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10.1113/jphysiol.2014.277277 http://scihub22266oqcxt.onion/10.1113/jphysiol.2014.277277 C4192710!4192710!24951620     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\24951620.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Physiol 2014 ; 592 (Pt 17): 3901-16 Nephropedia Template TP {{tp|p=24951620|t=2014. Hypometabolism and hypothermia in the rat model of endotoxic shock: independence of circulatory hypoxia |pdf=|usr=}}{{24951620}} gab.com Text Hypometabolism and hypothermia in the rat model of endotoxic shock: independence of circulatory hypoxia JO: J Physiol http://www.kidney.de/pget.php?&tw=1&pmid=24951620 #FOAvip We tested the hypothesis that development of hypothermia instead of fever in endotoxic shock is consequential to hypoxia. Endotoxic shock was induced by bacterial lipopolysaccharide (LPS, 500 ?g kg?1i.v.) in rats at an ambient temperature of 22°C. A ?3-adrenergic agonist known to activate metabolic heat production, CL316,243, was employed to evaluate whether thermogenic capacity could be impaired by the fall in oxygen delivery () during endotoxic shock. This possibility was rejected as CL316,243 (0.15 mg kg?1i.v.) evoked similar rises in oxygen consumption () in the presence and absence of endotoxic shock. Next, to investigate whether a less severe form of circulatory hypoxia could be triggering hypothermia, the circulating volume of LPS-injected rats was expanded using 6% hetastarch with the intention of improving tissue perfusion and alleviating hypoxia. This intervention attenuated not only the fall in arterial pressure induced by LPS, but also the associated falls in and body temperature. These effects, however, occurred independently of hypoxia, as they were not accompanied by any detectable changes in NAD+/NADH ratios. Further experimentation revealed that even the earliest drops in cardiac output and during endotoxic shock did not precede the reduction in that brings about hypothermia. In fact, and fell in such a synchrony that the / ratio remained unaffected. Only when hypothermia was prevented by exposure to a warm environment (30°C) did an imbalance in the / ratio become evident, and such an imbalance was associated with reductions in the renal and hypothalamic NAD+/NADH ratios. In conclusion, hypometabolism and hypothermia in endotoxic shock are not consequential to hypoxia but serve as a pre-emptive strategy to avoid hypoxia in this model. Twit Text FOAVip Hypometabolism and hypothermia in the rat model of endotoxic shock: independence of circulatory hypoxia ????J Physiol http://www.kidney.de/pget.php?&tw=1&pmid=24951620 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24951620 #FOAvip English Wikipedia <ref>{{Cite pmid|24951620}}</ref> Hypometabolism and hypothermia in the rat model of endotoxic shock: independence of circulatory hypoxia #MMPMID24951620 Corrigan JJ; Fonseca MT; Flatow EA; Lewis K; Steiner AA J Physiol 2014[Sep]; 592 (Pt 17): 3901-16 PMID24951620show ga We tested the hypothesis that development of hypothermia instead of fever in endotoxic shock is consequential to hypoxia. Endotoxic shock was induced by bacterial lipopolysaccharide (LPS, 500 ?g kg?1i.v.) in rats at an ambient temperature of 22°C. A ?3-adrenergic agonist known to activate metabolic heat production, CL316,243, was employed to evaluate whether thermogenic capacity could be impaired by the fall in oxygen delivery () during endotoxic shock. This possibility was rejected as CL316,243 (0.15 mg kg?1i.v.) evoked similar rises in oxygen consumption () in the presence and absence of endotoxic shock. Next, to investigate whether a less severe form of circulatory hypoxia could be triggering hypothermia, the circulating volume of LPS-injected rats was expanded using 6% hetastarch with the intention of improving tissue perfusion and alleviating hypoxia. This intervention attenuated not only the fall in arterial pressure induced by LPS, but also the associated falls in and body temperature. These effects, however, occurred independently of hypoxia, as they were not accompanied by any detectable changes in NAD+/NADH ratios. Further experimentation revealed that even the earliest drops in cardiac output and during endotoxic shock did not precede the reduction in that brings about hypothermia. In fact, and fell in such a synchrony that the / ratio remained unaffected. Only when hypothermia was prevented by exposure to a warm environment (30°C) did an imbalance in the / ratio become evident, and such an imbalance was associated with reductions in the renal and hypothalamic NAD+/NADH ratios. In conclusion, hypometabolism and hypothermia in endotoxic shock are not consequential to hypoxia but serve as a pre-emptive strategy to avoid hypoxia in this model. äHypometabolism and hypothermia in the rat model of endotoxic shock: in(epmc).pdf DeepDyve Pubget Overpricing