Sicuteri, F.; Fanciullacci, M.; Bavazzano, A.; Franchi, G.; del Bianco, P.L.
March 1970
Angiology;Mar1970, Vol. 21 Issue 3, p193
Academic Journal
Following subarachnoid hemorrhage, a plasmatic factor, capable of generating kinin in cerebrospinal fluid, becomes activated. This factor is activated by the mechanism of dilution of plasma (permeability factor dilute) with CSF. In cerebral hemorrhage, also, the activation of nervous tissue proteases probably involves the generation of kinins. Direct and indirect evidence, experimental and clinical pharmacology, of the activation of these two principal kinin-liberating factors (PF/dil and tissue proteases) is presented. Kinins, because of their potent triple action on capillaries, on pain receptors and on nerve function, may be involved in the pathogenesis of various symptoms of intracranial hemorrhage. A kallikrein inhibitor antagonizes both the PF/dil factor and kinin-liberating protease; pretreatment with this inhibitor protects animals from experimental cerebral hemorrhage. When administered early and in large doses in cerebral apoplexy and in subarachnoid hemorrhage, the kallikrein inhibitor exhibits therapeutic actions which, in comparison to conventional therapy, may be considered encouraging.


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