McDonald T P, Sullivan P S
Department of Animal Science, College of Veterinary Medicine, University of Tennessee, Knoxville.
Exp Hematol. 1993 Sep;21(10):1316-20.
Several recent studies show that production of platelets and red blood cells (RBC) are inversely related. For example, it is well established that hypoxia, a stimulator of erythropoiesis, causes thrombocytopenia in laboratory animals. The thrombocytopenia is most likely the result of a reduction in the production of platelets caused by a decrease in the number of colony-forming units-megakaryocyte (CFU-Meg), early precursor megakaryocytes (small acetylcholinesterase-positive cells, SAChE+), and recognizable megakaryocytes in the bone marrow. In all cases, active erythropoiesis was required for the thrombocytopenia. The hypoxia-induced thrombocytopenia was not caused by sequestration of platelets in an enlarged spleen or by expanding blood volumes. We speculate that this thrombocytopenia is caused by competition of a precursor cell of the erythrocytic and megakaryocytic cell lines; that is, marked stimulation of the erythroid cells by erythropoietin (Epo) causes a decrease in the number of immature megakaryocytes, leading to decreased thrombocytopoiesis. In support of this hypothesis, other recent work shows that thyroxine (a stimulator of erythropoiesis) and Epo (when given in large, chronic doses) elevate erythropoiesis and cause thrombocytopenia. Conversely, both endogenous and exogenous sources of thrombopoietin lead to elevated thrombocytopoiesis and anemia in mice. It should also be mentioned that megakaryocytes and erythrocytes have several biochemical similarities, and several clinical conditions point to an inverse relationship between RBC and platelet production. These in vivo, biochemical, and clinical data support the hypothesis that megakaryocytes and erythrocytes share a common precursor cell.
最近的几项研究表明,血小板和红细胞(RBC)的生成呈负相关。例如,众所周知,作为红细胞生成刺激因子的缺氧会导致实验动物出现血小板减少症。血小板减少症很可能是由于骨髓中集落形成单位-巨核细胞(CFU-Meg)、早期前体巨核细胞(小乙酰胆碱酯酶阳性细胞,SAChE+)和可识别的巨核细胞数量减少,导致血小板生成减少所致。在所有情况下,血小板减少症都需要活跃的红细胞生成。缺氧诱导的血小板减少症不是由血小板在肿大脾脏中的滞留或血容量增加引起的。我们推测这种血小板减少症是由红细胞系和巨核细胞系的前体细胞竞争所致;也就是说,促红细胞生成素(Epo)对红系细胞的显著刺激导致未成熟巨核细胞数量减少,从而导致血小板生成减少。支持这一假设的是,最近的其他研究表明,甲状腺素(一种红细胞生成刺激因子)和Epo(大剂量长期给药时)会提高红细胞生成并导致血小板减少症。相反,血小板生成素的内源性和外源性来源都会导致小鼠血小板生成增加和贫血。还应该提到的是,巨核细胞和红细胞在生化方面有几个相似之处,并且一些临床情况表明红细胞和血小板生成之间存在负相关。这些体内、生化和临床数据支持巨核细胞和红细胞共享一个共同前体细胞的假设。