D. Atar et al., COENZYME-Q(10) PROTECTS ISCHEMIC MYOCARDIUM IN AN OPEN-CHEST SWINE MODEL, The Clinical investigator, 71(8), 1993, pp. 190000103-190000111
Myocardial stunning, defined as a reversible decrease in contractility
after ischemia and reperfusion, may be a manifestation of reperfusion
injury caused by free oxygen radical damage. The aim of this study wa
s to test the hypothesis that pretreatment with coenzyme Q10 (ubiquino
ne), believed to act as a free radical scavenger, reduces myocardial s
tunning in a porcine model. Twelve swine were randomized to receive ei
ther oral supplementation with coenzyme Q10 or placebo for 20 days. A
normothermic open-chest model was used with short occlusion (8 min) of
the distal left descending coronary artery followed by reperfusion. R
egional contractile function was measured with epicardial Doppler crys
tals in ischemic and nonischemic segments by measuring thickening frac
tion of the left ventricular wall during systole. Stunning time was de
fined as the elapsed time of reduced contractility until return to bas
eline. Coenzyme Q10 concentrations were measured in blood and homogeni
zed myocardial tissue by high performance liquid chromatography. Plasm
a levels of reduced coenzyme Q10 (ubiquinol) were higher in swine pret
reated with the experimental medication as compared to placebo (mean 0
.45 mg/l versus 0.11 mg/l, respectively). Myocardial tissue concentrat
ions, however, did not show any changes (mean 0.79 mug/mg dry weight v
ersus 0.74 mug/mg). Stunning time was significantly reduced in coenzym
e Q10 pretreated animals (13.7+/-7.7 min versus 32.8+/-3.1 min, P < 0.
01). In conclusion, chronic pretreatment with coenzyme Q10 protects is
chemic myocardium in an open-chest swine model. The beneficial effect
of coenzyme Q10 on myocardial stunning may be due to protection from f
ree radical mediated reperfusion injury. This protective effect seems
to be generated by a humoral rather than intracellular mechanism.