Onabanjo A O
Eur J Appl Physiol Occup Physiol. 1978 Apr 15;38(3):207-13. doi: 10.1007/BF00430079.
In five subjects whose hands were exposed to heat, no depletion in the plasma kininogen level was observed when vasodilatation occurred. This might be due to the admixture of arterial and venous blood following the opening of arterio-venous (A--V) anastomoses. The small rise obtained by warming was not significant (P greater than 0.1). Consequently, the drop in kinonogen concentration recorded when the hand was allowed to cool to an ambient temperature of 23 degrees C as compared with the basal level and that during the period of warming, was also found to be non-significant. In another nine subjects whose A--V kininogen values were determined when their hands were immersed in a water bath at 37 degrees C, a significant A--V difference of the kininogen content was obtained. From this work, it is concluded that no appreciable depletion of venous kininogen concentration was obtained on hand warming. It is possible that sweat glands, vasodilator nerve fibres and the release of kinins contribute in part to the dilatation that occurs. Possible patho-physiological mechanisms involved are discussed.
在五名手部受热的受试者中,当出现血管舒张时,未观察到血浆激肽原水平的降低。这可能是由于动静脉(A-V)吻合开放后动脉血与静脉血混合所致。受热引起的小幅升高并不显著(P>0.1)。因此,与基础水平以及受热期间相比,当手部冷却至23摄氏度的环境温度时记录到的激肽原浓度下降也不显著。在另外九名受试者中,当他们的手浸入37摄氏度的水浴中时测定了A-V激肽原值,结果发现激肽原含量存在显著的A-V差异。从这项研究得出结论,手部受热时静脉激肽原浓度没有明显降低。汗腺、血管舒张神经纤维和激肽的释放可能部分促成了所发生的血管舒张。文中讨论了可能涉及的病理生理机制。