Platelet-Count Differences in Blood of the Rabbit Right and Left Heart Ventricles

The lungs and platelet production

“…If substantial thrombopoietic activity occurred in the lungs, a higher steady state PLT would be expected in radial arterial than in pulmonary arterial blood, resulting from pooling of pulmonary and systemic platelet production. This has been reported in cats, rabbits and rats by a number of authors (Howell & Donahue, 1937; Sharnoff & Scardino, 1960; Tinggaard Pedersen, 1974). While similar results have been reported in humans (Howell & Donahue, 1937; Bierman, 1955), these studies employed unphysiological experimental models (Jordan, 1940), imprecise counting methods, and, in some cases, unreliable statistical analyses.…”

“…Howell and Donahue (1937) reported a higher platelet count in blood leaving the lungs than in blood entering them and suggested that megakaryocytes concentrated in the lungs contribute actively to platelet production. This view, supported by Bierman (1955), Sharnoff and Scardino (1960) and Tinggaard Pedersen (1974), was challenged by Jordan (1940) and by Fidlar and Waters (1941).…”

Platelets in Lung Biology

“…A central observation is that platelet numbers are higher in the pulmonary veins and systemic arterial vessels than in the pulmonary artery in experimental animals and in humans. Comparison of platelet counts in venous versus arterial blood, the right versus left ventricles, and the inferior vena cava versus the aorta in cats, dogs, rabbits, and rats yielded platelet numbers that were higher on the left side than on the right side of the lungs in most determinations (27, 29, 46, 47). In one of these reports, retrograde perfusion of the lungs resulted in the recovery of large numbers of megakaryocytes with degenerative nuclear changes in the effluent, suggesting that platelets are released from intrapulmonary megakaryocytes (29).…”

The regulation of proplatelet production

“…In contrast, only three studies have been reported from the United States and Canada and they have all reported lower frequencies of both H. pylori infection and platelet count response rates following eradication treatment. [7][8][9] These data suggest that H. pylori infection may be merely an incidental observation, not excluding the diagnosis of ITP and not clinically important for management. In between these alternative interpretations are studies reporting partial platelet count responses, suggesting that H. pylori infection may contribute to the thrombocytopenia in ITP but is not the sole cause.…”

“…1 Alternatively, Sharnoff and colleagues suggested that megakaryocytes travel through the circulation to the lungs where they are physically fragmented into platelets within pulmonary capillaries. 7 In the former model, it is hypothesized that the role of the DMS is as a store of membrane to support proplatelet formation, whereas in the latter the DMS defines pre-formed platelet territories.…”