased significantly increased in the negative control group (p < 0.05). High dose AME significantly improved hemodynamic function, lowered MDA (8.75 ± 2.09 nmol/mL) and NO (22.14 ± 3.27 umol/L) levels (p < 0.05), and also decreased CK (0.57 ± 0.31 U/mL) and NOS (24.24 ± 3.38 U/mL) in CHF rats (p < 0.05). Conclusion: AME significantly improve adriamycin-induced chronic congestive heart failure in rats, which could be used for the therapeutic management of chronic congestive heart failure in future.

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Ophiopogon japonicas (Linn. f.) Ker-Gawl. extract ameliorates chronic heart failure in rats

Tropical Journal of Pharmaceutical Research ◽

10.4314/tjpr.v18i9.10 ◽

2021 ◽

Vol 18 (9) ◽

pp. 1853-1857

Author(s):

Hu-zhi Cai ◽

Yan-ping Tang ◽

Xin-yu Chen ◽

Hai-bo Xie ◽

Qing-yang Chen ◽

...

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Diastolic Pressure ◽

Left Ventricular ◽

Normal Control Group ◽

Heart Weight ◽

Control Group ◽

High Dose ◽

Chronic Congestive Heart Failure ◽

Whole Heart

Purpose: To investigate the effect of Ophiopogon japonicas (Linn. f.) Ker-Gawl. extract (OJKE) on oxidative stress and hemodynamics in chronic congestive heart failure (CHF) rats. Methods: The rats were modelled to congestive heart failure (except normal group) , and then randomly divided into normal control group, model (untreated) group, captopril group, high-dose, middle-dose and low-dose of OJKE groups. They were treated for 4 weeks as appropriate for each group. At the end of treatment, the hemodynamic function, whole heart weight index, and blood creatinine kinase (CK), as well as superoxide dismutase (SOD), malondialdehyde (MDA), nitric oxide (NO), nitricoxide synthase (NOS) were determined. Results: Compared with the normal control group, arterial systolic pressure (SBP), diastolic pressure (DBP), mean arterial pressure (MAP), heart rate (HR), left ventricular systolic peak (LVSP), and left ventricular pressure change rate (dp/dt max) significantly decreased (p < 0.05), while left ventricular end diastolic pressure (LVEDP), whole heart weight index, blood CK, MDA, NO, NOS significantly increased in the untreated group (p < 0.05). A high dose of OJKE significantly improved hemodynamic function, lowered MDA (8.33 ± 2.12 nmol/mL) and NO (20.58 ± 3.53 umol/L) levels (p < 0.05), and also decreased CK (0.53±0.37 U/mL) and NOS (22.46±3.29 U/mL) in CHF rats (p < 0.05). Conclusion: OJKE improved adriamycin-induced chronic congestive heart failure in rats significantly.

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Effect of Zhen-wu decoction on chronic heart failure in rats

Tropical Journal of Pharmaceutical Research ◽

10.4314/tjpr.v16i10.18 ◽

2017 ◽

Vol 16 (10) ◽

pp. 2439-2443

Author(s):

Zhongyong Liu ◽

Lin Li ◽

Shihua Luo ◽

Jia Fang

Keyword(s):

Heart Failure ◽

Diastolic Pressure ◽

Left Ventricular ◽

Normal Control Group ◽

Heart Weight ◽

Control Group ◽

High Dose ◽

Chronic Congestive Heart Failure ◽

Hemodynamic Function ◽

Whole Heart

Purpose: To investigate the effect of Zhen-wu decoction (ZWD) on oxidative stress and hemodynamics in chronic congestive heart failure (CHF) rats.Methods: After Sprague Dawley (SD) rats were successfully prepared into CHF, they were randomly divided into normal control group, model (untreated CHF) group, captopril group, high-dose, middledose and low-dose of ZWD groups, and were treated with drugs for 4 weeks respectively. At the end of the experiment, hemodynamic function, whole heart weight index, blood creatinine kinase (CK), superoxide dismutase (SOD), malondialdehyde (MDA), nitric oxide (NO) and nitric oxide synthase (NOS) were determined.Results: Compared with normal control group, ZWD group showed decreased arterial systolic pressure (SBP, 89.16 ± 17.27 mmHg), diastolic pressure (DBP, 72.54 ± 22.36 mmHg), mean arterial pressure (MAP, 72.64 ± 11.87 mmHg), heart rate (HR, 368.25 ± 39.12 beats/min), left ventricular systolic peak (LVSP, 105.27 ± 15.23 mmHg), and left ventricular pressure change rate (dp/dt max) (p < 0.05), while left ventricular end diastolic pressure (LVEDP) (19.52 ± 1.89 mmHg), whole heart weight index (2.74 ± 0.16 mg/g), blood CK (0.98 ± 0.16 U/mL), MDA (17.28 ± 2.94 nmol/mL), NO (36.35 ± 3.27 umol/L), NOS (39.89 ± 3.56 U/mL) significantly increased (p < 0.05). High dose of ZWD significantly improved hemodynamic function, lowered MDA (8.85 ± 2.14 nmol/mL) and NO (24.25 ± 3.21 umol/L) levels (p < 0.05), and also decreased CK (0.58 ± 0.37 U/mL) and NOS (26.12 ± 3.87 U/mL) in CHF rats (p < 0.05).Conclusion: ZWD improves adriamycin-induced chronic congestive heart failure in rats significantly, and therefore has potential to be developed for the management of chronic congestive heart failure.Keywords: Zhen-wu decoction, Chronic heart failure, Hemodynamic function, Oxidative stress

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1990.258.5.h1603 ◽

1990 ◽

Vol 258 (5) ◽

pp. H1603-H1605 ◽

Cited By ~ 12

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.

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Changing Strategies in the Management of Chronic Congestive Heart Failure

DICP ◽

10.1177/106002809102501214 ◽

1991 ◽

Vol 25 (12) ◽

pp. 1349-1354 ◽

Cited By ~ 1

Author(s):

Daniel E. Hilleman ◽

Syed M. Mohiuddin

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Mortality Rate ◽

Heart Transplantation ◽

Nyha Class ◽

Class Ii ◽

Left Ventricular ◽

Fixed Dose ◽

Chronic Congestive Heart Failure ◽

Organ Systems

Recent studies have more clearly defined the role of drug therapy in patients with chronic congestive heart failure (CHF). Treatment of patients with asymptomatic left ventricular dysfunction (New York Heart Association [NYHA] class I) cannot be recommended at this time. The benefit of prophylactic treatment with angiotensin-converting enzyme inhibitors (ACEIs) or vasodilators in patients at high risk for developing symptomatic CHF is currently being evaluated. Treatment of patients with symptomatic CHF (NYHA class II-IV) should be initiated with a combination of a diuretic, digoxin, and an ACEI. This combination has been shown to reduce the mortality rate in patients with NYHA class II-IV CHF. Patients who remain symptomatic despite treatment with this combination may benefit from the addition of the direct-acting, nonspecific vasodilators—hydralazine and a nitrate. The addition of the nonspecific vasodilators to an ACEI has not been tested in controlled trials. In patients who remain symptomatic despite treatment with diuretics, digoxin, ACEIs, and nonspecific vasodilators, treatment options are not clear. The use of beta-agonists, phosphodiesterase inhibitors, and intermittent fixed-dose, fixed-interval dobutamine should be avoided as these agents are associated with a high mortality rate. Heart transplantation should be considered early in the course of CHF to allow for preservation of other vital organ systems. Unfortunately, heart transplantation is available to only a very small minority of potential transplant candidates.

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Congestive Heart Failure in Copper-Deficient Mice

Experimental Biology and Medicine ◽

10.1177/15353702-0322807-06 ◽

2003 ◽

Vol 228 (7) ◽

pp. 811-817 ◽

Cited By ~ 44

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.

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Ginsenoside Re Improves Isoproterenol-Induced Myocardial Fibrosis and Heart Failure in Rats

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2019/3714508 ◽

2019 ◽

Vol 2019 ◽

pp. 1-9 ◽

Cited By ~ 2

Author(s):

Quan-wei Wang ◽

Xiao-feng Yu ◽

Hua-li Xu ◽

Xue-zhong Zhao ◽

Da-yuan Sui

Keyword(s):

Heart Failure ◽

Myocardial Fibrosis ◽

Group Treatment ◽

Transforming Growth Factor ◽

Diastolic Pressure ◽

Systolic Pressure ◽

Left Ventricular ◽

Heart Weight ◽

Hydroxyproline Content ◽

Ginsenoside Re

Objective. Panax ginseng is used widely for treatment of cardiovascular disorders in China. Ginsenoside Re is the main chemical component of P. ginseng. We aimed to investigate the protective effect of ginsenoside Re on isoproterenol-induced myocardial fibrosis and heart failure in rats. Methods. A model of myocardial fibrosis and heart failure was established by once-daily subcutaneous injection of isoproterenol (5 mg/kg/day) to rats for 7 days. Simultaneously, rats were orally administrated ginsenoside Re (5 or 20 mg/kg) or vehicle daily for 4 weeks. Results. Isoproterenol enhanced the heart weight, myocardial fibrosis, and hydroxyproline content in rat hearts. Ginsenoside Re inhibited (at least in part) the isoproterenol-induced increase in heart weight, myocardial fibrosis, and hydroxyproline content. Compared with the isoproterenol group, treatment with ginsenoside Re ameliorated changes in left ventricular systolic pressure, left ventricular end diastolic pressure, and the positive and negative maximal values of the first derivative of left ventricular pressure. Ginsenoside Re administration also resulted in decreased expression of transforming growth factor (TGF)-β1 in serum and decreased expression of Smad3 and collagen I in heart tissue. Conclusion. Ginsenoside Re can improve isoproterenol-induced myocardial fibrosis and heart failure by regulation of the TGF-β1/Smad3 pathway.

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Cardiac Triangle Mapping: A New Systems Approach for Noninvasive Evaluation of Left Ventricular End Diastolic Pressure

Fluids ◽

10.3390/fluids4010016 ◽

2019 ◽

Vol 4 (1) ◽

pp. 16

Author(s):

Niema M Pahlevan ◽

Ray V Matthews

Keyword(s):

Heart Failure ◽

Left Ventricle ◽

Systems Approach ◽

Diastolic Pressure ◽

Unmet Need ◽

Left Ventricular ◽

Time Interval ◽

Chronic Congestive Heart Failure ◽

Intrinsic Frequency ◽

Future Design

Noninvasive and practical assessment of hemodynamics is a critical unmet need in the treatment of both chronic and acute cardiovascular diseases. Particularly, the ability to monitor left ventricular end-diastolic pressure (LVEDP) noninvasively offers enormous benefit for managing patients with chronic congestive heart failure. Recently, we provided proof of concept that a new cardiac metric, intrinsic frequency (IF), derived from mathematical analysis of non-invasively captured arterial waveforms, can be used to accurately compute cardiovascular hemodynamic measures, such as left ventricle ejection fraction (LVEF), by using a smartphone. In this manuscript, we propose a new systems-based method called cardiac triangle mapping (CTM) for hemodynamics evaluation of the left ventricle. This method is based on intrinsic frequency (IF) and systolic time interval (STI) methods that allows computation of LVEDP from noninvasive measurements. Since the CTM method only requires arterial waveform and electrocardiogram (ECG), it can eventually be adopted as a simple smartphone-based device, an inexpensive hand-held device, or perhaps (with future design modifications) a wearable sensor. Such devices, combined with this method, would allow for remote monitoring of heart failure patients.

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Expectoration of bronchial casts in association with Ramipril treatment

Cardiology in the Young ◽

10.1017/s1047951119002294 ◽

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.

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