Search PubMed⌕ Search

Biomedical subjects

E C Rossi

Publications and source records attributed to E C Rossi.

At least 55 records · Page 3Linked to original sources
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↗
PubMed1973

Inhibition of primary ADP-induced platelet aggregation in normal subjects after administration of nitrofurantoin (furadantin).

The evidence indicating that platelets may play a role in the occurrence of certain thromboembolic phenomena has stimulated a search for inhibitors of platelet function. This report presents data to indicate that nitrofurantoin is a potent inhibitor of primary ADP-induced platelet aggregation. The addition of 10 muM nitrofurantoin to citrated platelet-rich plasma obtained from 12 normal subjects produced a 29+/-6% (2 SD) inhibition of the velocity of platelet aggregation induced by 2 muM ADP. The inhibitory effect of nitrofurantoin demonstrated competitive kinetics in respect to ADP. The intravenous (180 mg) or oral (200 mg) administration of nitrofurantoin produced a serum nitrofurantoin concentration ranging from 2.7 to 23 muM in 28 normal subjects. Platelet-rich plasma obtained from these subjects demonstrated inhibition of the velocity of ADP-induced platelet aggregation that correlated with the log of the serum nitrofurantoin concentration (P < 0.001). Collagen-induced platelet aggregation was also inhibited in a dose-related manner, and the bleeding time was significantly prolonged in the two subjects with the highest serum nitrofurantoin concentration. These studies indicate that nitrofurantoin in vivo inhibits platelet function to a degree that is proportional to the serum nitrofurantoin concentration.

Adenosine Diphosphate↗