KININOGEN CONSUMPTION IN CEREBRAL-CIRCULATION OF HUMANS DURING BRAIN ISCHEMIA AND POSTISCHEMIC REPERFUSION

1. Total kininogen, high molecular weight kininogen and low molecular weight kininogen were quantitated as bradykinin equivalents in the blo od flowing to and from the brain in patients with stenotic and occlusi ve carotid damage in the course of neurosurgical treatment. Although c onsiderable improvement in blood supply of ischemic brain areas was es tablished after surgery in all patients, improvement in postoperative neurological status was seen only in four patients (group I), while in six cases there were no or negative neurological changes (group II). 2. The biochemical study confirmed the principal difference between th ese two groups: 1) prior to surgery in the patients of group II, but n ot of group I, total kininogen in blood flowing from the brain was mar kedly lowered compared to its arterial level, the latter being close t o normal; the decrease was due only to low molecular weight kininogen. 2) After surgery, cerebral venous total kininogen levels were signifi cantly lowered in patients of both groups; however, for patients of gr oup II, these changes were more pronounced and they showed a decrease in both high and low molecular weight kininogen. 3. The major involvem ent of low molecular weight kininogen implicates tissue kallikrein in this process. The reduction of kininogen indicates that kinin formatio n occurred in the cerebral intravascular space during brain ischemia a nd following brain reperfusion and was most likely associated with the well-known actions of kinin on cerebral vessels, i.e., vasodilatation and brain edema.