glutamine prevents heart damage

From: Doug Skrecky (oberon@vcn.bc.ca)
Date: Fri Jul 02 1999 - 17:02:42 MDT


Authors
  Khogali SE. Harper AA. Lyall JA. Rennie MJ.
Institution
  Department of Anatomy & Physiology, University of Dundee, Scotland, UK.
Title
  Effects of L-glutamine on
  post-ischaemic cardiac function: protection and rescue.
Source
  Journal of Molecular & Cellular Cardiology. 30(4):819-27, 1998 Apr.
Abstract
  We investigated the effects of L-glutamine
  (0-20 mM) on cardiac function. The isolated perfused working rat heart (left
  atrial and aortic pressures of 5 and 70 cm H2O, respectively) was subjected
  to 20 min of normothermic low-flow ischaemia followed by reperfusion for 35
  min. In the absence of glutamine, ischaemia-reperfusion caused an immediate
  significant (P < 0.01) fall in cardiac output from 46 to 20 ml/min, with a
  further deterioration to 17 ml/min at 35 min reperfusion. Ischaemia also
  caused a significant (P < 0.05) fall in myocardial glutamate from 2.6 to 1.8
  mumol/g wet weight; and ischaemia-reperfusion caused significant (each P <
  0.05) diminutions of myocardial ATP from 3.5 to 1.0 mumol/g wet weight and
  phosphocreatine from 4.8 to 1.5 mumol/g wet weight and resulted in
  significant (P < 0.05) accumulation of myocardial lactate from 0.9 to 4.3
  mumol/g wet weight. Glutamine, present throughout the perfusion protocol
  (i.e. prior to ischaemia), at or above 1.25 mM, prevented the
  post-ischaemic diminution of cardiac output and the
  deleterious changes in myocardial metabolites.
  Post-ischaemic treatment with glutamine at 2.5 mM completely
  prevented the post-ischaemic diminution of cardiac output
  and restored the myocardial metabolites to normal. CONCLUSIONS: Glutamine may
  be suitable as a cardioprotective and rescue agent. These
  effects may be mediated by maintenance of myocardial
  glutamate, ATP and phosphocreatine: and prevention of lactate accumulation.



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