{"doi":"10.1055/s-0039-1689450","title":"Rabbit Subendothelium - Human Platelet Interaction, a New Tool for Pathogenesis of Long Bleeding Time","abstract":"<jats:p>Interaction of human platelets with previously denuded rabbit aorta provides a new tool for the estimation of platelet function in inherited and acquired platelet disorders. The interaction with the sub endothelium was estimated morphometrically by the Baumgartner technique.</jats:p><jats:p>It is already known that in the Bernard-Soulier syndrome, adhesion-aggregation to purified collagen and platelet aggregation in the presence of all the inducers acting through ADP are normal. In contrast bovine factor VIII and ristocetin do not aggregate the Bernard-Soulier platelets which adhere to subendothelium at only approximately 10 percent of the normal range.</jats:p><jats:p>In thrombasthenia, adhesion to collagen is normal but primary or secondary ADP-induced aggregation is absent. Adhesion to rabbit subendothelium is reduced by 50 percent but always a monolayer of cells was seen.</jats:p><jats:p>In a 65 year old patient who has an acquired haemorrhagic disorder with a long bleeding time and a normal platelet count her isolated platelets do not respond to ristocetin while they aggregate normally with collagen and ADP. Adhesion of her platelets to subendothelium is reduced by 50 per cent.</jats:p><jats:p>It is therefore postulated that rabbit subendothelium-human platelet interaction provides a method for a better understanding of pathogenesis of long bleeding time.</jats:p>","journal":"Thrombosis and Haemostasis","year":1975,"id":663296,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":0,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1731719,"name":"E. Bodevin","orcid":null,"position":1,"is_corresponding":false},{"id":1731721,"name":"J. P. Caen","orcid":null,"position":2,"is_corresponding":false},{"id":1731717,"name":"H. Michel","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"Rabbit Subendothelium - Human Platelet Interaction, a New Tool for Pathogenesis of Long Bleeding Time","abstract":"<jats:p>Interaction of human platelets with previously denuded rabbit aorta provides a new tool for the estimation of platelet function in inherited and acquired platelet disorders. The interaction with the sub endothelium was estimated morphometrically by the Baumgartner technique.</jats:p><jats:p>It is already known that in the Bernard-Soulier syndrome, adhesion-aggregation to purified collagen and platelet aggregation in the presence of all the inducers acting through ADP are normal. In contrast bovine factor VIII and ristocetin do not aggregate the Bernard-Soulier platelets which adhere to subendothelium at only approximately 10 percent of the normal range.</jats:p><jats:p>In thrombasthenia, adhesion to collagen is normal but primary or secondary ADP-induced aggregation is absent. Adhesion to rabbit subendothelium is reduced by 50 percent but always a monolayer of cells was seen.</jats:p><jats:p>In a 65 year old patient who has an acquired haemorrhagic disorder with a long bleeding time and a normal platelet count her isolated platelets do not respond to ristocetin while they aggregate normally with collagen and ADP. Adhesion of her platelets to subendothelium is reduced by 50 per cent.</jats:p><jats:p>It is therefore postulated that rabbit subendothelium-human platelet interaction provides a method for a better understanding of pathogenesis of long bleeding time.</jats:p>","is_dataset_classified":null,"base_score":0.0,"endowment":0.0,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"19162232","pmcid":null,"openalex_id":"https://openalex.org/W2992184344","authors":[],"funders":[],"total_grants":0,"fwci":0.0,"citation_percentile":0.15972222,"influential_citations":0,"citation_trend":[],"oa_status":"closed","license":null,"oa_locations":[{"url":"http://www.thieme-connect.de/products/ejournals/pdf/10.1055/s-0039-1689450.pdf","host_type":"publisher"},{"url":"https://doi.org/10.1055/s-0039-1689450","host_type":"journal"}],"fields_of_study":["Platelet Disorders and Treatments","Blood properties and coagulation","Antiplatelet Therapy and Cardiovascular Diseases"],"mesh_terms":[],"keywords":["Platelet","Ristocetin","Bernard–Soulier syndrome","Adhesion","Thrombasthenia","Chemistry","Platelet adhesion","Clot retraction","Pathogenesis","Bleeding time","Platelet aggregation","Immunology","Medicine"],"sdg_mappings":[],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-08-12T21:01:17.192006Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}