RESUMEN
<p><b>OBJECTIVE</b>To reveal the relationship of chronic pulmonary heart disease (CPHD) with the chemotactic factor Fractalkine (FKN) and tumor necrosis factor-alpha (TNF-alpha), and to explore the action mechanism of tetramethylpyrazine (TMP) for suppressing pulmonary hypertension.</p><p><b>METHODS</b>Patients with CPHD were randomly assigned to two groups, 19 in Group A and 16 in Group B, and a control group (group C) consisting of 18 healthy adults was setup. Conventional treatment were given to all patients, which consisted of Piperacillin 3. 375 g iv dripping twice a day, Levofloxacin 0.6 g + Ambroxol 60 mg + Doxofylline 0.2 g iv dripping once a day, all for 10-14 days, and acid-base and electrolytes balance in patients were monitored and corrected. At the same time, TMP (trade name: Chuanqing, containing 120 mg of TMP in a 2 mL ampoule) was given additionally to patients in Group B at the dosage of 240 mg/d by adding in 250 mL of normal saline via iv dripping. Serum levels of FKN and TNF-alpha were detected before and after treatment by enzyme-linked immunoassay, and the change of mean pulmonary arterial pressure (mPAP) was measured as well.</p><p><b>RESULTS</b>Before treatment, difference of FKN and TNF-alpha levels between the two patients' groups were insignificant (P > 0.05), but all higher than those in Group C respectively (P < 0.01). While after treatment, the two indices and mPAP levels in Group B were statistically lower than those before treatment, also than those in Group A. Regression analysis showed a positive correlation between TNF-alpha and FKN (r = 0.662, P < 0.001).</p><p><b>CONCLUSIONS</b>A high blood FKN and TNF-alpha expression state exists in CPHD patients, which could be suppressed by TMP, and these suppressive effects may be one of the important mechanisms responsible for the pulmonary arterial pressure lowering action of TMP.</p>