UNLABELLED: 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.
UNLABELLED: 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.
Authors: Jacquelyn M Walejko; Andrew Antolic; Jeremy P Koelmel; Timothy J Garrett; Arthur S Edison; Maureen Keller-Wood Journal: Am J Physiol Endocrinol Metab Date: 2019-01-08 Impact factor: 4.310
Authors: Wenjie Ma; Yoriko Heianza; Tao Huang; Tiange Wang; Dianjianyi Sun; Yan Zheng; Frank B Hu; Kathryn M Rexrode; JoAnn E Manson; Lu Qi Journal: Int J Epidemiol Date: 2018-02-01 Impact factor: 7.196
Authors: Benjamin Lauzier; Fanny Vaillant; Clemence Merlen; Roselle Gélinas; Bertrand Bouchard; Marie-Eve Rivard; Francois Labarthe; Vern W Dolinsky; Jason R B Dyck; Bruce G Allen; John C Chatham; Christine Des Rosiers Journal: J Mol Cell Cardiol Date: 2012-11-28 Impact factor: 5.000