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Carvedilol - Europe PMC

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Last Updated: 10 September 2022

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Mechanism of carvedilol induced action potential and calcium alternans.

Following carvedilol therapy, Carvedilol extended the sarcoplasmic reticulum Ca release refractoriness by more than four weeks of rehabilitation; however, no changes were observed in L-type calcium current recovery from activation or SR Ca load after carvedilol therapy. In experiments with a different u03b2-blocker, no effect was observed on the CaT or APD alternans ratios, leaving out the possibility that the carvedilol effect on CaT and APD alternans was determined by its u03b2-blocking properties.

Source link: https://europepmc.org/article/MED/35501948


Novel carvedilol-loaded pro-phytomicelles: formulation, characterization and enhanced protective efficacy against acetaminophen-inducedliverinjury in mice.

CAR pro-phytomicelles was manufactured with rebaudioside A and dipotassium glycyrrhizinate as mixed nanomaterials, according to this unique nanoformulation of CAR. Samples of CAR pro-phytomicelles may be easily dissolvable into aqueous media to produce clear phytomicelle solutions with CAR encapsulation yield of 99. 67 percent and a small micelle size of 15. 62 nm, with CAR encapsulation efficiency of 0. 02 % and small micelle size of 15. 62 nm. Acetaminophen overdose caused high mortality and severe liver injury in mice, according to a study by the CAR pro-phytomicelle, although acetaminophen overdose caused significant protective effects against acetaminophen overdose.

Source link: https://europepmc.org/article/MED/35995319


Anxiolytic Effect of Carvedilol in Chronic Unpredictable Stress Model.

Anxiety disorders are the most common psychiatric disorders, with Anxiety disorders being also a comorbid state of other disorders. In animals exposed to regular stress, we sought to investigate the anxiolytic-like effects of carvedilol, a drug used to treat elevated blood pressure and heart failure with potent antioxidant properties, in animals exposed to chronic stress. Female Swiss mice were exposed to different stressors for 21 days in order to do this. Behavior tests were administered on the 22nd day to determine locomotor activity and anxiety-like changes. The number of head dips in the HB was reduced by CUS, an effect that was reversed by CVD. In stressed animals, a decrease in the cortical layer thickness of the adrenal gland was found, which CVD reversed. Both brain regions' DVS and CVD's increased IL-6 levels. DVS resulted in an increase in IFN-u03b3 in the hippocampus, according to DVS. CVD has an anxiolytic effect partially related to immune-inflammatory mechanism regulation, according to our findings.

Source link: https://europepmc.org/article/MED/36035219


Carvedilol versus Metoprolol in Patients with Ventricular Tachyarrhythmias.

Patients with ventricular tachyarrhythmias are treated with carvedilol and metoprolol in the study. Patients on beta-blocker therapy with episodes of ventricular tachycardia or fibrillation from 2002 to 2015 were included in a large retrospective database. Patients with metoprolol were compared to patients with metoprolol. Patients with carvedilol were older, more likely to be experiencing VT and in more advanced stages of heart disease. When compared to metoprolol, treatment with carvedilol was associated with similar all-cause mortality. Higher incidences of the composite arrhythmic endpoint were still present in patients treated with carvedilol, however, the risk of cardiac rehospitalization was not influenced by the type of beta-blocker therapy. In patients with ventricular tachyarrhythmias, carvedilol and metoprolol are both associated with similar all-cause mortality, although the risk of the composite arrhythmic endpoint in patients with carvedilol therapy has risen.

Source link: https://europepmc.org/article/MED/36005438


Title: Neuroprotective repositioning and anti-tau effect of carvedilol on rotenone induced neurotoxicity in rats: Insights from an insilico&in vivo anti-Parkinson's disease study.

Current treatments forParkinson's Disease only help with symptoms relief; however, new treatment options should be considered. Carvedilol is a nonselective blocker with additional benefits as an anti-inflammatory, and neuroprotective agent. carvedilol was used principally to assess carvedilol as an anti-parkinsonian and anti-tau protein target in this report. In vivo research was conducted to determine the possible causes of PD in a rotenone-induced rat model and investigate the potential underlying mechanisms. The effects of carvedilol on the measured parameters of open field, catalepsy, Y-maze tests, as well as brain histology, and tyrosine hydroxylase were evaluated. In addition, carvedilol significantly reduced rotenone-induced decrease in TH expression in the rats' striata. tau protein hyperphosphosrylation by Glycogen synthase 3u03b2 inhibition and Phosphoinositide 3-kinase stimulation, reduced tau protein hyperphosphosrylation by Carvedilol. These findings, taken together, suggest that carvedilol may be a potential candidate for PD management.

Source link: https://europepmc.org/article/MED/35964655

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions