Objectives: Molecular mechanisms linking autonomic dysfunction with poorer clinical outcomes in critical illness remain unclear. We hypothesized that baroreflex dysfunction alone is sufficient to cause cardiac impairment through neurohormonal activation of (nicotinamide adenine dinucleotide phosphate oxidase dependent) oxidative stress resulting in increased expression of G-protein-coupled receptor kinase 2, a key negative regulator of cardiac function. Design: Laboratory/clinical investigations. Setting: University laboratory/medical centers. Subjects: Adult rats; wild-type/nicotinamide adenine dinucleotide phosphate oxidase subunit-2-deficient mice; elective surgical patients. Interventions: Cardiac performance was assessed by transthoracic echocardiography following experimental baroreflex dysfunction (sino-aortic denervation) in rats and mice. Immunoblots assessed G-protein-coupled receptor recycling proteins expression in rodent cardiomyocytes and patient mononuclear leukocytes. In surgical patients, heart rate recovery after cardiopulmonary exercise testing, time/frequency measures of parasympathetic variables were related to the presence/absence of baroreflex dysfunction (defined by spontaneous baroreflex sensitivity of
from Emergency Medicine via xlomafota13 on Inoreader http://ift.tt/1U9WW0K
Εγγραφή σε:
Σχόλια ανάρτησης (Atom)
Δημοφιλείς αναρτήσεις
-
Abstract Objectives Emergency departments (EDs) commonly analyze cases of patients returning within 72 hours of initial ED discharge as...
-
ORIGINAL ARTICLES Cone-beam computed tomography versus orthopantomography in sinus lift procedures: Two-dimensional versus three-dimension...
-
Haemovigilance programme of India: Comparative analysis of transfusion reactions reported over a 5-year period through two reporting formats...
Δεν υπάρχουν σχόλια:
Δημοσίευση σχολίου