Plasma Kallikrein Activity and Prekallikrein Levels during Endotoxin Shock in Dogs

1978 ◽  
Vol 10 (1) ◽  
pp. 50-62 ◽  
Author(s):  
A.O. Aasen ◽  
W. Frølich ◽  
O.D. Saugstad ◽  
E. Amundsen
Keyword(s):  
Endotoxin Shock ◽  
Plasma Kallikrein ◽  
Kallikrein Activity

Cold Promoted Activation of Factor VII VI. Effect of Inhibitors

1973 ◽  
Vol 29 (03) ◽  
pp. 633-643
Author(s):  
H Gjønnæss
Keyword(s):  
Soya Bean ◽  
Factor Vii ◽  
Plasma Kallikrein ◽  
Contact Activation ◽  
Activation Reaction ◽  
Hexadimethrine Bromide ◽  
Bean Trypsin Inhibitor ◽  
Plasma Arginine ◽  
Kallikrein Activity ◽  
Effect Of Inhibitors

SummaryThe cold promoted activation of factor VII occurs in parallel with an activation of a plasma arginine esterase, and, on inhibition of the cold activation of factor VII, the esterase activation also decreased. The inhibitor pattern supported our theory that the arginine esterase that is activated in the cold activation of factor VII is plasma kallikrein.The cold activation of factor VII was completely inhibited with soya bean trypsin inhibitor in doses that did not interfere with the contact activation. On the other hand, inhibition of the contact activation with hexadimethrine bromide did not interfere with the cold activation of factor VII except when this was kaolin induced. Contact and cold activation therefore appear to represent two different pathways for the activation of factor VII. The cold activation reaction is probably mediated by the activation of plasma prekallikrein, and inhibition of the plasma kallikrein activity correlates with the inhibition of the cold promoted activation of factor VII.

scholarly journals Changes in Levels of Plasma Pre-Kallikrein, Kallikrein and Kallikrein Inhibitors During Endotoxin Shock in Dogs

1977 ◽  
Author(s):  
M. J. Gallimore ◽  
A. O. Aasen ◽  
E. Amundsen
Keyword(s):  
Late Phase ◽  
Endotoxin Shock ◽  
Time Dependent ◽  
Plasma Kallikrein ◽  
Kinin System ◽  
E Coli ◽  
Dependent Inhibition ◽  
Kallikrein Kinin System ◽  
Time Dependent Inhibition ◽  
Kallikrein Inhibitors

Plasma protease activity is known to be increased during endotoxin shock and recent studies have indicated that the plasma kallikrein-kinin system becomes activated by circulating endotoxin. Plasma levels of pre-kallikrein kallikrein and kallikrein inhibitors were therefore determined in samples from dogs infused with E. coli endotoxin, using assays with a chromogenic substrate for plasma kallikrein(Chromozyme -PK, Pentapharm, Basle, Switzerland). “Fast-reacting” and “time-dependent” inhibitors of kallikrein were studied using purified human plasma kallikrein. Considerably reduced levels of plasma pre-kallikreiri and increased levels of kallikrein were detected in the late phase of shock and significant reductions in “fast-reacting” and “time-dependent” inhibition of kallikrein was observed. These results show that during endotoxin shock plasma pre-kallikrein becomes activated to kallikrein and indicate that kallikrein inhibitors play an important mediatory role in the pathophysiology of endotoxin shock.

Elevation in plasma kallikrein activity after rat kidney allografting

1974 ◽  
Vol 127 (3) ◽  
pp. 287-291 ◽  
Author(s):  
Thomas C. Moore ◽  
Michael C. Sinclair ◽  
Carlos A.E. Lemmi
Keyword(s):  
Rat Kidney ◽  
Plasma Kallikrein ◽  
Kallikrein Activity

Cold Promoted Activation of Factor VII

1972 ◽  
Vol 28 (02) ◽  
pp. 182-193 ◽  
Author(s):  
H Gjønniess
Keyword(s):  
Ellagic Acid ◽  
Factor Vii ◽  
Coagulation System ◽  
Plasma Kallikrein ◽  
Glandular Kallikrein ◽  
Kallikrein Activity

SummarySeveral known activators of the plasma kallikrein system were tested for the ability to induce cold promoted activation of factor VII.All the prekallikrein activators tested (EACA, trypsin, acetone, urokinase, kaolin, Liquoid, ellagic acid) revealed generation of factor VII activator activity (CPA). Simultaneously the plasma kallikrein system was activated. A good correlation was demonstrated between the factor VII activation and the kallikrein activity.Glandular kallikrein, bradykinin, or kallidin revealed no effect on the coagulation system. Thus, the correlation between the factor VII activation and the kallikrein system seemed to be restricted to plasma kallikrein.

scholarly journals Decreased plasma kallikrein activity is associated with reduced kidney function in individuals with type 1 diabetes

Diabetologia ◽  
2020 ◽  
Vol 63 (7) ◽  
pp. 1349-1354
Author(s):  
Mari-Anne Härma ◽  
◽  
Emma H. Dahlström ◽  
Niina Sandholm ◽  
Carol Forsblom ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Kidney Function ◽  
Plasma Kallikrein ◽  
Kallikrein Activity ◽  
Reduced Kidney Function

scholarly journals INHIBITION OF PLASMA KALLIKREIN WITH APROTININ IN PORCINE ENDOTOXIN SHOCK

1993 ◽  
Vol 34 (2) ◽  
pp. 193-198 ◽  
Author(s):  
Matthias Siebeck ◽  
Edwin Fink ◽  
Joachim Weipert ◽  
Marianne Jochum ◽  
Hans Fritz ◽  
...  
Keyword(s):  
Endotoxin Shock ◽  
Plasma Kallikrein

scholarly journals Kallikrein-kinin blockade in patients with COVID-19 to prevent acute respiratory distress syndrome

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Frank L van de Veerdonk ◽  
Mihai G Netea ◽  
Marcel van Deuren ◽  
Jos WM van der Meer ◽  
Quirijn de Mast ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Pulmonary Edema ◽  
Distress Syndrome ◽  
Vascular Leakage ◽  
Plasma Kallikrein ◽  
Early Disease ◽  
Kallikrein Activity

COVID-19 patients can present with pulmonary edema early in disease. We propose that this is due to a local vascular problem because of activation of bradykinin 1 receptor (B1R) and B2R on endothelial cells in the lungs. SARS-CoV-2 enters the cell via ACE2 that next to its role in RAAS is needed to inactivate des-Arg9 bradykinin, the potent ligand of the B1R. Without ACE2 acting as a guardian to inactivate the ligands of B1R, the lung environment is prone for local vascular leakage leading to angioedema. Here, we hypothesize that a kinin-dependent local lung angioedema via B1R and eventually B2R is an important feature of COVID-19. We propose that blocking the B2R and inhibiting plasma kallikrein activity might have an ameliorating effect on early disease caused by COVID-19 and might prevent acute respiratory distress syndrome (ARDS). In addition, this pathway might indirectly be responsive to anti-inflammatory agents.

Sign in / Sign up

Export Citation Format

Share Document