Abstract
The influence of coenzyme Q10 (CoQ10) in cold stress test (-15°C for 4 hours) cardiac functional impairment was studied in isolated isovolumic heart of control rats (C; n=12) and of placebo (P; n=11) and treated rats (CoQ10; n=10). In addition, electron microscopic evaluation of left ventricular (LV) slices (n=3 in each group) allowed us to analyze the myocardial ultrastructure. Maximal values of developed pressure (DPmax) were similarly decreased in cold stressed animals (C=129±3.9 mmHg; P=106±6.7 mmHg; CoQ10=91± 3.9 mmHg); however, volume-induced enhancement of pressure generation (slope of DP / volume relations: C=0.248±0.0203 mmHg / μl; P=0.2831±0.0187 mmHg / μl; CoQ10=0.2387 (0.0225 mmHg / μl; p > 0.05), and the duration of systole (C=80±1.6 ms; P=78±1.3 ms; CoQ10=80±2.7 ms) were not altered. Myocardial relaxation, evaluated by the relaxation constant (C=39±1.9 ms; P=42±3.4 ms; CoQ10=51±6.0 ms), as well as resting stress / strain relations were unaffected by cold stress. Myocardial samples showed that pretreatment with CoQ10 attenuates myofibrillar and mitochondrial lesions, and prevents mitochondrial fractional area increase (P: 53.11%>CoQ10: 38.78%=C: 33.87%; p< 0.005) indicating that the exogenous administration of CoQ10 can reduce cold stress myocardial injury.
