摘要
为探讨TXA2 在先天性心脏病 (先心病 )肺动脉高压形成中的作用 ,我们采用放免法测定了 36例实验对象血浆TXB2 的浓度 ,结果表明与对照组相比 ,血浆TXB2 在左向右分流先心病不伴肺动脉高压组 [(12 5 0 4± 2 3 5 5 )pg/mL与 (6 3 72± 15 5 1)pg/mL]、肺动脉高压组 [(12 6 4 2±31 2 8)pg/mL与 (6 3 72± 15 5 1)pg/mL]均明显升高 ,但左向右分流先心病不伴肺动脉高压组和肺动脉高压组之间[(12 5 0 4± 2 3 5 5 )pg/mL与 (12 6 4 2± 31 2 8)pg/mL]、中度和重度肺动脉高压组之间 [(12 6 79± 2 1 5 5 )pg/mL与(12 6 0 5± 4 1 0 9)pg/mL]无显著差异。表明血小板活化释放的TXA2 并不直接介导先心病肺动脉高压的形成。
Objectives To explore the role of thromboxane A 2 in pathogenesis of pulmonary hypertension (PH) associated with congenital heart disease (CHD). Methods The plasma concentrations of thromboxane B 2 in 36 subjects were measured by radioimmunoassay. Results Comparing with the control group, TXB 2 were significantly higher in the left-to-right shunt type of CHD without PH group [(125.04±23.55) pg/mL vs (63.72±15.51) pg/mL, mean±SD] and in group with PH associated with CHD [(126.42±31.28) pg/mL vs (63.72±15.51) pg/mL]. There were no significant differences between the group of left-to-right shunt type of CHD without PH and the group with PH [(125.04±23.55) pg/mL vs (126.42±31.28) pg/mL], even between the mode-rate PH group and the severe PH group [(126.79±21.55) pg/mL vs (126.05±41.09) pg/mL]. Conclusions Our findings suggested that TXA 2 released from platelet activation did not mediate the pathogenesis of PH associated with CHD directly.
出处
《岭南心血管病杂志》
2004年第1期38-40,共3页
South China Journal of Cardiovascular Diseases
