In order to evaluate the effects of hyperthermia on adriamycin cardiomyopathy and
its relationship with heat shock protein induction and myosin accumulation,
female Sprague-Dawley rats (21–24 days) were randomized into four groups: the
control, adriamycin, temperature and temperature-adriamycin groups. Adriamycin
was injected i.v. at a dose of 27 mg/Kg (0.1 ml). The rats were exposed to a
temperature of 45ºC for 35 min, followed by a recovery (1 h) at room temperature
prior to adriamycin treatment. Body weight was recorded weekly. The thickness of
the ventricular wall and percentage of cellular damage were biometrically and
ultrastructurally evaluated, respectively. Heat shock protein 25 and myosin
accumulation were determined through Western blot analysis. The determinations
were carried out monthly until the third month after treatment. At eight and
twelve weeks after treatment, the thickness of the ventricular wall seemed to
decrease in the adriamycin-treated rats in relation to the other groups. An
electron microscopic analysis of the adriamycin group’s left ventricular wall
samples, showed more sarcomeric changes and loss of myofibrils than the control,
temperature and temperature-adriamycin groups. At 24 hours after treatment with
adriamycin, higher levels of heat shock protein 25 and myosin were observed
(week 0) in the temperature-adriamycin group than in the control and adriamycin
groups (4, 8 and 12 weeks). Hyperthermia was confirmed by a multivariate
approach to induce heat shock protein 25 and myosin, which would strengthen
cardiac-sarcomeric myosin arrangement.