scholarly journals TMAO, a seafood-derived molecule, produces diuresis and reduces mortality in heart failure rats

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Marta Gawrys-Kopczynska ◽  
Marek Konop ◽  
Klaudia Maksymiuk ◽  
Katarzyna Kraszewska ◽  
Ladislav Derzsi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Protein Structure ◽  
Circulatory System ◽  
Correlation Spectroscopy ◽  
Sprague Dawley ◽  
Water Control ◽  
Spontaneously Hypertensive ◽  
Beneficial Effects ◽  
Contracting Heart

Trimethylamine-oxide (TMAO) is present in seafood which is considered to be beneficial for health. Deep-water animals accumulate TMAO to protect proteins, such as lactate dehydrogenase (LDH), against hydrostatic pressure stress (HPS). We hypothesized that TMAO exerts beneficial effects on the circulatory system and protects cardiac LDH exposed to HPS produced by the contracting heart. Male, Sprague-Dawley and Spontaneously-Hypertensive-Heart-Failure (SHHF) rats were treated orally with either water (control) or TMAO. In vitro, LDH with or without TMAO was exposed to HPS and was evaluated using fluorescence correlation spectroscopy. TMAO-treated rats showed higher diuresis and natriuresis, lower arterial pressure and plasma NT-proBNP. Survival in SHHF-control was 66% vs 100% in SHHF-TMAO. In vitro, exposure of LDH to HPS with or without TMAO did not affect protein structure. In conclusion, TMAO reduced mortality in SHHF, which was associated with diuretic, natriuretic and hypotensive effects. HPS and TMAO did not affect LDH protein structure.

scholarly journals TMAO, a seafood-derived molecule, produces diuresis and reduces mortality in heart failure rats

2020 ◽  
Author(s):  
Marta Gawrys-Kopczynska ◽  
Marek Konop ◽  
Klaudia Maksymiuk ◽  
Katarzyna Kraszewska ◽  
Ladislav Derzsi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Hydrostatic Stress ◽  
Oral Treatment ◽  
Circulatory System ◽  
Correlation Spectroscopy ◽  
Sprague Dawley ◽  
Spontaneously Hypertensive ◽  
Arterial Blood ◽  
Contracting Heart

ABSTRACTBackgroundThere is an ongoing debate whether trimethylamine-oxide (TMAO), a molecule present in seafood and a derivate of microbiota metabolism, is beneficial or harmful for the circulatory system. Interestingly, deep-water animals accumulate TMAO that protects proteins such as lactate dehydrogenase (LDH) against high hydrostatic pressure. We hypothesized that TMAO may benefit the circulatory system by protecting cardiac LDH exposed to hydrostatic stress (HS) produced by contracting heart.Methods and ResultsMale, 6-week-old, Sprague-Dawley (SD, n=40) and Spontaneously-Hypertensive-Heart-Failure (SHHF n=18) rats were divided into either Water or TMAO oral treatment. After 56 weeks, half of Water and TMAO SD rats were given isoprenaline (ISO) to produce catecholamine stress. In vitro, LDH with or without TMAO was exposed to HS (changes in pressure 0-250mmHg x 280min−1) and was evaluated using fluorescence correlation spectroscopy. After 58 weeks of the treatment survival was 100% in SD-Water, SD-TMAO, ISO-TMAO and 90% in ISO-Water. In SHHF-Water survival was 66% vs 100% in SHHF-TMAO. In general, TMAO-treated rats showed higher diuresis and natriuresis. In comparison to SHHF-Water, SHHF-TMAO showed significantly lower diastolic arterial blood pressure, plasma NT-proBNP and expression of angiotensinogen and AT1 receptors in the heart. In separate experiments, intravenous TMAO but not vehicle or urea significantly increased diuresis in SD. In vitro, exposure of LDH to HS with or without TMAO did not affect the protein structure.ConclusionsTMAO reduces mortality in SHHF rats that is associated with diuretic, natriuretic and hypotensive effects. HS produced by the contracting heart is neutral for cardiac LDH structure.

Diabetes and Heart Failure: Is it Hyperglycemia or Hyperinsulinemia?

2020 ◽  
Vol 18 (2) ◽  
pp. 148-157 ◽  
Author(s):  
Triantafyllos Didangelos ◽  
Konstantinos Kantartzis
Keyword(s):  
Heart Failure ◽  
Insulin Treatment ◽  
Close Association ◽  
Adverse Outcomes ◽  
Negative Effects ◽  
Beneficial Effects ◽  
Appropriate Treatment ◽  
Increased Risk ◽  
Treatment Of Diabetes

The cardiac effects of exogenously administered insulin for the treatment of diabetes (DM) have recently attracted much attention. In particular, it has been questioned whether insulin is the appropriate treatment for patients with type 2 diabetes mellitus and heart failure. While several old and some new studies suggested that insulin treatment has beneficial effects on the heart, recent observational studies indicate associations of insulin treatment with an increased risk of developing or worsening of pre-existing heart failure and higher mortality rates. However, there is actually little evidence that the associations of insulin administration with any adverse outcomes are causal. On the other hand, insulin clearly causes weight gain and may also cause serious episodes of hypoglycemia. Moreover, excess of insulin (hyperinsulinemia), as often seen with the use of injected insulin, seems to predispose to inflammation, hypertension, dyslipidemia, atherosclerosis, heart failure, and arrhythmias. Nevertheless, it should be stressed that most of the data concerning the effects of insulin on cardiac function derive from in vitro studies with isolated animal hearts. Therefore, the relevance of the findings of such studies for humans should be considered with caution. In the present review, we summarize the existing data about the potential positive and negative effects of insulin on the heart and attempt to answer the question whether any adverse effects of insulin or the consequences of hyperglycemia are more important and may provide a better explanation of the close association of DM with heart failure.

Abstract 131: Anti-inflammatory and Mitochondrial Effects of Butyrate in Shr Astrocytes in vitro

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Tao Yang ◽  
Ty Redler ◽  
Carla G Bueno Silva ◽  
Rebeca Arocha ◽  
Jordan Schmidt ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Rna Isolation ◽  
Inflammatory Factors ◽  
Pcr Analysis ◽  
Sprague Dawley ◽  
Beneficial Effects ◽  
Sd Rats ◽  
Anti Inflammatory

Emerging evidence demonstrates a significant link between gut dysbiosis and hypertension (HTN). Butyrate is one of the major fermented end-products of gut microbiota that reportedly produces beneficial effects on the immune system and metabolism. A contraction in butyrate-producing bacteria in the gut of spontaneously hypertensive rats (SHR) suggests that reduced butyrate may be associated with HTN. Considering its role in mitochondrial metabolism, we proposed that the positive anti-inflammatory effects of butyrate may be mediated via improvement in mitochondrial function in astrocytes. Methods: Sprague Dawley (SD) and SHR primary astrocytes from two-day old pups were cultured in DMEM, supplemented with 10% FBS and 1% pen/strep, for 14 days, prior to treatment with butyrate (0-1mM) for 4 hours. Cells were then subjected to the Seahorse XFe24 Extracellular Flux Analyzer to evaluate mitochondrial function following butyrate treatment. Additional samples were collected for total RNA isolation for real time PCR analysis of inflammatory factors and transcripts related to mitochondrial function and stress. Results: Butyrate significantly increased both basal and maximal mitochondrial respiration (by 3-4 fold, P<0.001) and elevated proton leak (by 4 fold, P<0.01) in astrocytes from SD rats but not SHR. Furthermore, we observed a trend for an increase in both ATP-linked and non-mitochondrial respiration in SD astrocytes compared to SHR (by 2-3 fold, P=0.07). This was associated with a significant reduction in relative expression levels in catalase (by 50%, P<0.05) and a trend in reduction in Sod1 and Sod2 (by 25%-50%, P=0.1) in astrocytes harvested from SD rats but not the SHR. Conversely, butyrate significantly lowered expression of pro-inflammatory Ccl2 (by 33%, P<0.05) and Tlr4 (by 48%, P <0.05) in astrocytes of SHR, but not SD rats. Conclusion: Butyrate modulated mitochondrial bioenergetics in SD but not the SHR, suggesting that the mitochondria of astrocytes may be less sensitive to the effects of butyrate in HTN. In addition, butyrate reduced inflammatory mediators in the SHR, but had no effect in the SD rat astrocytes. Thus, central anti-inflammatory effects of butyrate may be mediated via a mitochondria-independent mechanism.

Neurons from neonatal hypertensive rats exhibit abnormal membrane properties in vitro

1990 ◽  
Vol 259 (3) ◽  
pp. C389-C396 ◽  
Author(s):  
B. C. Jubelin ◽  
M. S. Kannan
Keyword(s):  
Action Potentials ◽  
Membrane Properties ◽  
Sprague Dawley ◽  
Spontaneously Hypertensive ◽  
Enzymatic Dissociation ◽  
Sd Rats ◽  
High Calcium ◽  
Cervical Ganglia ◽  
Wistar Kyoto

The in vitro membrane properties of neurons from superior cervical ganglia (SCG) of neonatal spontaneously hypertensive (SH), Wistar-Kyoto (WKY), and Sprague-Dawley (SD) rats were studied with microelectrodes. Neurons were obtained by enzymatic dissociation, plated, irradiated, and studied after 2-5 wk. Most SH neurons showed multiple action potentials in response to an intracellular long-duration depolarizing pulse (multiple firing), whereas most neurons from WKY or SD rats generated only one or two action potentials. Multiple firing was inhibited by low concentrations of cobalt (10(-5) M) but not by tetrodotoxin (TTX) (3 x 10(-6) M). Neither high calcium (5-10 x 10(-3) M) nor the Ca2+(-)channel opener BAY K 8644 (10(-6) M) could induce multiple firing in SD or WKY neurons. However, multiple firing was readily induced by apamin (10(-6) M) or tetraethylammonium chloride (5 x 10(-3) M) (Ca2+(-)activated K+(-)channels blockers), with cobalt and TTX sensitivities similar to native multiple-firing neurons. We conclude that 1) multiple firing is characteristic of neonate SH rats SCG neurons in vitro and depends on regenerative Ca2+ currents; 2) multiple firing in SH neurons results from a lack of activation of a Ca2+(-)activated K+ conductance and not from a lack of internal Ca2+ availability; and 3) multiple firing in SCG neurons mirrors a default in K+ conductance common to all cells in genetically hypertensive individuals.

scholarly journals EVALUATION OF BENEFICIAL EFFECTS OF LINUM USITATISSIMUM IN CONGESTIVE HEART FAILURE

2017 ◽  
Vol 9 (10) ◽  
pp. 62
Author(s):  
Pravin Tirgar ◽  
Limbasiya Kalpesh
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Linum Usitatissimum ◽  
Positive Inotropic Effect ◽  
Methanolic Extract ◽  
In Vitro Study ◽  
Control Group ◽  
Force Of Contraction ◽  
Beneficial Effects

Objective: Evaluation of beneficial effects of the seed of Linum usitatissimum in congestive heart failure.Methods: Methanolic extract of seeds of Linumusitatissimum (MELU) was prepared using soxhlet apparatus and oil of seed of Linumusitatissimum (OLU) was isolated using Clevenger apparatus. The positive inotropic action of methanolic extract of seeds of Linum usitatissimum was evaluated using Langendorff’s assembly (in vitro study). Beneficial effects of methanolic extract and oil of seeds of Linum usitatissimum were carried out by doxorubicin (1 mg/kg, i. p. within 3 w) to induce congestive heart failure (in vivo study). Parameters like electrocardiogram (ECG) recording and cytosolic Ca2+level and histopathology of the heart were carried out. In same study diuretic action was evaluated using Lipschitz model.Results: Methanolic extract of seeds of Linum usitatissimum showed significantly increased in positive inotropic effect (force of contraction 48.8±1.53 mm) as compared to control group (force of contraction 17.5±0.76 mm) on Langendorff”s study (in vitro study). In doxorubicin-induced congestive heart failure both MELU and OLU showed significant decreased QT (Note: In cardiology, the QT interval is a measure of the time between the start of the Q wave and the end of the T wave in the heart's electrical cycle. There is no full form for this medical word) interval. The histopathologic study indicated the least damage to the architecture of myocardial membrane. MELU and OLU increased urine output (5.66±0.16 ml and 6.58±0.15 ml respectively) significantly in Lipschitz model as compared to disease control group (4.58±0.15 ml).Conclusion: Present research work emphasizes that the seeds of Linum usitatissimum is beneficial in the management of congestive heart failure because of having positive inotropic effect, diuretic activity and control of rhythmicity of heart.

Validation of Cardiac Output as Reported by a Permanently Implanted Wireless Sensor

2015 ◽  
Vol 10 (1) ◽  
Author(s):  
Michael Tree ◽  
Jason White ◽  
Prem Midha ◽  
Samantha Kiblinger ◽  
Ajit Yoganathan
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Measurement Accuracy ◽  
Circulatory System ◽  
Left Heart Failure ◽  
Mock Circulatory System ◽  
System A ◽  
Reference Flow ◽  
Relevant Range

The CardioMEMS heart failure (HF) system was tested for cardiac output (CO) measurement accuracy using an in vitro mock circulatory system. A software algorithm calculates CO based on analysis of the pressure waveform as measured from the pulmonary artery, where the CardioMEMS system resides. Calculated CO was compared to that from reference flow probe in the circulatory system model. CO measurements were compared over a clinically relevant range of stroke volumes and heart rates with normal, pulmonary hypertension (PH), decompensated left heart failure (DLHF), and combined DHLF + PH hemodynamic conditions. The CardioMEMS CO exhibited minimal fixed and proportional bias.

scholarly journals Neuregulins: protective and reparative growth factors in multiple forms of cardiovascular disease

2020 ◽  
Vol 134 (19) ◽  
pp. 2623-2643
Author(s):  
Andrew Geissler ◽  
Sergey Ryzhov ◽  
Douglas B. Sawyer
Keyword(s):  
Heart Failure ◽  
Cardiovascular Disease ◽  
Tyrosine Kinases ◽  
Cardiac Myocyte ◽  
Diastolic Heart Failure ◽  
Systolic Heart Failure ◽  
Circulatory System ◽  
Cardiovascular Responses ◽  
Adaptive Responses ◽  
Beneficial Effects

Abstract Neuregulins (NRGs) are protein ligands that act through ErbB receptor tyrosine kinases to regulate tissue morphogenesis, plasticity, and adaptive responses to physiologic needs in multiple tissues, including the heart and circulatory system. The role of NRG/ErbB signaling in cardiovascular biology, and how it responds to physiologic and pathologic stresses is a rapidly evolving field. While initial concepts focused on the role that NRG may play in regulating cardiac myocyte responses, including cell survival, growth, adaptation to stress, and proliferation, emerging data support a broader role for NRGs in the regulation of metabolism, inflammation, and fibrosis in response to injury. The constellation of effects modulated by NRGs may account for the findings that two distinct forms of recombinant NRG-1 have beneficial effects on cardiac function in humans with systolic heart failure. NRG-4 has recently emerged as an adipokine with similar potential to regulate cardiovascular responses to inflammation and injury. Beyond systolic heart failure, NRGs appear to have beneficial effects in diastolic heart failure, prevention of atherosclerosis, preventing adverse effects on diabetes on the heart and vasculature, including atherosclerosis, as well as the cardiac dysfunction associated with sepsis. Collectively, this literature supports the further examination of how this developmentally critical signaling system functions and how it might be leveraged to treat cardiovascular disease.

scholarly journals Cytoprotective roles of epigallocatechin gallate and resveratrol on staurosporine-treated mesenchymal stem cells in in vitro culture

2021 ◽  
Vol 67 (3) ◽  
pp. 45-52
Author(s):  
Arkadiusz Burczak ◽  
Magdalena Kosiedowska ◽  
Paulina Borkowska ◽  
Jan Kowalski
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Negative Impact ◽  
Colorimetric Assay ◽  
Antioxidant Properties ◽  
Circulatory System ◽  
Epigallocatechin Gallate ◽  
Regenerative Capacity ◽  
Beneficial Effects

Summary Introduction: There are many scientific reports on the beneficial effects of epigallocatechin gallate and resveratrol on the human body, e.g. antioxidant properties, a protective effect on the circulatory system and reduction of inflammation. Objective: The aim of the study was to evaluate the effect of these substances on the survival of mesenchymal stem cells (MSC) in the presence of the pro-apoptotic factor staurosporine. Methods: Cell viability WST-1 colorimetric assay. Results: It was confirmed that both 25 µM/ml and 50 µM/ml of epigallocatechin and 50 µM/ml of resveratrol statistically significantly increased the MSC survival rate. Conclusion: An excess supply of epigallocatechin gallate (50 µM/ml and higher) has a cytotoxic effect on MSC, which may have a negative impact on the body’s auto-regenerative capacity. Under toxic and stressful conditions, resveratrol and epigallocatechin gallate perform cytoprotective functions, thereby reducing the negative impact of toxic environmental conditions on the mesenchymal stem cells.

Myocardial tumor necrosis factor-α secretion in hypertensive and heart failure-prone rats

1999 ◽  
Vol 277 (2) ◽  
pp. H543-H550 ◽  
Author(s):  
Marina R. Bergman ◽  
Ruey H. Kao ◽  
Sylvia A. McCune ◽  
Bethany J. Holycross
Keyword(s):  
Heart Failure ◽  
Tumor Necrosis Factor ◽  
Cardiac Function ◽  
Cardiac Remodeling ◽  
Tumor Necrosis ◽  
Left Ventricular ◽  
Sprague Dawley ◽  
Spontaneously Hypertensive ◽  
Tnf Α ◽  
Necrosis Factor

Acute increases in blood pressure (BP) increase myocardial tumor necrosis factor (TNF)-α production, but it is not known whether chronic hypertensive stress elevates myocardial TNF-α production, possibly contributing to cardiac remodeling, decreased cardiac function, and faster progression to heart failure. BP, cardiac function, and size were evaluated in normotensive [Sprague-Dawley (SD)], spontaneously hypertensive (SHR), and spontaneously hypertensive heart failure-prone (SHHF) rats at 6, 12, 15, and 18 mo of age and in failing SHHF. Left ventricular tissues were evaluated for secretion of bioactive TNF-α and inhibition of TNF-α secretion by phosphodiesterase inhibitors. All ventricles secreted bioactive and immunoreactive TNF-α, but secretion decreased with age. SHR and SHHF rats secreted more TNF-α than SD rats at 6 mo of age, but only failing SHHF rats secreted significantly more TNF-α at 18 mo. Amrinone inhibited TNF-α secretion in all rats and was less potent but more efficacious than RO-201724 in all strains. TNF-α secretion correlated with BP and left ventricular mass in 6-mo-old rats, but this relationship disappeared with age. Results suggest that hypertension and/or cardiac remodeling is associated with elevated myocardial TNF-α, and, although hypertension, per se, did not maintain elevated cardiac TNF-α levels, SHHF rats increase TNF-α production during the end stages of failure.

Age-dependent augmentation of cardiac endothelial NOS in a genetic rat model of heart failure

1997 ◽  
Vol 273 (3) ◽  
pp. H1223-H1230 ◽  
Author(s):  
F. H. Khadour ◽  
R. H. Kao ◽  
S. Park ◽  
P. W. Armstrong ◽  
B. J. Holycross ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Left Ventricular ◽  
Shr Rats ◽  
Sprague Dawley ◽  
Spontaneously Hypertensive ◽  
Nitrite Level ◽  
Sd Rats ◽  
Enhanced Expression ◽  
Nitrate And Nitrite

Alterations in nitric oxide (NO) biosynthesis in the heart have been implicated in the pathophysiology of heart failure. We compared changes in cardiac nitric oxide synthase (NOS) activity and expression in genetically heart failure-prone (SHHF) rats at 6, 12, and 18 mo of age with those in age-matched spontaneously hypertensive (SHR) and Sprague-Dawley (SD) rats. Systolic blood pressure was significantly higher in SHHF and SHR rats compared with SD rats; however, it declined with age in SHHF rats only. Left ventricular mass increased with age in SHR and SHHF, but not in SD rats. Plasma nitrate and nitrite level was elevated in SHHF and SHR rats at 18 mo only. In left ventricular homogenates from SHHF rats, Ca(2+)-dependent NOS activity increased markedly with age and was accompanied by enhanced expression of endothelial NOS (eNOS). In contrast, SHR rats showed a much smaller increase in Ca(2+)-dependent NOS activity over time without changes in eNOS expression; neither parameter was altered with age in SD rats. Ca(2+)-independent NOS activity was not detected in any heart. This is the first report of a unique alteration in myocardial NOS activity in hypertensive rats genetically prone to heart failure.

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