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Acute Hypotension (acute + hypotension)
Selected AbstractsCardiovascular dialysis instability and convective therapiesHEMODIALYSIS INTERNATIONAL, Issue 2006Antonio SANTORO Abstract Acute hypotension is a frequent hemodialysis complication. Intratreatment vascular instability is a multifactorial process in which procedure-related and patient-related factors may influence the decrease in plasma volume and induce an impairment of cardiovascular regulatory mechanisms. Identification of the most susceptible patients and of the various risk factors may contribute to significantly improve cardiovascular stability during dialysis. In some high-risk patients, monitoring and biofeedback of the various hemodynamic variables, together with an extensive use of convection, can prevent the appearance of symptomatic hypotension and help in averting its onset. [source] Acute hypotension associated with leucocyte depletion filters during cell salvaged blood transfusionANAESTHESIA, Issue 7 2010T. R. Sreelakshmi Summary Intra-operative cell salvage is used in more than 75% of NHS hospitals in the United Kingdom and is a safe and cost effective alternative to allogenic blood transfusion. We report a case of acute hypotension during reinfusion of cell salvaged blood through a leucocyte depletion filter that occurred during a caesarean section. We review the literature of hypotension associated with the use of bedside leucocyte depletion filters. [source] Importance of calcitonin gene-related peptide, adenosine and reactive oxygen species in cerebral autoregulation under normal and diseased conditionsCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2004Hwa Kyoung Shin Summary 1.,Mechanisms regulating cerebral circulation, including autoregulation of cerebral blood flow (CBF), have been widely investigated. Vasodilators such as nitric oxide, prostacyclin, calcitonin gene-related peptide (CGRP) and K+ channel openers are well known to have important roles in the physiological and pathophysiological control of CBF autoregulation. In the present review, the focus is on the mechanism(s) of altered CBF autoregulation after traumatic brain injury and subarachnoid haemorrhage (SAH) and on the effect of adenovirus-mediated transfer of Cu/Zn superoxide dismutase (SOD)-1 in amelioration of impaired CBF autoregulation. 2.,The roles of CGRP and adenosine are particularly emphasized, both being implicated in the autoregulatory vasodilation of the pial artery in response to hypotension. 3.,After fluid percussion injury, production of NADPH oxidase-derived superoxide anion and activation of tyrosine kinase links the inhibition of K+ channels to impaired autoregulatory vasodilation in response to acute hypotension and alterations in CBF autoregulation in rat pial artery. 4.,Subarachnoid haemorrhage during the acute stage causes an increase in NADPH oxidase-dependent superoxide formation in cerebral vessels in association with activated tyrosine phosphorylation-coupled increased expression of gp91phox mRNA and membrane translocation of Rac protein, thereby resulting in a significant reduction of autoregulatory vasodilation. 5.,Fluid percussion injury and SAH-induced overproduction of superoxide anion in cerebral vessels contributes to the impairment of CBF autoregulation and administration of recombinant adenovirus-mediated transfer of the Cu/Zn SOD-1 gene effectively ameliorates the impairment of CBF autoregulation of the pial artery. [source] |