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N Tabuchi

Publications and source records attributed to N Tabuchi.

32 records · Page 2Linked to original sources
PubMed1995

Shear-induced pathway of platelet function in cardiac surgery.

The contribution of platelet dysfunction to the impaired hemostasis after cardiac surgery remains to be established, because there is no sensitive method to assess platelet function. Measurement of the shear-induced pathway of platelet function, an important mechanism in inducing hemostasis, became possible by a novel shear-inducing technique, the in-vitro bleeding test (Thrombostat 4000). By using this test, the changes in platelet function during cardiopulmonary bypass and their contribution to hemostasis were investigated in patients undergoing cardiac surgery. Platelet function is quickly impaired shortly after the start of cardiopulmonary bypass, and partly recovered at the end of cardiopulmonary bypass. The function of aspirin-treated platelets is more severely affected than of nonaspirin platelets during cardiopulmonary bypass. Furthermore, the degree of platelet dysfunction at the end of the operation, but neither the platelet number nor the activated clotting time, was significantly correlated with blood loss from the chest drain after cardiac surgery. These results indicate the significant and variable effects of cardiopulmonary bypass on the shear-induced pathway of platelet function. Moreover, the impairment of this function of platelets appears to be a major cause of excessive bleeding in patients after cardiac surgery. Therefore, the routine use of the shear-inducing test seems helpful to make a proper diagnosis and design the therapy for bleeders after cardiac surgery.

Aspirin↗
PubMed1995

Platelet function analysis after in vitro treatment with hemostasis-affecting components.

An overall platelet function test in whole blood, which simulates conditions under arterial pressure, is useful in measuring the effect of polymer materials on blood hemostatic function. We performed biocompatibility tests with materials or plasma substitutes by interaction of blood from healthy volunteers and then subjected these blood samples to platelet function analysis (Thrombostat). We tested also the capacity of locally applied hemostatic agents for bleeding control by direct application of these agents onto the Thrombostat measuring cell. The biocompatibility tests with materials exposed to blood appeared very discriminating between compatible and noncompatible materials. The hemostatic capacity of blood exposed to noncompatible materials (assessed by binding of active thrombin) reduced markedly after one hour incubation of the material. The plasma substitutes did not affect hemostasis significantly. However, a blood dilution of 40%, as in cardiopulmonary bypass, increased the time required for closure of the measuring cell by a platelet plug exponentially. Local hemostatic agents could be selected according to their capacity to enhance platelet plug formation. In addition, ADP mixed with the hemostatic agent was most effective in improving capacity. We conclude that platelet function analysis contributes importantly to screening of materials and plasma substitutes with regard to their interaction with primary hemostasis.

Biocompatible Materials↗
PubMed1995

Gelatin use impairs platelet adhesion during cardiac surgery.

Artificial colloids based on gelatin are used as plasma expander to replace donor blood products. In laboratory experiments, gelatin reduced both the velocity and extend of platelet agglutination by ristocetin, and only the agglutination velocity by polybrene (p < 0.05). Furthermore, gelatin delayed the in-vitro platelet plug formation under shear-stress in the absence of ADP (p < 0.05), whereas gelatin induced no delay in the presence of ADP. Thus, after induction of vWF release from platelets by polybrene or ADP, platelet function was normal. These results indicate that gelatin affects in particular the functionality of plasma-vWF and partly inhibits platelet adhesion. These negative effects of gelatin on hemostasis were demonstrated in two clinical studies during cardiac surgery. In a randomized study of sixty patients undergoing cardiac surgery, gelatin as prime in the heart-lung machine appeared to result in diminished efficacy of aprotinin on hemostasis, whereas it did not affect hemostasis in non-aprotinin patients. An additional retrospective clinical study showed that only high dose of gelatin affected hemostasis. This suggests a limited role of plasma-vWF and a strong back-up mechanism of platelet-vWF in achieving hemostasis.

Aprotinin↗
PubMed1994

Aprotinin preserves hemostasis in aspirin-treated patients undergoing cardiopulmonary bypass.

Various clinical trials have shown that hemostasis is improved by the administration of aprotinin during cardiopulmonary bypass. However, this effect has not been proved for those patients treated preoperatively with aspirin. Therefore, a double-blind, placebo-controlled study was conducted to test the efficacy of low-dose aprotinin (2 x 10(6) KIU in the pump prime solution) in preserving hemostasis in 40 aspirin-treated (325 mg) patients undergoing coronary artery bypass grafting. Aprotinin brought about a decrease in the postoperative blood loss (p < 0.05). The in vitro bleeding test (Thrombostat) demonstrated that aprotinin preserved the platelet hemostatic function in aspirin-treated patients during cardiopulmonary bypass (p < 0.05). The inhibitory effects of aspirin on collagen-induced platelet aggregation and thromboxane production were not influenced by aprotinin treatment. The findings from the present study indicate that aprotinin preserves hemostasis in aspirin-treated patients during cardiopulmonary bypass, but aspirin's effect on platelets is maintained. Therefore, aprotinin seems to be a useful adjunct treatment in aspirin-treated patients undergoing coronary artery bypass grafting.

Aprotinin↗
PubMed1994

Monitoring of anticoagulation in aprotinin-treated patients during heart operation.

Since aprotinin has become extensively used during cardiopulmonary bypass the maintenance of safe anticoagulation is a concern. Aprotinin affects anticoagulation measurement by the activated clotting time. Therefore, a reliable new measurement is needed to monitor anticoagulation during cardiopulmonary bypass. In the present study, we tested the efficacy of two alternative measurements in which whole blood clotting was stimulated by high-dose thromboplastin or by high-dose thrombin. During cardiopulmonary bypass under standardized heparinization, the activated clotting time was twofold longer in the aprotinin group than in control group (p < 0.05), whereas high-dose thromboplastin and high-dose thrombin groups were not significantly affected by aprotinin. In laboratory tests using blood from healthy volunteers, all methods showed linear correlation with heparin concentration in the absence of aprotinin (p < 0.05). However, the activated clotting time measurement was prolonged more by heparin when aprotinin was present (p < 0.05), whereas high-dose thromboplastin and high-dose thrombin measurements were not. Moreover, these measurements were faster and more dependable than the activated clotting time. Therefore, high-dose thromboplastin time and high-dose thrombin time seem to be reliable for monitoring anticoagulation when aprotinin is used during cardiopulmonary bypass.

Aged↗
PubMed1994

Aprotinin effect on platelet function and clotting during cardiopulmonary bypass.

A variety of studies have been performed on the preservation of hemostasis by aprotinin during cardiopulmonary bypass (CPB). It appears that the mechanism of aprotinin to preserve hemostasis can be interpreted in different ways. Our previous studies suggested that preservation of platelet glycoprotein Ib (GpIb) antigen, and counteraction of heparin anticoagulation in the extrinsic clotting pathway might partly explain the preservative effect of aprotinin. A clinical study was therefore conducted to evaluate these effects during the use of low dose aprotinin. Improved agglutination by ristocetin (P < 0.05), and improved GpIb antigen expression (P < 0.05) during CPB showed better preserved platelet adhesive capacity in the aprotinin group than in the control group. Glycoprotein Ib antigen expression and the agglutination capacity with ristocetin during CPB were closely related (P < 0.05). Platelet GpIIb/IIIa antigen and adenosine diphosphate (ADP) aggregation were not significantly different between the aprotinin and control groups. Aprotinin had no effect on the extrinsic clotting pathway in the blood, since the thromboplastin clotting time was similar in both groups. These results indicate that the protection of platelet adhesive capacity during CPB is a main function of aprotinin, whereas no evidence was collected for enhanced extrinsic clotting by aprotinin during CPB.

Adult↗
PubMed1993

Activation of fibrinolysis in the pericardial cavity during cardiopulmonary bypass.

The clotting and fibrinolytic systems are activated by tissue factor and by tissue-type plasminogen activator in the pericardial cavity, where the thrombogenicity is greater than that of the surface of modern extracorporeal circuits. This local activation may have consequences for the systemic activation processes during cardiopulmonary bypass. To test this hypothesis, we investigated blood activation by interrupting the blood suction from the pericardial cavity during cardiopulmonary bypass in clinical coronary artery bypass operations. In blood collected in the pericardial cavity, thrombin-antithrombin III complex (p < 0.01), tissue-type plasminogen activator antigen (p < 0.05), fibrinogen degradation products (p < 0.01), and fibrin degradation products (p < 0.01) were significantly higher than in the systemic blood. Plasma heparin was significantly consumed in the pericardial cavity (p < 0.01). Once the pericardial blood was returned to the systemic circulation after resumed suction during cardiopulmonary bypass, thrombin-antithrombin III complex (p < 0.05), fibrinogen degradation products (p < 0.05), and fibrin degradation product (p < 0.05) concentrations increased significantly in the systemic blood. The effects of pericardial tissue on activation of clotting and fibrinolysis were also studied in vitro. When human plasma was incubated for 5 minutes with rabbit pericardium at reduced heparin concentrations, we found significant generation of thrombin (p < 0.05) and plasmin (p < 0.05). If the thrombin inhibitor hirudin was added, plasmin generation was also inhibited (p < 0.05). The results of the clinical and experimental study are in agreement with our hypothesis that tissue factor and tissue-type plasminogen activator accelerate the activation of clotting and sequentially of fibrinolysis under conditions of low heparin concentrations in the pericardial cavity and that this local activation contributes highly to the systemic activation, affecting hemostasis during cardiopulmonary bypass. Topical use of heparin in the pericardial cavity therefore seems indicated to reduce blood activation during cardiopulmonary bypass.

Blood Coagulation Factors↗
PubMed1992

[Surgical treatment of infected left atrial myxoma--a case report].

A 22-year-old man had undergone dental therapy following an intermittent fever, and the bacteriological examination by blood culture identified Streptococcus viridans. A left atrial myxoma was echocardiographically found out and the tumor was surgically resected with uneventful postoperative course. Multiple foci and Gram-positive cocci within the typical myxoma were revealed histopathologically. Reviewing previous reports on infected cardiac myxoma, the coexistence of cardiac myxoma and a confirmed positive blood culture has been considered diagnostic criteria for "infected cardiac myxoma". But, from the surgical viewpoint, the demonstration of infecting organisms within the tumor is essential for accurate diagnosis. Infected atrial myxoma has an extremely high incidence of systemic embolization, and its bacterial foci could be the source of persistent bacteremia. Therefore, in clinical situations suggesting infected cardiac myxoma, we recommend performing open heart surgery to prevent both the embolization and the infective progression into other cardiac valves, as soon as possible.

Adult↗
PubMed1987

[Neuronal and adrenomedullary catecholamine response to cardiopulmonary bypass: with special reference to comparative studies based on functional classification].

Plasma epinephrine (E) and norepinephrine (NE) levels during cardiopulmonary bypass (CPB) were studied in thirty-eight cardiac patients with various grades of NYHA classification. Striking increases of both E and NE levels after release of aortic cross clamp (stage 4) were noted. A thirteen fold increase in E (from 0.05 +/- 0.05 ng/ml to 0.62 +/- 0.48 ng/ml) and sixfold increase in NE (from 0.21 +/- 0.18 ng/ml to 1.26 +/- 0.78 ng/ml) occurred from prebypass (stage 1) to stage 4. The values of E and NE were peaked at stage 4 and rapidly decreased after heart beating (stage 5). At chest closure (stage 7), E returned to close to prebypass control (stage 1) value, however NE remained still in moderately high level. Patients were divided into three groups: The mild group (NYHA class I and II, fourteen patients), the ill group (NYHA class III and IV, nineteen patients) and the IABP group (IABP support since prior to CPB due to unstable angina and ventricular septal perforation, five patients). Whereas E value at either stage 4 or stage 5 in the mild group was statistically significantly higher (p less than 0.05) than each E value at corresponding stages in the ill group. NE value at each stage 3 (prior to aortic cross clamp), stage 4 or stage 5 in ill group significantly higher than each NE value at same stages in the mild group respectively. These data suggest that depletion of E and compensatory increase of NE in the ill group may be occurred during CPB.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗