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10.1016/j.autneu.2014.07.004 http://scihub22266oqcxt.onion/10.1016/j.autneu.2014.07.004 C4139450!4139450 !25081417     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25081417 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Auton+Neurosci 2014 ; 184 (?): 24-6 Nephropedia Template TP {{tp|p=25081417 |t=2014. Pathophysiology of neurally mediated syncope: Role of cardiac output and total peripheral resistance |pdf=|usr=}}{{25081417 }} gab.com Text Pathophysiology of neurally mediated syncope: Role of cardiac output and total peripheral resistance JO: Auton Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=25081417 #FOAvip Syncope is a common clinical condition occurring even in otherwise healthy people without underlying cardiovascular disease. Neurally mediated syncope is by far the most common cause of syncope in individuals without any structural heart disease. Based on traditional wisdom, loss of sympathetic tone with relaxation of vascular smooth muscle is the key mechanism underlying the pathophysiology of syncope, especially in patients without an acute decrease in heart rate. However, this concept has recently been challenged. Some microneurographic studies indicate that sympathetic withdrawal may not always be a prerequisite even for the development of classic "vasodepressor" forms of syncope. Conversely, a decrease in cardiac output appears to be a determinant factor for syncope in most circumstances. This article reviews the relative contribution of cardiac output versus sympathetic vasoconstriction in neurally mediated syncope in otherwise healthy individuals. It is suggested that a moderate to severe fall in cardiac output with or without vasodilatation may contribute to syncope. Twit Text FOAVip Pathophysiology of neurally mediated syncope: Role of cardiac output and total peripheral resistance ????Auton Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=25081417 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25081417 #FOAvip English Wikipedia <ref>{{Cite pmid|25081417 }}</ref> Pathophysiology of neurally mediated syncope: Role of cardiac output and total peripheral resistance #MMPMID25081417 Fu Q ; Levine BD Auton Neurosci 2014[Sep]; 184 (?): 24-6 PMID25081417 show ga Syncope is a common clinical condition occurring even in otherwise healthy people without underlying cardiovascular disease. Neurally mediated syncope is by far the most common cause of syncope in individuals without any structural heart disease. Based on traditional wisdom, loss of sympathetic tone with relaxation of vascular smooth muscle is the key mechanism underlying the pathophysiology of syncope, especially in patients without an acute decrease in heart rate. However, this concept has recently been challenged. Some microneurographic studies indicate that sympathetic withdrawal may not always be a prerequisite even for the development of classic "vasodepressor" forms of syncope. Conversely, a decrease in cardiac output appears to be a determinant factor for syncope in most circumstances. This article reviews the relative contribution of cardiac output versus sympathetic vasoconstriction in neurally mediated syncope in otherwise healthy individuals. It is suggested that a moderate to severe fall in cardiac output with or without vasodilatation may contribute to syncope. |Animals [MESH] |Cardiac Output/*physiology [MESH] |Humans [MESH] |Syncope/*physiopathology [MESH]Pathophysiology of neurally mediated syncope: Role of cardiac output a(epmc).pdf DeepDyve Pubget Overpricing