Verena Kise Capellini

TL;DR: The basic physiology of the endothelium is considered, especially related to the synthesis and function of nitric oxide, and the pathophysiology of vascular disease associated with DM is discussed, including the role of hyperglycemia in the induction of oxidative stress and therole of advanced glycation end-products.

TL;DR: A critical analysis of the state of art of acid-base balance and endothelium function is provided to provide a critical analysis and incentivate researchers to develop more studies about these issues.

TL;DR: The results suggest that extracellular acidosis promotes vasodilation mediated by NO, K(ATP) and SK(Ca), and maybe other K(+) channels in isolated rat thoracic aorta.

TL;DR: Results suggested that partial liver I followed by global liver R induced liver, kidney, and lung injuries characterized by neutrophil sequestration and increased oxidative stress, and the reduced NO formation via eNOS may be implicated in the moderate impairment of renal function, observed by others at 24 hours after liver I/R.

TL;DR: Not all changes in pHo did result in pHi changes, but disruption of acid-base balance in both directions induced NO synthesis in the endothelium and/or vascular smooth muscle.