Ribose treatment reduced the infarct size and improved heart function after myocardial infarction in rats.
OBJECTIVE
In this study the effect of ribose on heart function and infarct-size was analyzed 6 h after myocardial infarction (MI) in rats.


METHODS
Continuous i.v.-infusion of NaCl or ribose (200 mg/kg/h) was started one day prior to induction of MI in female Sprague-Dawley rats which was done by ligation of the left coronary artery. Six hours after MI heart function was measured with 3F tip catheter, cardiac output by thermodilution method. Thereafter the ischemic area was delineated by Evans Blue infusion, and the infarct area was visualized by triphenyltetrazolium chloride staining. The mRNA expression of interleukin (IL)-1beta, IL-6, matrix-metalloproteinase (MMP)-8, and -9 was measured by ribonuclease protection assay.


RESULTS
Heart function was severely depressed 6 hours after coronary artery occlusion, but recovered significantly under the influence of ribose. Left ventricular (LV) systolic pressure (LVSP) and contractility (LVdP/dtmax) were restored to the normal levels of sham-operated animals, while parameters of LV relaxation (LVdP/dtmin and time constant of relaxation tau) were impaired compared to sham-operated animals, but significantly improved by ribose treatment compared to sham-treated MI-rats. Moreover, the infarct size was significantly smaller in the ribose treated animals despite a comparable ischemic area at risk in all MI-rats. The cytokine mRNA expression after MI was significantly reduced after ribose treatment, while there were no differences regarding MMP expression.


CONCLUSIONS
MI size was significantly reduced and LV function significantly improved by ribose treatment at 6 h after MI. This seemed to be based on slowing the velocity of the necrotic wave front across the LV wall after MI resulting in smaller infarcts.
Gonzalez
Germán E
GE
Institute of Cardiovascular Physiopathology, Department of Pathology, Faculty of Medicine, University of Buenos Aires.
Rabald
Steffen
S
Briest
Wilfried
W
Gelpi
Ricardo J
RJ
Seropian
Ignacio
I
Zimmer
Heinz-Gerd
HG
Deten
Alexander
A
D000818:Animals; D005260:Female; D006321:Heart / Q000187:drug effects / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects; D007238:Infarction / Q000473:pathology*; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012266:Ribose / Q000494:pharmacology*; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology / Q000517:prevention & control*; D016277:Ventricular Function, Left / Q000187:drug effects
D012266:Ribose