Effect of thermal injury on the kinin system in rabbit hind limb lymph

Abstract

Summary The kinin‐forming activity of hind limb lymph and of plasma has been examined in rabbits before and after thermal injury. Neither plasma nor lymph contained much active kallikrein activity but the enzyme was evident in samples treated with glass or with acid. There was little or no increase in the activity of enzyme activated by glass after thermal injury, but an increase in the activity of enzyme activated by acid regularly occurred. There were two increases in the activity of enzyme activated by acid—one about 2 h and the other 4–6 h after thermal injury. They corresponded to increases in vascular permeability as indicated by increases in the concentration of lymph protein. There was considerably more kininogen in the lymph and plasma than was used in the assays of kallikrein activity, showing that the increased kinin‐forming activity in lymph was not the result of the passage of kininogen from the plasma. The increase in activity in lymph was not usually accompanied by a similar increase in the plasma. However, an increase in the activity of enzyme activated by acid sometimes occurred in the plasma simply as a result of prolonged anaesthesia. It is suggested that whereas the enzyme activated by glass is a measure of prekallikrein, the acid activatable enzyme appears as a result of the dissociation of a kallikrein‐inhibitor complex. An increase in the concentration of this complex is therefore an indication of the preceding activation of kallikrein.

The effect of anti‐inflammatory agents on the changes in local lymph after thermal injury

“…Although no effect was observed when the drugs were infused immediately after the injury, when they were infused 90 min after burning, the lymph protein was significantly reduced. Since Lewis & Wawretschek (1971) using the same technique showed that there were two phases of increase in lymph protein it is possible that it is this second phase, which corresponds to a second phase of increased vascular permeability (Sevitt, 1958;Burke & Miles, 1958) which was inhibited by the antiinflammatory agents. The fact that neither hydrocortisone nor indomethacin affected the increase in lymph /3-glucuronidase activity is consistent with this view, since it has been shown (Lewis, 1969) that /3-glucuronidase leaks into the lymph after injury not from the injured cells but from the plasma as a result of the initial increase in vascular permneability.…”

Effect of external lymph drainage and of coumarin treatment on thermal injury in the rat hind leg

“…According to Lewis & Wawratschek (1971), there is, after thermal injury, a pronounced increase in the lymph of an inactive form of kallikrein which can be activated by acid treatment (but not by contact with a glass surface). According to these authors, increase in vascular permeability leads to the passage of prekallikrein from the plasma into the interstitial space of the injured area.…”