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Biomedical subjects

E C Rossi

Publications and source records attributed to E C Rossi.

At least 37 records · Page 2Linked to original sources
PubMed1981

Haemorrhagic thrombocytopathy associated with dilatation of the platelet--membrane complex.

We evaluated eight patients from four families because of a history of excessive bleeding. Most patients had prolonged bleeding times, absent secondary wave of platelet aggregation in response to epinephrine, collagen and adenosine diphosphate (ADP), and defective 14C-serotonin release and platelet factor 3 availability. These findings are characteristic of a platelet release defect. Electron-microscopy examination of the platelets of seven patients revealed a common abnormality. From 30% to 70% of the platelets in any given sample exhibited a prominent membrane complex and dilated, tortuous surface-connected canalicular system ('swiss-cheese' platelet). In two patients there was coincident storage-pool disease, but the remainder had adequate dense bodies and a normal ratio of ATP to ADP. SDS-polyacrylamide gel electrophoresis of platelet proteins and glycoproteins showed no abnormalities. The patency of the canalicular system was demonstrated in one patient by the observation that dense bodies appeared in the cannaliculi and outside the platelets following collagen-induced aggregation of polylysine-treated platelets. Since platelet-aggregation responses to the calcium ionophore A23187 were normal, we conclude that the defective platelet function in these patients may be due to impaired calcium mobilization from the morphologically abnormal membrane complex.

Bleeding Time↗
PubMed1981

Hereditary bleeding disorder due to a primary defect in platelet release reaction.

A large family with a hereditary bleeding disorder was investigated. Easy bruising, epistaxis and menorrhagia were noted in seven members of three generations and at least one member in each generation was affected. Platelet function abnormalities were characterized by reduced 14C-serotonin release, absent second wave aggregation in response to ADP or epinephrine and reduced aggregation in response to collagen. Bleeding time was prolonged in three individuals and platelet factor 3 availability was abnormal in four. Platelet count, morphology, adhesiveness and clot retraction were normal in all. Platelet ADP and ATP as well as ATP to ADP ratio were normal. This family probably represents the first documented instance of hereditary platelet primary release disorder. To elucidate the pathogenetic mechanism, further functional studies were performed. No appreciable shape change, 14C-serotonin release of aggregation was observed when the propositus' platelets were stimulated with sodium arachidonate or a PGH2 analogue. By contrast, platelets responded normally to ionophore A23187, thrombin and ristocetin. The findings indicate that the hereditary primary release disorder is probably due to a reduced thromboxane A2 production secondary to thromboxane synthetase deficiency. Alternatively, it may be due to platelet membrane abnormalities which render platelets unresponsive to thromboxane A2.

Adolescent↗
PubMed1980

Hemodialysis-exchange transfusion for treatment of thrombotic thrombocytopenic purpura.

Remission in thrombotic thrombocytopenic purpura (TTP) was achieved in two patients after repeated exchange transfusion. Since both patients had renal insufficiency, exchange was performed with hemodialysis. This provided optimal volume control and facilitated the rapid exchange of blood. The infusion of plasma did not maintain the clinical improvement achieved with exchange transfusion. Until a concentrate of the putative factor deficient in TTP becomes available, an exchange procedure remains the most expeditious method for the replacement of any deficient factor. The procedure of hemodialysis can be adapted to perform exchange transfusion safely and efficiently.

Acute Kidney Injury↗
PubMed1980

Sequential changes in factor VIII and platelets preceding deep vein thrombosis in patients with spinal cord injury.

The relationships between factor VIII associated activities, platelet function, and venous thrombosis were studied in 18 patients with lower limb paralysis following acute spinal cord injury (SCI). Deep vein thrombosis (DVT) was detected in 13 patients (72%). Eight of the 13 thromboses were documented between 6 and 8 d following injury while the other five episodes were noted on days 11 (two), 13, 18 and 22. The detection of thrombosis was preceded by marked increases in VIIIR:Ag and VIII:RCoF whereas VIII:C was only marginally increased. The platelet aggregation response to collagen was hyperactive by the sixth day while the platelet aggregate ratio (PAR) did not become abnormal until after DVT was detected. These studies suggest a chronology in the series of events leading to DVT in patients with lower limb paralysis following SCI. Initial elevations in VIII:Ag and VIII:RCoF are followed in sequence by increased platelet responsiveness to collagen, the occurrence of DVT, and the appearance of circulating platelet aggregates. Conceivably, VIIIR:Ag elaborated by endothelial cells alters platelet reactivity and provides an important determinant for venous thrombosis.

Adolescent↗
PubMed1979

The treatment of the hemolytic-uremic syndrome with inhibitors of platelet function.

In four patients with clinical and laboratory manifestations of the hemolytic-uremic syndrome, the administration of aspirin and dipyridamole was associated with a dramatic and rapid increase in the platelet count. In three of the four patients there was also improvement in neurologic or renal function. No subject experienced bleeding or other untoward effects. We conclude that a trial of aspirin and dipyridamole therapy is warranted early in the course of the hemolytic-uremic syndrome.

Adult↗
PubMed1979

Structure activity relationships between catecholamines and the alpha-adrenergic receptor responsible for the aggregation of human platelets by epinephrine.

PEA is a potent inhibitor (Ki approximately 13 microM) of human platelet aggregation induced by epinephrine. This led us to perform an SAR study of a congeneric series of compounds in an effort to identify the molecular components of epinephrine critical to its aggregating effect upon human platelets. Phenylethanolamine was similar to PEA in inhibitory potency. However, hydroxylation of the phenyl ring diminished the inhibitory effect (Ki tyramine approximately 87 microM; Ki octopamine approximately 88 microM). Dopamine, the weakest inhibitor (Ki approximately 150 microM), was a partial agonist capable of inducing platelet aggregation in some samples of PRP. The order of potency of catecholamines as aggregating agents was epinephrine greater than norepinephrine greater than Epinine greater than dopamine. Phenylephrine, the prototype alpha-agonist, did not induce aggregation but was a potent inhibitor (Ki approximately 12 microM) of the aggregation induced by epinephrine. Isoproterenol, the prototype beta-agonist, was neither an aggregant nor an inhibitor of epinephrine-induced platelet aggregation. These findings suggest that the binding of epinephrine to the alpha-adrenergic receptor responsible for platelet aggregation is accomplished by the N-methyl amino group whereas intrinsic aggregating activity is a function of the catechol moiety.

2-Hydroxyphenethylamine↗
PubMed1979

Inhibitors of platelet function and atherogenesis.

Platelets play an important role in atherogenesis. This has given rise to the speculation that inhibitors of platelet function may prevent atherosclerotic changes. Two distinct therapeutic goals might be achieved by the use of inhibitors of platelet function in vascular disease - one, the prevention of thrombosis and, two, the prevention of atherosclerosis. The choice of inhibitor may well determine the goal achieved. Thus far, the data available indicate that inhibitors of platelet aggregation, such as aspirin, are the most effective in the prevention of thrombosis, while inhibitors of platelet adherence, such as dipyridamole, are likely to be the most effective in the prevention of atherosclerosis.

Animals↗
PubMed1978

Platelet monoamine oxidase and epinephrine-induced platelet aggregation.

Platelet MAO activity and the aggregation response to epinephrine, ADP, and collagen were measured in normal subjects. There was a direct correlation between the amount of platelet MAO activity and the per cent aggregation induced by 1 and 2 micrometer epinephrine. There were lesser correlations between platelet MAO and ADP or collagen-induced aggregation. These findings suggest that platelet MAO may play a role in determining the response of human platelets to epinephrine.

Adenosine Diphosphate↗
PubMed1977

Kinetic parameters of platelet aggregation as an expression of platelet responsiveness.

The kinetics of platelet aggregation induced by collagen and by ADP were studied. The maximum aggregation (deltaLTmax) and the ADP and collagen concentrations required to produce half-maximum aggregation (Kd) were determined using platelets obtained from normal individuals, individuals who ingested aspirin and individuals whose platelet-rich plasma (PRP) demonstrated spontaneous aggregation. The Kd and deltaLTmax for ADP-induced platelet aggregation were variable and markedly affected by the citrate concentration. Conversely, kinetic parameters of collagen-induced aggregation were more reproducible and less affected by citrate. The Kd for collagen in platelet aggregation was increased following aspirin ingestion and decreased in samples of PRP that demonstrated spontaneous aggregation. These results suggest that kinetic parameters of platelet aggregation may be useful to express the responsiveness of platelets.

Adenosine Diphosphate↗
PubMed1977

Sulindac.

Explore the source record for details and available documents.

Anti-Inflammatory Agents↗
PubMed1977

Abnormalities in platelet function and morphology in a case of thrombocythemia.

A patient with "life-long" bleeding problems and thrombocythemia had normal results on routine coagulation and fibrinolysis tests, but platelet function tests, including bleeding time, platelet adhesiveness, aggregation, and uptake and release of labeled serotonin were markedly altered. In addition, several types of ultrastructural abnormalities not reported previously were observed in some of the patient's platelets. The relationship between thrombocythemia, platelet dysfunction, and abnormal morphology is discussed.

Adenosine Diphosphate↗