Coenzyme Q(10) exogenous administration attenuates cold stress cardiac injury

The influence of coenzyme Q(10) (CoQ(10)) in cold stress test (-15 degreesC for 4 hours) cardiac functional impairment was studied in isolated isovolu mic heart of control rats (C; n=12) and of placebo (P; n=11) and treated ra ts (CoQ(10); n=10). In addition, electron microscopic evaluation of left ve ntricular (LV) slices (n=3 in each group) allowed us to analyze the myocard ial ultrastructure. Maximal values of developed pressure (DPmax) were simil arly decreased in cold stressed animals (C=129 +/-3.9 mmHg; P=106 +/-6.7 mm Hg; CoQ(10)=91 +/-3.9 mmHg); however, volume-induced enhancement of pressur e generation (slope of DP / volume relations: C=0.248 +/-0.0203 mmHg/mul; P =0.2831 +/-0.0187 mmHg/mul; CoQ(10)=0.2387 (0.0225 mmHg/mul; p >0.05), and the duration of systole (C=80 +/- .6 ms; P=78 +/-1.3 ms; CoQ(10) = 80 +/-2. 7 ms) were not altered. Myocardial relaxation, evaluated by the relaxation constant (C=39 +/-1.9 ins; P=42 +/-3.4 ms; CoQ(10)=51 +/-6.0 ms), as well a s resting stress / strain relations were unaffected by cold stress. Myocard ial samples showed that pretreatment with CoQ(10) attenuates myofibrillar a nd mitochondrial lesions, and prevents mitochondrial fractional area increa se (P: 53.11%> CoQ(10): 38.78%=C: 33.87%; p <0.005) indicating that the exo genous administration of CoQ(10) can reduce cold stress myocardial injury.