Basic research of factors affecting the formation of granulation tissue in wound healing.

1.口服和腹腔注射吡拉西坦可促进大鼠创面愈合。结论：1.在切开创面和开放创面中，吡拉西坦均可提高创面破裂强度。S-1452；阻断血栓素A2，并未显示出对大鼠创面愈合的任何有利作用。这项研究的失败将归因于抗血小板作用。我们在大鼠身上检验了一个简单的实验模型，并研究了压疮的形成机制。我们设计了三种不同的缺血再灌流程序。在每种模型中，治疗部位的压力和总缺血时间相同。监测皮肤血流，未见一型反应性充血。实验一周后，在两种模式下，治疗部位均出现皮肤坏死。本实验表明，压疮的形成不仅取决于总压力，而且还取决于压力的模式。我们评价了瘢痕疙瘩植入裸鼠和在兔耳形成增生性瘢痕的效果。植入的瘢痕疙瘩迅速消失。烧灼创缘后兔耳创面明显增厚。因此上皮化的延迟在瘢痕疙瘩的形成中起着关键作用。对同一患者的增生性瘢痕组织和部位匹配的对照组的表皮增殖和分化标志物的表达进行了免疫组织学检测。与对照组相比，全增生性瘢痕的表皮明显增厚。Ki-67抗原染色显示14例中12例增生性瘢痕基底细胞增多。在增生性瘢痕和对照组中，分化标记物的表达没有差异。我们的结果提出了这样的可能性，即增生性瘢痕中的棘皮病是一种特征，这与组织扩张和许多情况下表皮覆盖增生性真皮肿瘤是相同的。

1. Intraperitoneal and oral administration of Piracetam accelerated wound healing in rats. In both incisional wounds and open wounds, piracetam raised wound breaking strength.2. S- 1452 ; thromboxane A2 blockade, did not show any beneficial effects of rat wound healing. The failure of this study would be attributed to the antiplatelet actions.3. We examined a simple experimental model in the rat and investigated the mechanism of formation of pressure ulcers. We planned three patterns of ischemia-reperfusion procedure. In each pattern the pressure of the treated site and total time of ischemia was same. Monitoring the skin blood flow, reactive hyperemia was not seen in one pattern. One week after experiment, in two patterns, skin necrosis of the treated sites were recognized. By this experiment, it is suggested that the formation of pressure ulcers is not dependent upon only the total pressure but also the patterns of pressure.4. We estimated the efficacy of keloid implantation to nude mouse and creating hypertrophic scar in the rabbit ears. The implanted keloid disappeared rapidly. The rabbit ear wound were got hypertrophic with cauterized the wound margin. So the delay of epithelization has the key role for keloid formation.5. The expression of markers of epidermal proliferation and differentiation was assessed immunohistologically in hypertrophic scar tissue and site-matched controls from the same patients. The epidermis appeared thicker in all-hypertrophic scars when comparing with controls. Staining for Ki-67 antigen revealed an increase in hypertrophic scar basal cells in twelve cases out of fourteen cases. No difference in the expression of differentiation markers was observed between hypertrophic scars and controls.Our results raise the" possibility that acanthosis in hypertrophic scar represents a feature, which is shared with tissue expansion and, a number of conditions with the epidermis covering proliferative dermal tumors.