Bekemeier H, Hirschelmann R
Agents Actions. 1986 Jan;17(3-4):363-5. doi: 10.1007/BF01982647.
Vasodepression was found ex vivo in the isolated perfused hind legs of rats, mice and guinea-pigs with paw inflammation using maximum pressure amplitude, EAm, pD2-value and intrinsic sensitivity (i.s.) as the test parameters of dose-response curves of vasopressor substances (noradrenaline, lys- and arg-vasopressin, angiotensin II, substance P, Na2-ATP). Vasodepression is strong in the anaphylactic and dextran paw edema, moderate in the carrageenin paw edema and adjuvant arthritis, but weak in the pertussis vaccine and kaolin paw edema. It is partly long-lasting, does not closely correlate with edema strength and can also be shown in the contralateral non-inflamed leg. Thus, a vasoreactivity depressing factor(s) must be liberated from the site of inflammation and reach the general circulation. Here, the method is described using the adjuvant arthritis as an example.
在大鼠、小鼠和豚鼠患有爪部炎症的离体灌注后肢中发现血管抑制现象,使用最大压力幅度、EAm、pD2值和内在敏感性(i.s.)作为血管升压物质(去甲肾上腺素、赖氨酸和精氨酸血管加压素、血管紧张素II、P物质、Na2-ATP)剂量反应曲线的测试参数。血管抑制在过敏性和右旋糖酐爪部水肿中较强,在角叉菜胶爪部水肿和佐剂性关节炎中中等,但在百日咳疫苗和高岭土爪部水肿中较弱。它部分是持久的,与水肿强度没有密切相关性,并且也可以在对侧未发炎的腿部显示出来。因此,一种血管反应性抑制因子必须从炎症部位释放出来并进入体循环。在此,以佐剂性关节炎为例描述该方法。