Background. Extreme hemodilution caused by relatively large prime volumes required for cardiopulmonary bypass in infants causes a dilutional coagulopathy, characterized by low concentrations of fibrinogen and other circulating coagulation factors. Modified ultrafiltration results in hemoconcentration and is associated with decreases in postoperative bleeding and transfusion requirements in children. This study was undertaken to quantify the effect of modified ultrafiltration on concentrations of fibrinogen, plasma proteins, and platelets in infants and small children.
Methods. Twenty patients less than 15 kg were studied. Cardiopulmonary bypass circuits were primed with crystalloid solutions. Red blood cells were added during cardiopulmonary bypass for hematocrits less than 15%. Colloid solutions were not administered. Concentrations of fibrinogen, plasma proteins, and platelets, and hematocrit were measured before cardiopulmonary bypass, before modified ultrafiltration, and after modified ultrafiltration.
Results. Modified ultrafiltration was associated with significant (p < 0.001) increases in hematocrit (19% ± 6% to 31% ± 9%), fibrinogen (65 ± 29 to 101 ± 45 mg/dL), and total plasma proteins (2.7 ± 0.3 to 4.9 ± 0.7 g/dL), but no change (p = 0.129) in platelet count.
Conclusions. We conclude that modified ultrafiltration significantly attenuates the dilutional coagulopathy associated with cardiopulmonary bypass in infants. 相似文献
Triflavin, an Arg-Gly-Asp (RGD)-containing peptide, purified from snake venom of Trimeresurus flavoviridis, inhibits human platelet aggregation through the blockade of fibrinogen binding to fibrinogen receptors associated with glycoprotein IIb/IIIa complex. In this report, we examined the effect of triflavin on tumor cells (human hepatoma J-5)-induced platelet aggregation (TCIPA) of heparinized platelet-rich plasma (PRP). ADP-scavenger agents, apyrase (10 U/ml) and creatine phosphate (5 mM)/creatine phosphokinase (5 U/ml) did not inhibit TCIPA while hirudin (5u/ml) completely inhibited it. J-5 cells initially induced platelet aggregation, then blood coagulation occurred. J-5 cells concentration-dependently shortened the recalcification time of normal as well as Factor VIII, IX-deficient human plasmas, while it was inactive at shortening the recalcification time of Factor VII-deficient plasma, suggesting J-5 cells induced platelet aggregation through activation of extrinsic pathway, leading to thrombin formation as evidenced by the amidolytic activity on S-2238 by expressing tissue factor-like activity. Triflavin inhibited TCIPA in a dose-dependent manner (IC50, 0.02 μM). When compared on molar ratio, triflavin was approximately 30,000 times more potent than GRGDS (IC50,0.58 mM). On the other hand, GRGES showed no significant effect on TCIPA, even its concentration was raised to 4 mM. Additionally, the monoclonal antibodies, raised against glycoprotein IIb/IIIa complex (i.e., 7E3 and 10 E5) inhibited J-5 TCIPA. In conclusion, we suggest the inhibitory effect of triflavin on J-5 TCIPA may be chiefly mediated by the binding of triflavin to the fibrinogen receptor associated with glycoprotein IIb/IIIa complex on platelet surface membrane. 相似文献
The purpose of this study was to investigate whether, to whatextent, and through which mechanisms intravenous heparin, administeredbefore and after streptokinase, affects the plasma levels ofD-dimer and fibrinogen in myocardial infarction. Data concerningmortality and incidence of coronary recanalization in patientsreceiving heparin and thrombolytic therapy after acute myocardialinfarction are controversial; furthermore, the mechanisms throughwhich heparin acts in combination with thrombolytic therapyare unclear. Thirty-eight patients with acute myocardial infarctiontreated with streptokinase were considered. Nineteen of themreceived, immediately before the beginning of thrombolytic treatment,a bolus of heparin (100 U. kg1 intravenously) and, 2 h later,intravenous heparin in doses raising the partial thromboplastintime to 2-2.5 times the normal value (Group 1); the remaining19 did not receive anticoagulant treatment (Group 2). Multipledeterminations of plasma D-dimer and fibrinogen levels wereobtained in all patients before, and in the seven days followingthrombolytic treatment. Six hours after streptokinase, fibrinogendecreased from 304 ± 34 to 61 ± 34 mg. dt1 inGroup 1 and from 312 ± 29 to 38 ±21 mg. dt1 inGroup 2 (P<002 versus Group 1). The same difference betweengroups persisted at the 12th and at the 18th hour. D-dimer values,from 0-5 ± 01 \ig. dl1 in Group 1 and 04 ±01 fig.dt1 in Group 2, increased at the 1st hour to 37.2 ± 36.5fig. dt1 and 52.2 ± 39.8 µg. dl1, respectively.A peak value was reached in both groups at the 6th hour, whichwas followed by a slow decrease. A significant difference betweenthe two groups (P<0.05) was observed at the 1st, 2nd, 4thand 6th hour. An inverse correlation between maximal changesof fibrinogen and of D-dimer was found in both groups (r= 0.89,P<0.001 in Group 1; r=-0.81, P<0.001 in Group 2). The relationship between D-dimer and fibrinogen variations afterstreptokinase and changes induced by heparin, support the hypothesisthat the decrease of fibrinogen, following thrombolysis, isnot only the consequence of its direct degradation, but alsothe result of its transformation by streptokinase into fibrin,fibrin cross-linked (with facilitation of thrombogenic condition)and then into the stable catabolite, D-dimer. These data confirma thrombogenic effect of streptokinase therapy; this tendencycan be limited by prompt use of high doses of heparin. 相似文献
SUMMARY: A comparative immunohistological study was performed for the glomerular deposition of complements (C1q and C3c), fibrin/fibrinogen‐related antigen (FRA), the expression of intercellular adhesion molecule‐1 (ICAM‐1), and the infiltration of leucocytes bearing β2 integrins (leucocyte function associated antigen‐1 (LFA‐1), complement receptor 3 (CR3) and complement receptor 4 (CR4)) on renal biopsy specimens from 49 cases with Henoch‐Schoenlein purpura nephritis (HSPN), and 49 age‐matched cases with immunoglobulin A nephropathy (IgAN). the glomerular expression of ICAM‐1 was signifcantly correlated with the glomerular infiltration of leucocyte function associated antigen (LFA)‐1+ leucocytes in both diseases, and with that of CR3+ leucocytes in HSPN. the expression of ICAM‐1 was closely localized with the infiltration of LFA‐1+ leucocytes in the study with double immunostaining. the incidence and intensity of glomerular deposition of FRA were significantly higher in HSPN than in IgAN (P< 0.001), and those of C3c were significantly lower in HSPN than in IgAN (P< 0.001). the glomerular deposition of FRA was significantly correlated with the glomerular infiltration of CR4+ leucocytes in HSPN (P<0.05) but not in IgAN. In contrast, the glomerular deposition of C3c was significantly correlated with the glomerular infiltration of CR4+ leucocytes in IgAN (P<0.05), but not in HSPN. Studies with double immunostaining revealed a close association of CR4+ leucocytes with FRA deposition in HSPN and with C3c deposition in IgAN, respectively. the number of glomerular leucocytes bearing β2 integrins was significantly correlated with urinary protein at the time of renal biopsy in both diseases. These results suggested the differential roles of β2 integrins in the induction of glomerular injury in HSPN and IgAN. the ICAM‐1/LFA‐1 interaction may commonly be involved in the glomerular infiltration of leucocytes in both diseases. the ICAM‐1/CR3 interaction may be involved only in HSPN. Complement receptor 4 may function as a fibrin/fibrinogen receptor in HSPN, while CR4 may function as a complement receptor in IgAN. 相似文献