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Background: Paroxysmal sympathetic hyperactivity (PSH) occurs with high prevalence among critically ill patients with traumatic brain injury (TBI) and is associated with worse outcomes. The PSH-Assessment Measure (PSH-AM) consists of a Clinical Features Scale and a diagnosis likelihood tool (DLT) intended to quantify the severity of sympathetically mediated symptoms and the likelihood that they are due to PSH, respectively, on a daily basis. Here, we aim to identify and explore the value of dynamic trends in the evolution of sympathetic hyperactivity following acute TBI using elements of the PSH-AM.

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Background: Previous literature has highlighted that excessive alcohol use (EAU) is directly linked with permanent neurological damage. Studies have also highlighted gradual improvements in heart rate variability (HRV) after cessation of alcohol use. Moreover, chronic alcohol consumption has also been correlated with reduced HRV and an increase in skin conductance (SC) among healthy adults, leading to a combined decline in cognitive performance.

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Effects of Sympathetic Denervation in Metabolism Regulation: A Novel Approach for the Treatment of MASLD?

Cardiol Rev

January 2025

From the First Department of Cardiology, School of Medicine, National and Kapodistrian University of Athens, Hippokration General Hospital, Athens, Greece.

Although metabolic dysfunction-associated steatotic liver disease (MASLD), previously termed nonalcoholic fatty liver disease, has become the most common chronic liver disorder, its complex pathophysiology has not been fully elucidated up to date. A correlation between elevated sympathetic activation and MASLD has been highlighted in recent preclinical and clinical studies. Furthermore, increased sympathetic activity has been associated with the main mechanisms involved in MASLD, such as lipid accumulation in the liver, insulin resistance, and metabolic dysregulation, while it has been also correlated with the progression of MASLD, leading to liver fibrosis.

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Anorectal neuropathy causes anorectal dysfunction, yet it is poorly recognized. This stems from both a lack of understanding of the extrinsic and intrinsic innervation of the anorectum and tools for evaluation of neuronal function. Our objective was to provide an improved understanding of the neuronal networks of the anorectum and discuss its functional significance.

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This study aimed to investigate the effects of chronic sympathoinhibition on glucose uptake by the myocardium and by the skeletal muscle in an animal model of obesity associated with leptin signaling deficiency. 6 obese Zucker rats (OZR) and 6 control Lean Zucker rats (LZR) were studied during basal conditions, chronic clonidine administration (30 days, 300 µg/kg), and washout recovery period. Glucose uptake in the myocardium and in the skeletal muscle was measured using positron emission tomography (PET) and 2-[18F] fluoro-2-deoxy-D-glucose ([18F]FDG).

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