Sharma J N, Zeitlin I J, Mackenzie J F, Russell R I
Department of Physiology and Pharmacology, University of Strathclyde, Glasgow, Scotland.
Fundam Clin Pharmacol. 1988;2(5):399-403. doi: 10.1111/j.1472-8206.1988.tb01005.x.
Plasma kinin-precursor (kininogen) concentrations were measured in the peripheral venous blood of 7 untreated patients with inflammatory bowel diseases, 12 healthy subjects, and 5 uncomplicated fracture cases. The mean plasma kininogen levels were significantly raised (P less than 0.025) in patients with intestinal inflammation (7.0 +/- 1.0 micrograms BK Eq/ml), as compared with the value found in healthy subjects (5.7 +/- 0.7 micrograms BK Eq/ml), and in fracture cases (5.0 +/- 1.2 micrograms BK Eq/ml). The packed cell volume did not differ (P greater than 0.05) between patients and control groups. Thus, the raised plasma kininogen levels observed in patients were not the result of nonspecific changes in plasma volume. It is suggested that raised plasma kininogen might be due to increased synthesis to provide substrate for excessive kinin-formation, to a potent inflammatory agent, or to high synthesis of acute-phase reactants. The possible significance of this observation is discussed.
在7例未经治疗的炎症性肠病患者、12名健康受试者和5例无并发症骨折患者的外周静脉血中检测了血浆激肽前体(激肽原)浓度。与健康受试者(5.7±0.7微克BK当量/毫升)和骨折患者(5.0±1.2微克BK当量/毫升)相比,肠道炎症患者的平均血浆激肽原水平显著升高(P<0.025)(7.0±1.0微克BK当量/毫升)。患者与对照组之间的红细胞压积无差异(P>0.05)。因此,患者中观察到的血浆激肽原水平升高并非血浆容量非特异性变化的结果。提示血浆激肽原升高可能是由于合成增加以提供过量激肽形成的底物、一种强效炎症介质或急性期反应物的高合成所致。讨论了这一观察结果的可能意义。