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J Villaro

Publications and source records attributed to J Villaro.

7 recordsLinked to original sources
PubMed1989

[Role of the contact plasma system in human physiopathology].

The possible implications of the plasma contact system in several human pathological conditions have been reviewed. The mechanism of activation and the biochemistry of the different components of this physiological system are described. The activation of the plasma contact system and its important physiological consequences are considered. The implication of the plasma contact system in the pathogenesis of different human and experimental pathological conditions (shock, disseminated intravascular coagulation, extracorporeal circulation...) is reviewed. A particular consideration is given to the pathogenesis of glomerulonephritis where the plasma contact system has been more directly implicated.

Factor XI↗
PubMed1988

Role of the plasma contact system in the pathogenesis of experimental anti-GBM glomerulonephritis.

To study the participation of the Hageman factor-related contact system of plasma in the pathogenesis of glomerulonephritis (GN), an anti-BM GN was induced in a group of 10 normal Brown Norway rats and another of seven Brown Norway BN/Mai Pfd f rats. The latter strain is characterized by a congenital deficiency of plasma prekallikrein and of high-molecular weight kininogen, with lengthening of the activated partial thromboplastin time. In the deficient group, one animal developed crescents in less than 25% of glomeruli, five in 25-50% and one in 50-75%. In the group of normal rats, extracapillary proliferation was of greater severity: one animal showed crescents in less than 25% of glomeruli, two in 50-75% and five in more than 75% of glomeruli. Although in both groups intense glomerular fibrin deposition was documented, the intensity of these deposits was less severe in the deficient animals. These data suggest, in the first place, that functional integrity of the contact system is not a necessary requirement for glomerular fibrinogenesis, other mechanisms being implicated in this phenomenon. On the other hand, this functional deficit has exerted a protective effect on crescent formation, which suggests that the contact system can play a role as a mediator of injury in glomerulonephritis, perhaps through the release of contact system-dependent mediators of inflammation.

Animals↗