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Biomedical subjects

G Fuhrer

Publications and source records attributed to G Fuhrer.

At least 19 recordsLinked to original sources
PubMed1992

Aprotinin in cardiopulmonary bypass--effects on the Hageman factor (FXII)--Kallikrein system and blood loss.

Aprotinin has been used in our hospital in open heart surgery for almost 20 years and recently published studies have revealed a reduction in postoperative blood loss under this therapy. In the present study patients undergoing aorto-coronary bypass operations received either 20,000 KIU aprotinin/kg body weight (group 2) or 60,000 KIU aprotinin/kg body weight (group 3). Another group of patients without aprotinin served as a control (group 1) and postoperative bleeding was more pronounced in these patients compared with the other groups. In parallel, slight reductions in kallikrein-like activity were observed in patients treated with aprotinin. Furthermore, we have shown that the main inhibitor of the contact phase, C1-esterase-inhibitor, loses some of its activity against beta-FXIIa in the presence of heparin. Aprotinin was able to partly antagonize this phenomenon. All studies dealing with the effect of aprotinin in extracorporeal circulation demonstrate hyperfibrinolysis in untreated patients. Aprotinin is known to inhibit plasmin at low concentrations and thus reduced the postoperative bleeding tendency (group 2). In addition, plasma kallikrein is inhibited by high aprotinin concentrations and is responsible for a reduced activation of the contact phase system. This effect led to a further reduction in blood loss (group 3).

Aprotinin↗
PubMed1992

The effects of fractionated and unfractionated heparins with and without aprotinin on plasma inhibition of alpha and beta FX11a.

Chromogenic peptide substrate assays were used to compare the effects of fractionated and unfractionated heparins on plasma inhibition of alpha and beta FX11a, with and without various concentrations of aprotinin. All of the heparins reduced beta FX11a inhibition at 1 or 2U/ml. Four heparins increased alpha FX11a inhibition. Aprotinin counteracted the reduction in beta FX11a inhibition and augmented the heparin potentiation of alpha FX11a inhibition.

Aprotinin↗
PubMed1990

FXII.

The plasma protein FXII (Hageman factor) has been shown to be linked with the plasma defence systems of coagulation, fibrinolysis, kallikrein-kinin and complement. It can be activated by surface contact activation and in solution. Surface contact activation is a complex phenomenon involving negatively charged surfaces, FXII, high molecular weight kininogen and plasma kallikrein. Fluid-phase activation can be effected by a variety of serine proteases. In both types of activation the FXII zymogen is converted to active enzymes. FXII levels in plasma are low or undetectable in both inherited deficiencies and in a variety of clinical conditions. FXII levels can also be elevated in some clinical conditions. Although discovered as a clotting protein FXII appears to play an important role in the kallikrein-kinin and fibrinolytic systems and also has effects on cells. Recent studies suggest that therapeutic blockade of activation of FXII can be of benefit in certain clinical conditions.

Animals↗
PubMed1988

[Changes in the kallikrein-kinin and complement system in angiography using non-ionic contrast media].

To examine alterations of the kallikrein-kinin system and of the complement due to the bolus injection of newer non-ionic contrast agents, venous blood samples were taken before and 3 min after angiography. There were no adverse contrast reactions clinically evident. Prekallikrein, kallikrein inhibition, beta-factor XIIa inhibition, C1-esterase inhibitor, C1q, C3, ATIII, HMW-kininogen, fibrinogen and factor XII were determined. Bolus injection of the contrast medium caused an activation of the kallikrein-kinin system (p less than 0.05) with reduction of prekallikrein, kallikrein-inhibition, beta-factor XIIa inhibition and C1-esterase inhibitor. The levels of C1q and C3 were also decreased (p less than 0.05) indicating an activation of the complement. Our results demonstrate, that angiography causes a significant activation of the kallikrein-kinin as well as of the complement system in spite of the use of newer non-ionic contrast agents.

Angiography↗
PubMed1988

[Activation of the kallikrein-kinin system by intravenous administration of ionic and non-ionic radiographic contrast media].

Conventional ionic contrast media (sodium meglumine and amidotrizoate) were injected intravenously in 22 patients (group A); the nonionic, low-osmolar contrast medium iohexol was similarly administered to 24 patients (group B). This resulted in a significant (group A: P less than 0.05; group B: P less than 0.01) reduction in prekallikrein (93 and 94%, respectively), inhibition of kallikrein (90 and 88%), beta-factor XIIa inhibition (86 and 85%), and C1 inhibition (90 and 91%). Factor XII levels remained unchanged in both groups. These results indicate that the kallikrein-kinin system is activated even during routine, complication-free radiographic procedures involving contrast-media injection. There was no difference between ionic and nonionic contrast media.

Complement C1 Inactivator Proteins↗