BackgroundTobacco smoke exposure is an important risk factor for cardiac remodeling.
Under this condition, inflammation, oxidative stress, energy metabolism
abnormalities, apoptosis, and hypertrophy are present. Pentoxifylline has
anti‑inflammatory, anti-apoptotic, anti-thrombotic and anti-proliferative
properties.ObjectiveThe present study tested the hypothesis that pentoxifylline would attenuate
cardiac remodeling induced by smoking.MethodsWistar rats were distributed in four groups: Control (C), Pentoxifylline
(PX), Tobacco Smoke (TS), and PX-TS. After two months, echocardiography,
invasive blood pressure measurement, biochemical, and histological studies
were performed. The groups were compared by two-way ANOVA with a
significance level of 5%.ResultsTS increased left atrium diameter and area, which was attenuated by PX. In
the isolated heart study, TS lowered the positive derivate (+dp/dt), and
this was attenuated by PX. The antioxidants enzyme superoxide dismutase and
glutathione peroxidase were decreased in the TS group; PX recovered these
activities. TS increased lactate dehydrogenase (LDH) and decreased
3-hydroxyacyl Coenzyme A dehydrogenases (OH-DHA) and citrate synthase (CS).
PX attenuated LDH, 3-OH-DHA and CS alterations in TS-PX group. TS increased
IL-10, ICAM-1, and caspase-3. PX did not influence these variables.ConclusionTS induced cardiac remodeling, associated with increased inflammation,
oxidative stress, apoptosis, and changed energy metabolism. PX attenuated
cardiac remodeling by reducing oxidative stress and improving cardiac
bioenergetics, but did not act upon cardiac cytokines and apoptosis.