Effect of brinase (protease I from aspergillus oryzae) on the elimination of fibrin from the lungs and pulmonary damage in rats with induced intravascular coagulation and inhibited fibrinolysis

Diffang, Charles; Saldeen, Tom

doi:10.1016/0049-3848(76)90108-0

Cited by 9 publications

(3 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…After blocking of the fibrinolytic system with AMCA, however, fibrin depositions were re corded, and simultaneously a more pro nounced decrease in fibrinogen levels oc curred, as well as a further increase in the incidence of positive EGT. After infusion of ancrod to rabbits similar observations have been reported [20], AMCA is not an inhibitor of brinase and it does not interfere with the degrading effect of brinase on fibrinogen/fibrin [7], The sub stance may, however, influence the fate of the partially degraded fibrinogen, i.e. the inhibi tion of fibrinolytic activity after administra tion of AMCA may counteract the dissolu tion of fibrinogen/fibrin aggregates.…”

Section: Discussionsupporting

confidence: 63%

See 1 more Smart Citation

Influence of Brinase on Fibrinogen: Fibrin Transition in in vitro and in vivo Studies

Saldéen¹,

Frisch²

1982

Pathophysiol Haemos Thromb

View full text Add to dashboard Cite

The influence of brinase on fibrinogen levels, ethanol gelation test (EGT), fibrin content of lungs and kidneys (125I-fibrinogen) and brinase inhibitor capacity was investigated in the rat. The animals were either treated with i.v. infusions of brinase (4 mg/kg), tranexamic acid (AMCA) + brinase or heparin + AMCA + brinase. A control group was given i.v. saline, a reference group AMCA + thrombin. Brinase caused a decrease in fibrinogen levels and an increase in the incidence of positive EGT, deposition of fibrin was not observed. Infusion of brinase into rats with inhibited fibrinolytic system (AMCA), caused a more pronounced decrease in fibrinogen levels, a further increase in the incidence of positive EGT and also fibrin deposition in the kidneys. In rats treated with AMCA + thrombin a similar decrease in fibrinogen levels was recorded, the EGT was positive in all animals, and extensive fibrin deposits were observed in the kidneys and lungs of the animals. Heparinization before infusion of AMCA + brinase antagonized the lowering in fibrinogen levels and the increase in incidence of positive EGT and, moreover, fibrin deposits were no longer observed.

show abstract

Section: Discussionsupporting

confidence: 63%

“…In the present study brinase was infused into rats treated with a synthetic fibrinolysis inhibitor, tranexamic acid (AMCA), which, however, does not interfere with the fibrino lytic effect of brinase [7], Plasma fibrinogen levels, the incidence of positive EGT and the fibrin content in lungs and kidneys were as sessed.…”

mentioning

confidence: 99%

Influence of Brinase on Fibrinogen: Fibrin Transition in in vitro and in vivo Studies

Saldéen¹,

Frisch²

1982

Pathophysiol Haemos Thromb

View full text Add to dashboard Cite

show abstract

“…Among these arachidonate metabo-lites, thromboxane is known to be associated with sequences of events that follow infusion of thrombin in the rat (20), and with the development of thrombin-induced pulmonary edema in sheep (8,9). lncreased permeability to protein may also result from entrapment of fibrin (6) and leukocytes (2 1,s) in the lung. The cyclooxygenase inhibitor indomethacin is known to inhibit prostaglandin synthesis (24) and the release of thromboxane A2 in guinea pig lung parenchymal strips (26).…”

Section: Introductionmentioning

confidence: 99%

Effect of Indomethacin on Thrombin-Induced Pulmonary Edema in the Rat

Ahn

Sandler²,

Wegener³

et al. 1995

Upsala Journal of Medical Sciences

Self Cite

View full text Add to dashboard Cite

The preventive effect of indomethacin on thrombin-induced pulmonary edema was studied in rats.Administration of thrombin caused a significant increase in lung weight, wet weight to dry weight ratio (WWDW), and relative lung water content. During infusion of thrombin, mean pulmonary artery pressure rose and mean systemic artery pressure fell, Pa02 decreased progressively and there was a continuous rise in pH and PaC02.An inhibitor of cyclooxygenase, indomethacin, at a dose of 1 mgkg body weight, induced a significant further increase in lung weight (p<0.05), and a tendency towards an increase in WW/DW and water content compared with animals given thrombin alone. Treatment with indomethacin, however, counteracted the elevated pulmonary artery pressure occurring in the early phase after thrombin infusion, but not that in the late phase. Systemic artery pressure was not affected by indomethacin. The increases in pH and PaCOz after thrombin infusion were attenuated and remained stable almost at baseline level after indomethacin administration. Tndomethacin did not prevent the hypoxemia induced by thrombin infusion.In conclusion, although indomethacin prevented the early increase in pulmonary artery pressure due to thrombin and the decrease in pH and the increase in PaC02, it caused lung vascular permeability to protein to increase more than with thrombin alone.

show abstract

Studies on the role of thromboxane in thrombin-induced pulmonary insufficiency in the rat

Sandler

Gerdin

Saldeen

1986

Thrombosis Research

View full text Add to dashboard Cite

Effect of brinase (protease I from aspergillus oryzae) on the elimination of fibrin from the lungs and pulmonary damage in rats with induced intravascular coagulation and inhibited fibrinolysis

Cited by 9 publications

References 15 publications

Influence of Brinase on Fibrinogen: Fibrin Transition in in vitro and in vivo Studies

Influence of Brinase on Fibrinogen: Fibrin Transition in in vitro and in vivo Studies

Effect of Indomethacin on Thrombin-Induced Pulmonary Edema in the Rat

Studies on the role of thromboxane in thrombin-induced pulmonary insufficiency in the rat

Contact Info

Product

Resources

About