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目的观察布-加综合征(B-CS)患者血浆中前列环素(PGI2)含量,探讨PGI2在肝后型门静脉高压症患者发病中的作用。方法采用放免法检测19例B-CS患者分流减压手术前后、21例B-CS患者口服肠道抗菌药物前后静脉血PGI2含量,光电比色法检测患者口服肠道抗菌药物前后静脉血内毒素含量。结果对照组患者血浆PGI2含量为(9.46±3.74)ng/L。分流减压手术前后,B-CS患者门静脉压力由(37.2±4.5)cmH2O下降至(25.8±4.2)cmH2O(P<0.01);血浆中PGI2含量由(17.71±6.93)ng/L下降至(12.43±3.54)ng/L(P<0.01),且其含量下降与门静脉压力下降呈正相关(r=0.54,P<0.05)。口服肠道抗菌药物前、后,B-CS患者血浆内毒素含量由(0.328±0.188)Eu/ml下降至(0.226±0.147)Eu/ml(P<0.01);而血浆PGI2含量分别为(14.08±5.54)ng/L和(14.21±4.98)ng/L,差异无统计学意义(P>0.05),但高于对照组(P<0.01)。结论布-加综合征患者血浆PGI2含量增高,且参与了门静脉的高压状态的维持。PGI2含量增高之原因部分地由于机体合成PGI2增多所致。增高的门静脉压力是刺激机体合成PGI2增多的原因之一,内毒素水平可能与机体合成PGI2增多无关。
Objective To observe the content of prostacyclin (PGI2) in patients with Budd-Chiari syndrome (B-CS) and to explore the role of PGI2 in the pathogenesis of post-hepatic portal hypertension. Methods The radioimmunoassay was used to detect the content of PGI2 in venous blood before and after oral administration of antimicrobial drugs in 21 patients with B-CS before and after bypass decompression in 19 patients with B-CS. The levels of venous blood endotoxin before and after oral administration of antibiotics content. Results The plasma PGI2 level in the control group was (9.46 ± 3.74) ng / L. The portal pressure of B-CS patients decreased from (37.2 ± 4.5) cmH2O to (25.8 ± 4.2) cmH2O before and after bypass decompression (P <0.01), and the plasma PGI2 level decreased from (17.71 ± 6.93) ng / L to ± 3.54) ng / L (P <0.01), and the decrease was positively correlated with the decrease of portal pressure (r = 0.54, P <0.05). The levels of endotoxin in B-CS patients decreased from (0.328 ± 0.188) Eu / ml to (0.226 ± 0.147) Eu / ml before and after oral administration of gut antibiotics (P <0.01) ± 5.54) ng / L and (14.21 ± 4.98) ng / L, respectively. There was no significant difference between them (P> 0.05), but higher than that of the control group (P <0.01). Conclusion The plasma PGI2 level in patients with Budd-Chiari syndrome is increased, and is involved in the maintenance of high pressure state in the portal vein. The reason for the increased PGI2 content is due in part to the increased synthesis of PGI2 in the body. Increased portal pressure is one of the reasons to stimulate the synthesis of PGI2 in the body. Endotoxin levels may not be related to the increase of PGI2 synthesis in the body.