The dysfunction of ammonia in heart failure increases with an increase in the intensity of resistance exercise, even with the use of appropriate drug therapy

Medeiros, Wladimir Musetti; Ac, Carvalho; Peres, Paulo Alberto Tayar; Luca, Fabio A De; Gun, Carlos

doi:10.1177/2047487312460520

Cited by 9 publications

(13 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Dependent on the redox state, E. coli and Lactobacillus plantarum reduce nitrites to ammonia (denitrification) [116] or ammonia is oxidized by Nitrosomonas back to nitrite (nitrification) [117]. Dysregulation of this pathway can lead to pathological accumulation of gut-derived ammonia or nitrite, gut dysbiosis and related cardiovascular problems [118,119,120]. A limitation of this hypothesis is that the presence of ammonia-oxidizing bacteria and archaea is described only in soil, water and plants [121].…”

Section: Gut Bacteria-derived Molecules and The Circulatory Systemmentioning

confidence: 99%

See 1 more Smart Citation

Gut Bacteria and Hydrogen Sulfide: The New Old Players in Circulatory System Homeostasis

2016

View full text Add to dashboard Cite

Accumulating evidence suggests that gut bacteria play a role in homeostasis of the circulatory system in mammals. First, gut bacteria may affect the nervous control of the circulatory system via the sensory fibres of the enteric nervous system. Second, gut bacteria-derived metabolites may cross the gut-blood barrier and target blood vessels, the heart and other organs involved in the regulation of the circulatory system. A number of studies have shown that hydrogen sulfide (H 2 S) is an important biological mediator in the circulatory system. Thus far, research has focused on the effects of H 2 S enzymatically produced by cardiovascular tissues. However, some recent evidence indicates that H 2 S released in the colon may also contribute to the control of arterial blood pressure. Incidentally, sulfate-reducing bacteria are ubiquitous in mammalian colon, and H 2 S is just one among a number of molecules produced by the gut flora. Other gut bacteria-derived compounds that may affect the circulatory system include methane, nitric oxide, carbon monoxide, trimethylamine or indole. In this paper, we review studies that imply a role of gut microbiota and their metabolites, such as H 2 S, in circulatory system homeostasis.

show abstract

Section: Gut Bacteria-derived Molecules and The Circulatory Systemmentioning

confidence: 99%

“…Moreover, it has been found that NH 3 inhalation in healthy adults results in cerebrovascular vasodilatation without affecting the arterial blood pressure [165]. Finally, patients with HF show increased plasma levels of NH 3 [119,120].…”

Section: Gut Bacteria-derived Molecules and The Circulatory Systemmentioning

confidence: 99%

Gut Bacteria and Hydrogen Sulfide: The New Old Players in Circulatory System Homeostasis

2016

View full text Add to dashboard Cite

show abstract

“…Sarcopenia or loss of skeletal muscle mass is a frequent complication of cirrhosis, advanced heart failure, and chronic lung disease that adversely impacts outcomes . Despite the high clinical significance, there are limited data on the mechanisms of sarcopenia and consequently a lack of effective therapies .…”

mentioning

confidence: 99%

“…S arcopenia or loss of skeletal muscle mass is a frequent complication of cirrhosis, advanced heart failure, and chronic lung disease that adversely impacts outcomes. (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12) Despite the high clinical significance, there are limited data on the mechanisms of sarcopenia and consequently a lack of effective therapies. (3) Hyperammonemia is a consistent abnormality in cirrhosis due to impaired ureagenesis capacity and portosystemic shunting.…”

mentioning

confidence: 99%

Ammonia lowering reverses sarcopenia of cirrhosis by restoring skeletal muscle proteostasis

Kumar¹,

Davuluri²,

Silva³

et al. 2017

Hepatology

173

151

View full text Add to dashboard Cite

Sarcopenia or skeletal muscle loss is a frequent, potentially reversible complication in cirrhosis that adversely affects clinical outcomes. Hyperammonemia is a consistent abnormality in cirrhosis that results in impaired skeletal muscle protein synthesis and breakdown (proteostasis). Despite availability of effective ammonia lowering therapies, whether lowering ammonia restores proteostasis and reverses muscle mass is unknown. Myotube diameter, protein synthesis and molecular responses in C2C12 murine myotubes to withdrawal of ammonium acetate following 24 h exposure to 10mM ammonium acetate were complemented by in vivo studies in the hyperammonemic portacaval anastomosis rat (PCA) and sham operated, pair-fed (SO) Sprague- Dawley rats treated with ammonia lowering therapy by L-ornithine L-aspartate and rifaximin orally for 4 weeks. We observed reduced myotube diameter, impaired protein synthesis and increased autophagy flux in response to hyperammonemia that were partially reversed following 24h and 48h withdrawal of ammonium acetate. Consistently, 4 weeks of ammonia lowering therapy resulted in significant lowering of blood and skeletal muscle ammonia, increase in lean body mass, improved grip strength and higher skeletal muscle mass, diameter and an increase in type II fibers in the treated compared to untreated PCA rats. Increased skeletal muscle myostatin expression, reduced mTORC1 function, and the hyperammonemic stress response including autophagy markers were also reversed in the PCA rats treated with ammonia lowering therapy. Despite significant improvement, molecular and functional readouts were not completely reversed by ammonia lowering measures. Conclusions Ammonia lowering therapy results in improvement in skeletal muscle phenotype, function and molecular perturbations of hyperammonemia. These preclinical studies complement previous studies on ammonia induced skeletal muscle loss and lay the foundation for prolonged ammonia lowering therapy to reverse sarcopenia of cirrhosis.

show abstract

“…Therefore, high ammonia levels signify a state of rapid energy consumption or potential de cits in the aerobic tricarboxylic acid (TCA) cycle. (11)(12)(13)) Accordingly, hyperammonemia can be representative of an insu cient energy supply or defective metabolism in critically ill patients.…”

Section: Introductionmentioning

confidence: 99%

Prognostic Value of Serum Ammonia in Critical Patients with Non-Hepatic Disease : A Prospective, Observational, Multicenter Study

Li¹,

Yao²,

Li³

et al. 2021

Preprint

View full text Add to dashboard Cite

Background: Non-hepatic hyperammonemia can damage the central nervous system (CNS) and possible prognostic factors are lacking. This study aimed to investigate the prognostic and risk factors for patients admitted to the intensive care unit (ICU).Methods: This prospective, observational, multicenter study was conducted between November and December 2019 at 11 ICUs in the Chinese Heilongjiang province. Changes in blood ammonia level during and after ICU admission were continuously monitored, expressed as the high-level (H-), mean-level (M-), and initial-level (I-) of ammonia. The risk factors of poor prognosis were investigated by conducting univariate and multivariate logistic regression analyses. Receiver operating characteristic curve (ROC) analysis was conducted to compare predictive ability of APACHE-II score, lactic acid, TBil, M-ammonia.Results: A total of 1060 patients were included in this study, of which 707 (67%) had a favorable prognosis and 353 (33%) had a poor prognosis. As shown by univariate models, a poor prognosis was associated with elevated serum levels of lactic acid, TBil, and ammonia (P<0.05), and pathologic scores from three assessments: APACHE-II, GCS, and SOFA. Multivariate analysis revealed that circulating mean ammonia levels in ICU patients were independently associated with a poor prognosis (OR=1.73, 95% CI: 1.07-2.80, P=0.02). However, the APACHE-II score (AUC: 0.714, sensitivity: 0.86, specificity: 0.68, P <0.001) remained the most predictive factor for patient prognosis by ROC analysis.Conclusions: Elevated serum levels of ammonia in the blood were independently prognostic for ICU patients without liver disease.Trial registration: ChiCTR1900026632. Registered 16 October 2014.

show abstract

The dysfunction of ammonia in heart failure increases with an increase in the intensity of resistance exercise, even with the use of appropriate drug therapy

Abstract: We conclude that in HF, there is an inefficiency of purine metabolism that increases with increasing exercise intensity, but not with an increase of total volume. These findings suggest that hyperkalemia may play an important role in the disorders of purine metabolism.

Cited by 9 publications

References 35 publications

Gut Bacteria and Hydrogen Sulfide: The New Old Players in Circulatory System Homeostasis

Gut Bacteria and Hydrogen Sulfide: The New Old Players in Circulatory System Homeostasis

Ammonia lowering reverses sarcopenia of cirrhosis by restoring skeletal muscle proteostasis

Prognostic Value of Serum Ammonia in Critical Patients with Non-Hepatic Disease : A Prospective, Observational, Multicenter Study

Contact Info

Product

Resources

About