Wester J, Sixma J J, Geuze J J, van der Veen J
Lab Invest. 1978 Sep;39(3):298-311.
The in vivo formation of hemostatic plugs was studied in humans in skin wounds made using the template bleeding procedure of Mielke (34). The wounds were excised by punch biopsy 10 seconds, 30 seconds, 2 minutes, and 3 minutes after they were made. The wounds were V-shaped and approximately 0.4 mm. deep. Within 30 seconds small hemostatic plugs were observed at the end of transected vessels. The plugs grew in size in the subsequent minutes and became impermeable. The platelets degranulated and formed pseudopods which became strongly interdigitated. The platelets at the periphery of the plugs showed discontinuities of the membranes. Cytoplasmic matrix and cell organelles had disappeared in many of these peripheral cells. Small fibrin fibers were already found at 30 seconds, mostly along the margins of the wounds and also at the periphery of the hemostatic plugs. Fibrin was absent from the center of the plugs and from the lumen of transected vessels. When part of a plug was extending into the vessel lumen, the platelets inside the vessel were less degranulated and less interdigitated than the rest of the plug. The effect of acetysalicylic acid (ASA) was studied in wounds before and 2.5 hours after ingestion of 2 gm. of ASA. Wounds were excised by punch biopsy 3 or 10 minutes after they had been made. Platelets in ASA were less degranulated, had fewer pseudopods, and showed less interdigitation than platelets in control plugs. Ballooning and fibrin deposition were similar in control and ASA plugs. Pronounced differences between control and ASA plugs were observed in a subject who exhibited a considerably prolonged bleeding time after ASA. The ASA plugs were very large; many plugs had fused and in addition numerous small platelet clumps, most likely fragments from the plugs, were found in the superficial scab of the wound. It is postulated that ASA plugs are less stable due to decreased interdigitation. This allows more disruption of the plugs and rebleeding. Consequently, more platelets are needed and longer time is required for hemostasis to occur.
利用米尔克(34)的模板出血程序在人体皮肤伤口中研究了体内止血栓的形成。伤口在形成后10秒、30秒、2分钟和3分钟通过打孔活检切除。伤口呈V形,深度约0.4毫米。在30秒内,在横断血管末端观察到小的止血栓。这些栓子在随后的几分钟内体积增大并变得不透水。血小板脱颗粒并形成伪足,伪足相互强烈交错。栓子周边的血小板显示出膜的连续性中断。许多这些周边细胞的细胞质基质和细胞器已经消失。在30秒时已经发现小的纤维蛋白纤维,主要沿着伤口边缘以及止血栓的周边。栓子中心和横断血管腔内没有纤维蛋白。当栓子的一部分延伸到血管腔内时,血管内的血小板比栓子的其余部分脱颗粒少且交错少。研究了在摄入2克乙酰水杨酸(ASA)之前和之后2.5小时,伤口中ASA的作用。伤口在形成后3或10分钟通过打孔活检切除。与对照栓子中的血小板相比,ASA中的血小板脱颗粒少,伪足少,交错也少。对照栓子和ASA栓子中的气球样变和纤维蛋白沉积相似。在一名服用ASA后出血时间明显延长的受试者中,观察到对照栓子和ASA栓子之间有明显差异。ASA栓子非常大;许多栓子融合在一起,此外,在伤口的浅表痂皮中发现了许多小的血小板团块,很可能是栓子的碎片。据推测,由于交错减少,ASA栓子不太稳定。这使得栓子更容易破裂和再出血。因此,需要更多的血小板,并且止血需要更长的时间。