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RESPONSE OF PULMONARY (CIRCULATING) MEGAKARYOCYTES TO EXPERIMENTALLY INDUCED CONSUMPTION COAGULOPATHY IN RABBITS
Author(s) -
HANSEN KNUD BENDIX,
AABO KRISTIAN,
MYHREJENSEN OLAF
Publication year - 1979
Publication title -
acta pathologica microbiologica scandinavica section a pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0365-4184
DOI - 10.1111/j.1699-0463.1979.tb00038.x
Subject(s) - megakaryocytopoiesis , platelet , medicine , megakaryocyte , saline , thrombopoiesis , thromboplastin , partial thromboplastin time , bone marrow , fibrinolysis , coagulation , cardiology , haematopoiesis , immunology , endocrinology , biology , stem cell , genetics
The effects of slow temporary infusion of a tissue thromboplastin solution into the superior vena cava on pulmonary as well as circulating megakaryocytes were studied in 40 rabbits (2–48 hours after infusion) and related to 6 noninfused and 7 infused with normal saline. This is a simple and specific method of inducing a fall in blood platelet levels and thereby an activation of thrombocytopoiesis and megakaryocytopoiesis. The induced intravascular coagulation is probably counterbalanced by an activated fibrinolysis allowing the animals to survive the infusion and thereby offering the possibility of studying the long‐term effects. An increase to about 300% of the normal values in circulating as well as pulmonary megakaryocytes was found 20 and 24 hours after the onset of the infusions respectively. The number of circulating and pulmonary megakaryocytes, showing great individual variations, however, dropped to normal levels within 28 hours after onset of the infusions, which means that megakaryocytes remain detectable for less than eight hours in the lungs. No increase was found in pulmonary megakaryocytes in the control (saline infused) group. In our opinion the entrance of megakaryocytes from the bone marrow into the blood circulation is an incidental event, the number in the circulation reflecting the activity of megakaryocytopoiesis. This experiment supports our suggestion that intravascular coagulation is one of the major pathophysiological mechanisms leading to an increase in pulmonary megakaryocytes.