glutamine prevents heart damage

Doug Skrecky (oberon@vcn.bc.ca)
Fri, 2 Jul 1999 16:02:42 -0700 (PDT)

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.