ABSTRACT
ObjectiveTo investigate the effects of tirofiban on microvascular flow in infarction zone after coronary reperfusion in pigs with acute myocardial infarction (AMI),and to explore its mechanism of decreasing microvessel obstruction (MO) and the relationship with inflammatory factors. MethodsChinese mini pigs were randomized into control group and tirofiban treatment group.Acute myocardial infarction was induced by balloon occluding the medium segment of the left anterior descending artery for 90 min,and then reperfusion was created by withdrawing the balloon.The infarct myocardium and MO area were detected with delayed enhancement multi-slice spiral CT (DE-MSCT),the serum levels of IL-6 and IL-10 were measured with enzyme linked immunosorbent assay (ELISA).The pigs were killed, the heartwere excised and stained with 2, 3, 5-triphenyltetrazolium chloride (TTC). Results6 pig models were successfully established in each group.4 pigs in control group and 3 pigs in tirofiban treating group experienced MO.The MO volume was increased at every time after reperfusion in both groups,while the MO volume was significantly reduced in tirofiban treatment group compared with control group at 1 h [(9.6 ± 3.1) ％ vs.(4.8 ±0.7)％],24 h[(13.4±3.3) ％ vs.(5.8±-1.2)％],48 h[(15.1±3.8)％ vs.(6.4±1.2)％] and 72 h [(15.9±4.6) ％ vs.(6.6±0.8)％ after reperfusion (t=6.99,13.76,14.21,11.38,all P＜0.05).Compared with the baseline,the levels of serum IL-6 and IL-10 in both groups were increased at 30 min after AMI.In tirofiban treatment group,the level of serum IL-6 was significantly lower and serum IL-10 was higher than those in control group (P＜0.05 and P＜0.01) from 10 min to 72 h after reperfusion. Conclusions Tirofiban may lessen the MO area in infarction zone of AMI after reperfusion,which may be ascribed to its anti-inflammation besides anti-platelets.
ABSTRACT
Objective To identify the gene mutations of platelet membrane glycoprotein Ⅱ b,Ⅲa(GPⅡb/Ⅲa)in three Chinese pedigrees with Glanzmann thrombastIlenia.Methods All exons and exonintron boundaries of GP Ⅱ b/Ⅲ a gene were amplified by PCR analysis followed by DNA sequencing.DNA sequencing was used to exclude gene polymorphisms.Results The probands in the three pedigrees had a normal platelet count,coagulation profiles,scattered platelets on the blood film,a prolonged cutaneous bleeding time,and impaired or minimal ex vivo platelet aggregation in response to ADP,thrombin,collagen,adrenaline and arachidonic acid,but normal platelet aggregation in response to ristoeetin.Both FACS and Western blotting demonstrated trace content of αⅡb in the platelets from proband 1 and proband 3,who were classified as type Ⅰ GT,and a small amount of αⅡb in the platelets from proband 2,who was classified as type Ⅱ GT.Compound heterozygous mutations,T2255G(Leu721Arg)and C2671T(Gln860Stop)were identified in proband 1.The proband 2 had homozygous A2334C(Gln747Pro)missense mutation.Nonsense mutations C1750T (Arg584Stop)and 69-79 deletion mutation were identified in proband 3. Conclusions Compound heterozygous mutations T2255G and C2671T of αⅡb gene lead to type Ⅰ Glanzmann thrombasthenia for proband 1. Homozygous mutation A2334C of αⅡb gene leads to type Ⅱ Glanzmann thrombasthenia for proband 2. Compound heterozygous mutations C1750T and 69-79del αⅡb gene lead to type Ⅰ Glanzmann thrombasthenia for proband 3. T2255G,C1671T and 69-79del aye novel mutations for αⅡb gene.