Objective: To investigate the effect of tetramethylpyrazine on pulmonary artery hypertension in patients with chronic obstructive pulmonary disease at acute exacerbation. Method: Seventy-six patients with chronic obstructive pulmonary disease at acute exacerbation and pulmonary artery hypertension were randomly divided into two groups: the tetramethylpyrazine group and the control group (n=38 each). Basic routine therapy plus alprostadil was given to underlying diseases of both groups

Beside this basis

patients in the tetramethylpyrazine group were given tetramethylpyrazine injection 120 mg plus 5% glucose solution

intravenous infusion

once a day. Continuous medication lasted 14 days in both groups. Forty normal persons in outpatient were chosen as the health group. Blood gas analysis indicators

including partial pressure of oxygen in artery (PaO2) and blood oxygen saturation (SaO2); hemodynamic indicators

including left ventricular ejection fraction (LVEF)

pulmonary artery systolic pressure (PASP)

pulmonary artery diastolic pressure (PADP)

mean pulmonary artery pressure (MPAP); biochemical indicators

including endothelin-1 (ET-1) and nitric oxide (NO) were detected in the health group and in both groups before and after treatment. Result: Before the treatment

there were significant differences in eight indicators (PaO2

SaO2

LVEF

PASP

PADP

MPAP

ET-1

NO) between the two groups and the health group (P<0.01)

there were no significant difference in eight indicators of two groups. After 14 days

eight indicators had significantly improved compared with before treatment in patients of the two groups (P<0.05 or P<0.01)

however patients in the tetramethylpyrazine group improved more significantly (P<0.05 or P<0.01). There were no adverse reactions associated with tetramethylpyrazine. Conclusion: It was safe and effective that tetramethylpyrazine for the treatment of patients with chronic obstructive pulmonary disease and pulmonary artery hypertension. The possible mechanism is likely related with inhibiting of the vasoconstrictor ET-1 and increasing in vasodilator factor NO to reduce pulmonary artery hypertension.