大剂量抑制环加氧酶,增加TXA2生成,抗血小板聚集及抗血栓形成

小剂量激活环加氧酶,增加PGI2生成,抗血小板聚集及抗血栓形成

小剂量抑制环加氧酶,减少TXA2生成,抗血小板聚集及抗血栓形成

小剂量抑制环加氧酶,减少PGI2生成,抗血小板聚集及抗血栓形成

大剂量抑制环加氧酶,减少TXA2生成,抗血小板聚集及抗血栓形成

视神经萎缩

阿托品中毒

休克、深昏迷

有机磷中毒

大剂量抑制环加氧酶,增加TXA2生成,抗血小板聚集及抗血栓形成

小剂量激活环加氧酶,减少PGI2生成,抗血小板聚集及抗血栓形成

小剂量抑制环加氧酶,减少TXA2生成,抗血小板聚集及抗血栓形成

大剂量激活环加氧酶,增加PGI2生成,抗血小板聚集及抗血栓形成

大剂量抑制环加氧酶,减少TXA2生成,抗血小板聚集及抗血栓形成

低钾血症

高钠血症

高钾血症

消化功能紊乱

中毒性肠麻痹

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Microtubules and motor proteins play an important part in positioning organelles within a eukaryotic cell. In most animal cells, for example, the tubules of the endoplasmic reticulum (ER) reach almost to the edge of the cell, whereas the Golgi apparatus is located in the cell interior, near the centrosome. The ER extends out from its points of connection with the nuclear envelope along microtubules, which reach from the centrally located centrosome out to the plasma membrane.

As a cell grows, kinesins attached to the outside of the ER membrane (via adaptor proteins) pull the ER outward along microtubules, stretching it like a net. Cytoplasmic dyneins attached to the Golgi membranes pull the Golgi apparatus along microtubules in the opposite direction, inward toward the nucleus. In this way, the regional differences in these internal membranes—crucial for their respective functions—are created and maintained.

When cells are treated with colchicine—a drug that promotes microtubule disassembly—both the ER and the Golgi apparatus change their location dramatically. The ER, which is physically connected to the nuclear envelope, collapses around the nucleus; the Golgi apparatus, which is not attached to any other organelle, fragments into small vesicles, which then disperse throughout the cytoplasm.

When the colchicine is removed, the organelles return to their original positions, dragged by motor proteins moving along the re-formed microtubules.