Biomedical subjects
Publications and source records attributed to I Juhan.
The authors used a disposable original system to recover total blood during surgery and realized 17 transfusions of autologous blood in sheep. No biological or clinical disturbance was observed.
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We used a simple single process to recover total blood during surgery. All the process stands on a low burdensome jib and does not require additional staff in theater. Its cost is low. The indications concern all surgical operations enduring low or mean bleeding, except in septic and cancer surgery. It may be used in emergencies, even in war surgery with an incorporated source of depression.
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We investigated thromboxane B2 (TxB2), 6-keto-PGF1 alpha (6KPGF1 alpha reflecting prostacyclin), PGE2 and PGF2 alpha plasma levels; TxB2, PGE2 and PGF2 alpha platelet production and platelet aggregation response in ascending aorta (reflecting trans-pulmonary difference) and in venous coronary sinus (reflecting transcardiac difference) simultaneously in patients with ischemic heart disease, before and after right-atrial administration of 3 mg ISDN bolus. Transcardiac differences were scarce before as well as after ISDN administration. In aortic blood, ISDN administration into the right atria resulted in a significant increase in prostacyclin and PGF2 alpha plasma levels (472% and 242%, respectively), a decrease of both PGE2 plasma level (-173%) and PGE2 platelet production (-485%) and a marked lowering of platelet aggregation response to ADP, concomittantly. In contrast, TxB2-related features were poorly affected by ISDN. In coronary sinus blood, the aortic increase in 6KPGF1 alpha and PGF2 alpha plasma levels was detected to a lower extent whereas the characteristics of platelet aggregation had returned to control levels. By contrast, PGE2 plasma level (-191%) and PGE2 platelet production (-133%) were lower than prior ISDN administration. The results we report here, strongly support the view that ISDN promotes release of prostacyclin and PGF2 alpha from the lung and inhibit PGE2 production. These prostanoids may be responsible for the concomittant platelet reactivity lowering, thus providing a basis for understanding how ISDN might relieve myocardial ischemia favoring prostanoid mediated vasodilation and inhibition of platelet reactivity.
A case is reported of a young female patient with a circulating lupus anticoagulant. The illness, associated with several spontaneous abortions, is characterized as a "Soulier and Boffa syndrome". No severe bleeding occurred when she underwent several major operations. The clinical picture of lupus anticoagulant is discussed, as well as the perioperative management of such patients. The presence of a lupus anticoagulant, if not associated with other hemostatic defects, is not a contraindication to surgery. The risks and benefits of postoperative heparinization are recalled. Thrombin time seems to be the best coagulation test for adapting heparin doses.
Abnormalities of rheologic and hemostatic properties of blood are present in uncontrolled diabetics and play a role in the development of structural micro- and macroangiopathies. Red blood cell deformability is decreased in diabetics and shows negative correlation with fast hemoglobin and actual blood glucose levels. In uncontrolled insulin-dependent diabetics, normalization of plasma glucose by an insulin infusion improves red cell deformability in 2 h. Insulin infusion (0.2 U/kg/h) [the initial hyperglycemia being maintained (hyperglycemic clamp)] also improves red cell deformability. Deformability of normal erythrocytes is reduced by incubation in plasma from uncontrolled diabetics but is normal in plasma from diabetics controlled by a 24-h insulin infusion or in diabetic plasma with insulin added in vitro. Therefore, insulin appears to have a direct effect on erythrocyte deformability. Platelet aggregation measured in whole blood is raised in uncontrolled diabetics. Aggregation of normal platelets rises in the presence of "diabetic" red cells but not in the presence of red cells from the same patients controlled by 24-h treatment with insulin. The effect of insulin on platelet aggregation, therefore, seems to be at least partly mediated by erythrocytes.
Erythrocyte deformability is lower than normal in uncontrolled insulin-dependent diabetics and returns towards normal after 24 h treatment with a feedback-controlled insulin infusion. Deformability of normal erythrocytes is reduced by incubation in plasma from uncontrolled insulin-dependent diabetics but is normal in plasma from insulin-dependent diabetics controlled by 24 h insulin infusion, or in plasma from uncontrolled insulin-dependent diabetics with insulin added in vitro. Therefore, insulin has a direct action on erythrocyte deformability. Platelet aggregation measured in whole blood is raised in uncontrolled insulin-dependent diabetics and returns to normal after 24 h treatment with a feedback-controlled insulin infusion. Aggregation of normal platelets rises in the presence of erythrocytes from uncontrolled insulin-dependent diabetics, but not erythrocytes from the same patients after 24 h treatment with insulin. The effect of insulin on platelet aggregation therefore seems to be at least partly mediated by erythrocytes. The enhanced platelet aggregation seen in uncontrolled insulin-dependent diabetics can be explained either by a direct effect of erythrocyte rigidity or by an increased release of nucleotides (ADP) by the erythrocytes.
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Erythrocyte deformability was studied by the filtration technique of Reid & Dormandy using whole blood and washed erythrocytes from insulin-dependent diabetics (IDD) under insulin delivery by an artificial pancreas (AP). The same technique was employed to study deformability in vitro using normal erythrocytes incubated in the presence of insulin. Results of this study show that in IDD the initially poor erythrocyte deformability is improved within hours of insulin administration. Improved deformability was accompanied by increased levels of intra-erythrocyte ATP but without changes in levels of HbG and 23 DPG. Incubation of erythrocytes in medium containing glucose showed that deformability was significantly improved in the presence of insulin. These results indicate that insulin favourably affects erythrocyte deformability in IDD. Before and after 24 hours treatment by AP, platelet aggregation was studied in IDD by the technique of Born using platelet-rich plasma (PRP) and by a modified Breddin technique using PRP, whole blood or whole blood treated by chlorpromazine and mixtures of erythrocytes from IDD with normal PRP. Platelet hyperaggregation was only found in the presence of erythrocytes from untreated diabetics. Chlorpromazine, at a dose (10 mumole) which inhibits haemolysis without inducing platelet hyperaggregation, eliminated the above anomaly. In conclusion, it is conceivable that the insulin-induced correction of poor erythrocyte deformability eliminates excessive fragility of erythrocytes and their haemolysis wit release of ADP, thus avoiding platelet hyperaggregation.
A new case of congenital dysfibrinogenaemia was found in 2 members of the same family. The anomaly was characterized by an abnormal polymerization of fibrin monomers, whereas the release of fibrinopeptides by thrombin and fibrin stabilization by F XIII were normal. Investigation of the fibrinogen molecule did not lead to localizing the structural abnormality.
Two cases of the development of anti-VIII antibody during the postoperative period are reported. The methods used to demonstrate the antibodies, the different aetiologies, the course and current treatment are reviewed. The cause was found in only one of the two cases.
In 81 obese subjects the following studies were performed: --measurement of fat mass and its distribution in the body, --exploration of carbohydrate tolerance and lipid plasma level, --assessment of platelet aggregation and coagulation activity, --investigation of the chemical composition of platelet phospholipids. Platelet hyperactivity was demonstrated in certain patients, as evidenced by the presence of irreversible platelet aggregation with low doses of aggregation agents and by an increase in platelet coagulant activity; the latter phenomenon was not accompanied by a change in the biochemical composition of platelet phospholipids. Results of this work showed that platelet activity was not related to body weight and displayed no correlation or a slightly negative one to fat mass excess. Platelet activity was significantly increased in cases where obesity predominated in the upper body (hyperandroid obesity). The classical association of diabetes and atherosclerosis with hyperandroid obesity did not allow us to distinguish between the relative importance of hyperandroid obesity and diabetes in the observed platelet hyperactivity. Regardless of the causal mechanism involved, the relationship between platelet hyperactivity and upper body fat excess should be kept in mind.
In 36 treated diabetics (15 with insulin, 21 with oral hypoglycaemic agents) without any detectable arterial atheromatous lesion, there was a negative correlation between the filtrability of red cells and blood glucose levels (r = - 0.60) on the one hand and, secondly, glycosylated haemoglobin levels (r = - 0.40). In 17 insulindependents diabetics connected to an artificial pancreas, normalisation of blood glucose was accompanied by a concomitant increase in the filtrability of red cells, and improvement of spontaneous platelet agregation. Good control of diabetes would thus appear to be necessary to reduce the incidence of microangiopathy.
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The authors report on two cases of congenital thrombopenia with radial aplasia. Both children display several formative abnormalities and a mild thrombopenia; hemorragic manifestations occurred in the first case only. Megacryoblastic to platelets series, as studied with electronic microscopy, show small-sized, "microcytic" and hypogranular megacaryocytes, displaying a maturative disorder (dysmegacaryocytopoiesis). In functional studies, platelets of the first patient show an imperfect nucleotidic release and do not agregate normally with ristocetin. The second case exhibits mostly a PF3 reduction. The variety of expression of the megacaryocytic-platelets disorders appears likewise in the squelettal and visceral malformations. The whole disorder could be ascribed to a pleiotropic abnormal gene with a variable expressivity.
Five months experience with the Hemalog D has enabled the authors to define the mode of integration of the apparatus into a central hematology laboratory of a hospital without a clinical hematology department. The incidence and importance of such factors as the alarms set off by the apparatus, the time-course of blood basophils in patients receiving heparin and the clinical picture in patients for whom the apparatus revealed a peroxidase deficiency are discussed.