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The authors attempted experimental and clinical use of argatroban as an alternative anticoagulant in left heart bypass with the centrifugal pump, percutaneous cardiopulmonary support (PCPS), and extracorporeal membrane oxygenation (ECMO) to determine if it has complementary effects in preventing thrombus formation without aggravating bleeding tendency. Its reversible binding to thrombin and its short half-life contributed to reduce the risk of excessive blood loss without clot formation within the extracorporeal circulation circuit during thoracic aortic surgery using left heart bypass. PCPS and ECMO were safely performed at doses ranging from 0.5 to 10 micrograms/kg/min to maintain activated clotting time at approximately 200 seconds. Although experimental studies showed argatroban to be advantageous in preserving platelet and fibrinogen, further clinical investigations are necessary.

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Systemic heparinization often increases the risk of fatal bleeding from other injured organs in surgical repair of the aorta using extracorporeal circulation in patients with traumatic aortic rupture associated with multisystem injuries. We used an antithrombin agent, argatroban, as an alternative anticoagulant in left heart bypass with the Bio-Medicus centrifugal pump in 7 of 9 recent patients who underwent aortic repair using left heart bypass. All these patients survived without obvious evidence of systemic thromboembolization. Surgical treatments for other organ injuries were carried out in 3 patients concomitantly or immediately after aortic repairs without undue blood loss. Argatroban may have a complementary effect for preventing thrombus formation without aggravating bleeding tendency because of its monotarget specificity to thrombin. We believe intravenous administration (0.5 to 2 micrograms/kg/min) of argatroban is a safe anticoagulant for left heart bypass in repairs of traumatic aortic rupture associated with multiple organ injuries.

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BACKGROUND/PURPOSE: Fibronectin (FN) plays an important role in fibrin matrix formation during the wound healing process. The authors investigated whether exogenous FN increases the bursting strength (BS) of surgical wounds in malnourished rats. METHODS: Ninety rats were grouped according to three nutritional conditions (n = 30 in each group). All animals underwent a transverse celiotomy after 3 weeks of feeding, and FN (2 mg/body/day) was given postoperatively to 15 rats in each of the three groups. Wound BS was measured on postoperative days (PODs) 3, 5, and 7 after removal of the sutures. RESULTS: BS in normally nourished rats (group N; 142.6+/-23.4 mmHg) was significantly higher than that in protein malnourished rats (group PM, 110.2+/-11.2 mm Hg) and protein/ calorie (Cal)-malnourished rats (group PCM, 76.5+/-10.7 mm Hg) on POD 7 (P<.01). However, BS values for groups PM + FN (147.0+/-21.1 mmHg) and PCM + FN (115.1+/-28.9 mm Hg) were intensified significantly in comparison with groups PM and PCM (P<.01). Plasma FN levels in rats of the three FN nontreated groups were similarly decreased on POD 3 or 5, but returned to the preoperative level on POD 7, whereas those for the other three FN-treated groups increased after POD 3. CONCLUSION: Intravenous administration of FN might strengthen the weakened wounds of malnourished animals.

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A study was conducted to characterize the platelet aggregation induced by neuroblastoma tissue to investigate the mechanism of hypercoagulability in patients with neuroblastoma. The patients whose tumor tissues were examined had been shown clinically to have enhanced platelet activity. Platelet aggregation induced by neuroblastoma tissue extract was compared with that of other pediatric tumors. The effects of pretreatment with an antithrombin agent and prostacyclin (PGI2) on the platelet aggregation induced by tumor tissue extracts were also evaluated. Tissue extracts of 12 of 15 neuroblastomas, 3 of 3 Wilms' tumors, and 1 pheochromocytoma were demonstrated to have an activity that potentiated platelet aggregation in vitro. The platelet aggregation induced by tissue extracts of neuroblastomas and other tumor tissues was suppressed almost completely by pretreatment with a PGI2 analogue. The aggregation induced by neuroblastomas and the pheochromocytoma was also suppressed by pretreatment with an antithrombin agent, argatroban, whereas the aggregation induced by Wilms' tumors was not suppressed by this agent. These results suggest that (1) malignant tumors in children also have some chemical substances that sensitize platelet activity, such as those in adult cancers, and (2) thrombin is one of the mediators stimulating platelet aggregation in cases of neuroblastoma, although it is unlikely to be a contributing factor in other pediatric malignancies such as Wilms' tumor.

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This article reports a case of a thoracoabdominal aneurysm complicated with disseminated intravascular coagulopathy (DIC). The thoracoabdominal aneurysm was successfully replaced with a prosthetic graft following the short terms of heparin pretreatment. Although heparin pretreatment had been effective for the temporal remission of DIC, a large amount of blood transfusion was necessary because of prolonged bleeding from surgical wound. However, hematological evidence of DIC and bleeding tendency were dramatically arrested in the immediate postoperative period. It was concluded that the definitive treatment for DIC was removal of the aneurysm. Heparin was usefull for the preservation of coagulation factors and platelet, but it did not lessen operative bleeding.

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Adenosine (1), guanosine (2), and tryptophan (3), as well as beta-sitosterol beta-D-glucoside (4) were isolated from the n-butanol-soluble fraction of Xiebai, the tuber of Allium bakeri Reg., which was recognized to have an anti-platelet aggregation effect. Moreover, 1 and 2 were also isolated from the n-butanol-soluble fraction of Dasuan, the tuber of A. sativum L. Compound 1 showed a significant inhibitory activity against both the primary and secondary wave aggregation of human platelet induced by 2 microM ADP, whereas compounds 2-4 showed no or very low inhibitory effects. The structure-activity relationships on human platelet aggregation with regard to 1, 2 and their derivatives, adenosine 2'-monophosphate (5), adenosine 5'-monophosphate (6), adenosine triphosphate (7), guanosine 3'-monophosphate (8), and guanosine 5'-monophosphate (9), and guanylyl(3'----5')adenosine (10) are discussed. Compounds 5-7 and 10 also inhibited the primary and secondary wave aggregation with a dose-dependent response.

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