The kallikrein-kinin system as mediator in vasogenic brain edema. Part 2: Studies on kinin formation in focal and perifocal brain tissue - PubMed (original) (raw)

The kallikrein-kinin system as mediator in vasogenic brain edema. Part 2: Studies on kinin formation in focal and perifocal brain tissue

K Maier-Hauff et al. J Neurosurg. 1984 Jul.

Abstract

Vasogenic edema was induced in mongrel cats by cold injury to study uptake and activation of the plasma-kallikrein-kinin system in central nervous system (CNS) tissue. A method was developed for quantitative assessment of kinin formation in affected brain tissue areas. Gross disruption of the blood-brain barrier by focal trauma causes marked penetration of plasma kininogens into necrotic and edematous brain tissue. Moreover, the kallikrein-kinin (KK) system was activated in both necrotic and perifocal edematous areas, and was markedly enhanced by additional cerebral ischemia. Formation of kinins in necrotic brain tissue led to consumption of approximately 60% to 80% of the amount of kininogens being taken up. In perifocal edematous tissue, formation of kinins was less pronounced, or even absent. However, if cerebral ischemia evolved after severe intracranial hypertension, kinins were also formed in the perifocal edematous brain. The intravascular origin of kininogens found in pathological tissue areas secondary to injury was deduced from the observation that cerebral tissue of the contralateral hemisphere with an intact blood-brain barrier had no measurable quantities of kininogens. Consumption of plasma kininogens or formation of kinins were assessed as the difference of the total amount of plasma kininogens taken up into the tissue minus the amount of kininogens found in the brain at postmortem examination. The data indicate that uptake and activation of the plasma-KK system might occur under all pathological conditions in which blood-brain barrier damage permits cerebral penetration of plasma proteins, such as with cerebral contusion, focal ischemia, and tumors. The potent pathophysiological mechanisms induced by kinins in CNS tissue, such as formation of brain edema, microcirculatory dysfunction, and enhancement of blood-brain barrier permeability, together with their formation in focal and perifocal pathological brain tissue, provide further support for a mediator function of the KK system. Methods that specifically interfere with the formation of kinins in damaged brain should therefore be expected to attenuate vasogenic edema.

PubMed Disclaimer

Cited by

The role of bradykinin in the etiology of vasogenic brain edema and perilesional brain dysfunction.
Whittle IR, Piper IR, Miller JD. Whittle IR, et al. Acta Neurochir (Wien). 1992;115(1-2):53-9. doi: 10.1007/BF01400591. Acta Neurochir (Wien). 1992. PMID: 1595396
Transient Receptor Potential Vanilloid in the Brain Gliovascular Unit: Prospective Targets in Therapy.
Luo H, Declèves X, Cisternino S. Luo H, et al. Pharmaceutics. 2021 Mar 4;13(3):334. doi: 10.3390/pharmaceutics13030334. Pharmaceutics. 2021. PMID: 33806707 Free PMC article. Review.
TRPV1 activation results in disruption of the blood-brain barrier in the rat.
Hu DE, Easton AS, Fraser PA. Hu DE, et al. Br J Pharmacol. 2005 Oct;146(4):576-84. doi: 10.1038/sj.bjp.0706350. Br J Pharmacol. 2005. PMID: 16056236 Free PMC article.
Immunolocalization of plasma kallikrein in human brain.
Cerf ME, Raidoo DM. Cerf ME, et al. Metab Brain Dis. 2000 Dec;15(4):315-23. doi: 10.1023/a:1011179426420. Metab Brain Dis. 2000. PMID: 11383556

The kallikrein-kinin system as mediator in vasogenic brain edema. Part 2: Studies on kinin formation in focal and perifocal brain tissue - PubMed (original) (raw)