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Biomedical subjects

E C Rossi

Publications and source records attributed to E C Rossi.

16 recordsLinked to original sources
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↗
PubMed1976

Inhibition of platelet aggregation by 5-nitro-2-furaldehyde diacetate with observations on structure-activity relationships.

Nitrofurantoin [1-(5'-nitro-2'-furfurylideneamino)-2, 4-diketoimidazole] is a potent inhibitor of primary ADP-induced platelet aggregation. The nitro group on the furan ring and the specific arrangement of the two keto groups on the imidazole ring are the molecular characteristics of nitrofurantoin critical to its inhibitory effect. The present studies report that 5-nitro-2-furaldehyde diacetate is also a potent inhibitor of primary ADP-induced platelet aggregation. 5-Nitro-2-furaldehyde diproprionate, 5-nitro-2-furaldehyde dibutyrate, and 5-nitro-2-furfuryl acetate are essentially inactive. These results indicate that a diacetate moiety can replace the diketoimidazole moiety of nitrofurantoin and form a compound that fully retains the inhibitory effect upon primary ADP-induced platelet aggregation.

Adenosine Diphosphate↗
PubMed1975

A time-dependent increase in the responsiveness of platelet-rich plasma to epinephrine.

The variable responsiveness of platelet-rich plasma (PRP) to epinephrine and collagen was studied. These studies revealed that as PRP is allowed to stand at room temperature it becomes progressively more responsive to the aggregating effects of epinephrine and collagen. Samples of PRP obtained from 10 normal subjects showed only 8 plus or minus 8 per cent aggregation when tested after 5 minutes with "near threshold" concentrations of epinephrine. After 45 minutes the addition of the same concentrations of epinephrine to portions taken from the same samples of PRP yielded 72 plus or minus 12 per cent aggregation. Although similar results were obtained with "near threshold" concentrations of collagen, the variability of responsiveness to collagen could be easily overcome by increasing the collagen concentration. Such was not the case with epinephrine, and, a time-dependent acquisition of responsiveness was demonstrable over a broad range of epinephrine concentration. These findings suggest that variations in the amount of platelet aggregation observed with epinephrine may be a reflection of differences in the time factor involved in testing. This time factor should be taken into account before epinephrine-induced platelet aggregation curves are compared and defined as "normal" or "abnormal".

Blood↗
PubMed1975

Some factors affecting fibrinogen precipitation by ristocetin: ultrastructure of precipitates.

Fibrinogen in aqueous solution is precipitated by the antibiotic ristocetin. This reaction is inhibited by albumin and facilitated by low temperature. Resolubilized fibrinogen clots in the presence of thrombin. Ristocetin-precipitated fibrinogen takes the form of fibrils or clumps, composed of irregularly spaced, structure-less particles. The addition of ristocetin to washed platelets suspended in fibrinogen-containing media produces fibrinogen clumps in both the media and in the surface cannalicular system of the platelets. The changes in light transmission (aggregation curves) are due to both platelet aggregation and fibrinogen clumping. The role of the latter is confirmed by the observation that the addition of ristocetin to inert latex particles suspended in fibrinogen solution produces typical aggregation curves. This phenomenon is prevented by the addition of albumin to the media. We conclude that (1) if fibrinogen is present in any artificial system, albumin should be included in the media to prevent fibrinogen precipitation; and (2) statements about aggregation of any particulated materials by ristocetin should not be based solely on light-transmission changes, but should also include a description of the morphologic appearance.

Blood Platelets↗