作者: James T. Patrie , Eugene J. Barrett , Linda A. Jahn , William B. Horton , Kevin W. Aylor
DOI: 10.1113/JP281286
关键词:
摘要: Key points Multiple clinical studies report that acute hyperglycaemia (induced by mixed meal or oral glucose) decreases arterial vascular function in healthy humans. Feeding, however, impacts autonomic output, blood pressure, and insulin incretin secretion, which may themselves alter function. No prior have examined the effect of on both macro- microvascular while controlling plasma concentrations. Macrovascular functional responses to euglycaemia were compared. Octreotide was infused throughout protocols prevent endogenous release. Acute intravenous enhanced brachial artery flow-mediated dilatation, increased skeletal muscle volume flow, expanded cardiac volume. Compared other published findings, results suggest differ based study population (i.e. normal weight vs. overweight/obese) and/or glucose delivery method glucose). Abstract High concentrations acutely provoke endothelial cell oxidative stress are suggested trigger diabetes-related injury each independently obscure per se. Surprisingly, no effects glucose-induced In this randomized young adults, we compared macrovascular carotid-femoral pulse wave velocity post-ischaemic flow velocity) (heart perfusion contrast-enhanced ultrasound) hyperglycaemia. dilatation (P = 0.004), 0.001), 0.014). measure changed during octreotide-maintained euglycaemia. Our findings unlike meal-provoked hyperglycaemia, 4 h enhances provokes function, does not impair aortic stiffness. Previous large dysfunction ingestion be due differences populations meal-induced humoral neural factors beyond (ClinicalTrials.gov number NCT03520569.).