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Thromb Haemost 1977; 38(04): 0971-0983
DOI: 10.1055/s-0038-1651915
Original Article
Schattauer GmbH

Adenylate Cyclase and Phosphodiesterase Activity in the Platelet Release Abnormality

Carolyn Mci. Chesney   *
1   Hematology Research Laboratory, Department of Medicine, Massachusetts General Hospital and Harvard Medical School and the Pathology Department, Rhode Island Hospital, and Brown University Medical School
,
Ann S. Baker
1   Hematology Research Laboratory, Department of Medicine, Massachusetts General Hospital and Harvard Medical School and the Pathology Department, Rhode Island Hospital, and Brown University Medical School
,
Angelina Ca. Carvalho
1   Hematology Research Laboratory, Department of Medicine, Massachusetts General Hospital and Harvard Medical School and the Pathology Department, Rhode Island Hospital, and Brown University Medical School
,
Asli Ozer   **
1   Hematology Research Laboratory, Department of Medicine, Massachusetts General Hospital and Harvard Medical School and the Pathology Department, Rhode Island Hospital, and Brown University Medical School
,
George F. Meissner
1   Hematology Research Laboratory, Department of Medicine, Massachusetts General Hospital and Harvard Medical School and the Pathology Department, Rhode Island Hospital, and Brown University Medical School
,
Robert W. Colman   ***
1   Hematology Research Laboratory, Department of Medicine, Massachusetts General Hospital and Harvard Medical School and the Pathology Department, Rhode Island Hospital, and Brown University Medical School
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Publikationsdatum:
04. Juli 2018 (online)

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Summary

11 patients with histories of clinical bleeding were selected as examples of platelet release abnormality. Mean bleeding time was 18 ± 2.6 min (normal ±SEM; 6 ±0.44); mean platelet adhesiveness was 9.9 ± 4.3% (normal ±SEM; 30 ±2.2). Clot retraction and platelet factor 3 were normal. Platelet aggregation with adenosine diphosphate (ADP), epinephrine and collagen was decreased, as was 14C-serotonin release. Electron microscopic studies of platelets exposed to epinephrine showed 2 subgroups: one which failed to aggregate or have centralization of organelles and a second which developed pseudopodia and centralization of organelles, but rarely aggregated or degranulated.

Measurements of activity of adenylate cyclase and phosphodiesterase under basal conditions were performed on platelets from patients and control subjects. Adenylate cyclase activity was significantly lower and phosphodiesterase activity significantly higher in the patient group. Prostaglandin E1 was a potent stimulator of adenylate cyclase in both groups, as was NaF. It was concluded that the causative defects in patients with “platelet release abnormality” do not reside in either the activity of adenylate cyclase or of phosphodiesterase. Changes in formation and destruction of cyclic adenosinemonophosphate (AMP) may instead be regarded as a compensatory response to a defect in another effector system.

* Present address: Hematology Division, University of Tennessee Center for the Health Sciences, Memphis, Tennessee 38163, U.S.A.


** Present address: Department of Pharmacology, Hacettepe University, Ankara, Turkey.


*** Present address: Coagulation Unit of the Hematology-Oncology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania 19104, U.S.A.