Carotid stenting stenosis of the internal carotid artery. Carotid stenting may be considered an alternative to carotid surgery in average surgical risk patients, albeit with a higher risk of death or stroke as seen in the SAPPHIRE and CREST trials. Features that favor carotid stenting include non-atherosclerotic cause of the stenosis (fibrodysplasia, radiation, early post-surgical stenosis or flap) an experienced center and experienced physician performing the procedure. Features that make stent placement more difficult include significant aortic arch tortuosity, thrombus containing lesions, occluded carotid artery, heavily calcified vessels, symptomatic patients and very tortuous and twisting vessels. None of these affect open, surgical
Carotid body acid-base transporters (e.g. Na-H) which raise intracellular pH, and activates transporters (e.g. Cl-HCO) which decrease it. Changes in proton concentration caused by acidosis (or the opposite from alkalosis) inside the cell stimulates the same pathways involved in P sensing. Another mechanism is through oxygen sensitive potassium channels. A drop in dissolved oxygen lead to closing of these channels which results in depolarization. This leads to release of the neurotransmitter dopamine in the glossopharyngeal and vagus afferente to the vasomotor area. The type I (glomus) cells in the carotid (and aortic bodies) are derived from neuroectoderm and are thus electrically excitable.