The supportive value of pre-bypass L-glutamate loading in patients undergoing coronary artery bypass grafting.
OBJECTIVE
Experimental studies have demonstrated that an exogenous supply of glutamate improves mechanical function and recovery of ischemic myocardium. The aim of the present study was to investigate the effect of myocardial pre-bypass loading with glutamate on myocardial protection during global ischemia and reperfusion of patients undergoing coronary artery bypass grafting (CABG).


METHODS
The study was double blinded. Twenty patients undergoing elective CABG were randomized to receive L-glutamate (n = 10) or normal saline (n = 10). Intracellular levels of glutamate, ATP and lactate were measured in left ventricular biopsies collected 10 min after aortic clamp release. Hemodynamic data, and postoperative release of CK-MB and troponin T were also measured.


RESULTS
Pre-bypass administration of glutamate resulted in myocardial glutamate loading since glutamate levels were significantly higher in the glutamate group of patients than in controls (18.6 +/- 3.1 versus 8.7 +/- 1.2 microg/g tissue, P < 0.001). In the same group ATP levels were also significantly higher (2.4 +/- 0.7 versus 1.5 +/- 0.4 microg/g tissue, P < 0.05) and lactate levels significantly less than in controls (6.9 +/- 1.9 versus 12.0 +/- 2.1 microg/g tissue, P < 0.001). Glutamate patients had statistically significantly superior post-bypass hemodynamic performance (cardiac index, left ventricular stroke work index, systemic vascular resistance and pulmonary vascular resistance). Statistically significantly lower levels of CK-MB (6 h postoperative), total and peak CK-MB, troponin T (24 h postoperative), and total troponin T were found in the glutamate group.


CONCLUSIONS
The results of this preliminary study indicate that pre-bypass intravenous administration of glutamate in patients undergoing CABG has a supportive effect on myocardial metabolism during global ischemia and reperfusion, improves patients' postoperative hemodynamic performance and reduces postoperative cardiac enzyme release.
Bitzikas
G
G
Department of Cardiothoracic Surgery, AHEPA Hospital, Aristotles University of Thessaloniki, Thessaloniki, Greece. gbitzika@med.duth.gr
Papakonstantinou
C
C
Lazou
A
A
Bougioukas
G
G
Toumpouras
M
M
Tripsianis
G
G
Spanos
P
P
D000255:Adenosine Triphosphate / Q000378:metabolism; D000368:Aged; D002315:Cardiopulmonary Bypass; D001026:Coronary Artery Bypass; D003324:Coronary Artery Disease / Q000378:metabolism / Q000503:physiopathology / Q000601:surgery*; D052279:Creatine Kinase, MB Form / Q000097:blood; D004311:Double-Blind Method; D005260:Female; D018698:Glutamic Acid / Q000008:administration & dosage* / Q000378:metabolism; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D007262:Infusions, Intravenous; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D020127:Recovery of Function / Q000502:physiology*; D016896:Treatment Outcome; D020107:Troponin T / Q000097:blood
D020107:Troponin T; D019344:Lactic Acid; D018698:Glutamic Acid; D000255:Adenosine Triphosphate; D052279:Creatine Kinase, MB Form