Data also point to a facilitatory role played by the activation of BST alpha 2-adrenoceptor on the pressor response to PND-1186 dynamic exercise. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Blunt cerebrovascular injuries, defined as blunt injuries to the internal carotid or vertebral arteries, are uncommon and usually occur in victims of high-speed deceleration motor vehicle crashes. A blunt cerebrovascular injury after an equestrian accident is an extremely unusual presentation. In recent years, advances in screening
and treatment with pharmacologic anticoagulation before the onset of neurologic symptoms have improved outcomes for these patients. Endovascular stenting and embolization, although unproven, offer a new potential approach for these complex injuries. We present a unique case of four-vessel blunt cerebrovascular injuries after a horse-riding injury that required multidisciplinary KPT-8602 manufacturer management. (J Vasc Surg 2010;52:1052-7.)”
“The caudal pressor area (CPA) is a brainstem area located close to the spinal cord. The activation of the CPA increases sympathetic activity and mean arterial pressure (MAP) by mechanisms dependent
on the commissural nucleus of the solitary tract (commNTS) and rostroventrolateral medulla, however, the signals that activate the CPA to produce these responses are still unknown. Therefore, in the present study, we investigated the activity of glutamatergic and GABAergic mechanisms from the CPA and commNTS in rats exposed to hypoxia and the effects of the inhibition of CPA neurons on cardiorespiratory responses to peripheral chemoreceptor activation with i.v. sodium cyanide (NaCN). Male Sprague-Dawley rats (250-280 g, n=5-8/group) were used. In conscious rats, most of the commNTS neurons (66 +/- 11%) and part of the CPA neurons (36 +/- 7%) activated by hypoxia (8% O2) were glutamatergic (contained VGLUT2mRNA). Small part of the neurons activated during hypoxia was GABAergic (contained GAD-67mRNA) in the commNTS (9 +/- 4%) or the CPA (6 +/- 2%). In urethane anesthetized rats, the inhibition of CPA neurons with bilateral injections of muscimol (GABA-A agonist,
2 mM) reduced baseline MAP, splanchnic sympathetic nerve discharge (SND) and phrenic Calpain nerve discharge (PND). Muscimol into the CPA also reduced by around 50% the pressor and sympathoexcitatory responses and the increase in PND to peripheral chemoreceptor activation with NaCN (50 mu g/kg i.v.), without changing sympathetic baroreflex responses. These data suggest that CPA mechanisms facilitate cardiorespiratory responses to peripheral chemoreflex activation. Immunohistochemistry results also suggest that at least part of the CPA mechanisms activated by hypoxia is glutamatergic. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“We report a case of traumatic right subclavian artery pseudoaneurysm, which failed initial treatment by endovascular covered stent.