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Blood Fibrinolysis / -i BLOOD FIBRINOLYSIS ISBN 90 6231 046 X STELLINGEN I De meeste klinische studies op het gebied van de bloedfibrinolyse behoeven herevaluatie vanwege het gebruik van onjuist gebleken werkhypothesen en in­ adequate meetmethoden. II Alvorens studies met gezuiverde-komponenten over molekulaire mechanismen van kontaktaktivatie zinvol kunnen worden voortgezet, dient de verschijningsvorm van die komponenten in bloed te worden vastgesteld. J.H. Griffin: Thrombosis and Haemostasis 38 (1977) 117. R.J. Handle, R.W. Colman en A.P. Kaplan: Proc. Nat. Acad. Sei. USA 73 (1976) 4179-^183. Ill Als de modellen voor humaan serum HDL, zoals voorgesteld door Verdery en Nichols juist zijn, is dat ondanks de door hun uitgevoerde berekeningen. R.B. Verdery en A.V. Nichols: Chem. Phys. of Lipids 14 (1975) 123-134. IV Ten onrechte verwerpen Yu en Yu de authenticiteit van de door Downer e.a. gevonden derde grote hydrofobe subunit van cytochroom c oxidase uit runder- hart. CA. Yu en L. Yu: Biochim. Biophys. Acta 495 (1977) 248-259. N.W. Downer, N.C. Robinson en R.A. Capaldi: Biochemistry 15 (1976) 2930-2936. Het is misleidend synthetische substraten voor proteolytische enzymen aan te duiden met de naam van een enzym. E. Amundsen en L. Svensen. In: New Methods for the Analysis of Coagulation using chromogenic substrates (Ed. I. Witt), de Gruyter, Berlin (1977) p 211-220. VI De betekenis van plasma kallikreine als piasminogeenaktivator is gering. VII Doseringen bij infusietherapie voor patiënten met hemofilie dienen gebaseerd te zijn op halfwaardetijden in plasma van de betreffende stollingsfaktor. De meeste literatuurgegevens over deze waarden zijn echter fout. W.Th. Hermens. In: Handbook of Hemophilia (Eds. K.M. Brinkhous en H.C. Hemker), Excerpta Medica, Amsterdam (1975) p 569-589. VIII Het is niet waarschijnlijk dat de hoeveelheid circulerend anodaal antigeen bij Schistosoma mansoni infekties een nauwkeurige maat is voor de wormlast van de gastheer. M.P. Bawden en T.H. Weiler: Am. J. Trop. Med. Hyg. 23 (1974) 1077-1084. IX Voor het meten van de aktiviteit van extrinsieke plasminogeenaktivatoren in bloed verdienen de technieken met fibrine als substraat nog de voorkeur boven die met synthetische chromogene substraten. H. Stormorken: Thrombosis and Haemostasis 36 (1976) 299-301. Het rijksvaccinatieprogramma dient te worden uitgebreid met vaccinatie tegen bacteriële meningitis-verwekkers zoals Neisseria meningitidis, Haemophilus influenzae en Diplococcus pneumoniae. XI Het is gewenst dat exploitanten van legbatterijen eieren voor hun geld kiezen. XII De voortschrijdende ontkoppeling tussen lichaamsbeweging en werk betekent voor verstandige mensen een vermindering van de vrijheid vrije tijd te besteden. XIII Dat het bloed ons van schrik in de aderen zou kunnen stollen moet onwaarschijn­ lijk worden geacht. C. Kluft 22 februari 1978 BLOOD FIBRINOLYSIS PROACTIVATORS AND ACTIVATORS IN HUMAN PLASMA by CORNELIS KLUFT Gaubius Institute, Health) Research Organization TNO, Leiden, The Netherlands 1978 Dutch Efficiency Bureau - Pljnacker Published as a thesis, Leiden, 1978 PROMOTOR : PROF. DR. H. C. HEMKER CO-REFERENTS : PROF. DR. A. A. H. KASSENAAR DR. P. BRAKMAN l\/lanuscript : Mrs. C. Horsting-Been Drawings : Mr. J. J. NIeboer to my parents to mini and the ahildren CONTENTS General Introduction 10 Chapter I : Occurrence of CI inactivator and other proteinase inhibitors in euglobulin fractions and their influence on fibrinolytic activity. 22 Introduction 22 Materials and Methods 23 Results 25 Discussion 29 Chapter II : Elimination of inhibition in euglobulin fibrinolysis by use of flufenamate: Involvement of CI inactivator. 34 Introduction 34 Materials and Methods 35 Results 38 Discussion 47 Chapter III : Studies on the fibrinolytic system in human plasma: Quantitative determination of plasminogen activators and proactivators. 54 Introduction 55 Materials and Methods 55 Experimental 59 Discussion 73 Chapter IV : Cl-inactivator-resistant fibrinolytic activity in plasma euglobulin fractions: Its relation to vascular activator in blood and its role in euglobulin fibrinolysis. 80 Introduction 80 Materials and Methods 81 Results 84 Discussion 97 Chapter V : Determination of prekallikrein in human plasma: Optimal conditions for activating prekallikrein. 104 Introduction 104 Materials and Methods 105 Results 107 Discussion 116 Chapter VI : Factor Xll-dependent fibrinolysis: A double function of plasma kallikrein and the occurrence of a previously undetermined factor XII- and kallikrein-dependent plasminogen proactivator. 124 Introduction 124 Materials and Methods 126 Results 129 Discussion 139 Summary 148 Samenvatting 150 Acknowledgements 154 GENERAL INTRODUCTION Fibrin formed in the body by coagulation of fibrinogen has a temporary function or is part of a pathological process and should again disappear. This disappearance is due to the capacity of compounds present in the organism to break down the fibrin matrix into soluble components: a process called fibrinolysis. The serine protease plasmin is an important agent in the proteolytic degradation of the network of fibrin. Plasmin is generated from a precursor in plasma, plasminogen, by a process catalyzed by activators (scheme. Fig. 1). PLASMINOGEN ACTIVATOR PLASMINOGEN ^^ ^^ PUSHIN FIBRINOGEN ^*^ FIBRIN ^"^ ^^ FIBRIN DEGRADATION PRODUCTS Fig. 1. Scheme for plasma fibrinolysis. Mechanism of fibrinolysis Initiation of fibrinolysis appears to take place preferentially at the surface of fibrin. The mechanism of plasminogen activation has been more extensively studied for only two activators: human urinary activator (uroki­ nase) and a porcine tissue activator. Urokinase is only weakly adsorbed to fibrin, while, in contrast, the tissue activator is strongly bound to fibrin and its effect on plasminogen is greatly stimulated by the presence of fibrin (Thorsen et al., 1972; Robbins et al., 1975; Wallen, 1977). Native plasminogen (with glutamic acid as NHa-terminal amino acid) has a weak affinity for fibrin, whereas the modified form of plasminogen (resulting from limited proteolysis of the NHz-terminal end and with lysine as the NHz-termi- nal amino acid) has a much stronger affinity (Thorsen, 1975); (for reviews on plasminogen, see Collen and Verstraete, 1975; Collen and De Maeyer, 1975). These interactions with fibrin are related to the presence of a lysine-binding site in the plasminogen molecule (Wiman and Wallen, 1977). 10 The plasmin formed accumulates on fibrin (Celander and Guest, 1957). The active site of plasmin which is located in the light chain (Summaria et al., 1967) as well as the lysine-binding sites on the heavy chain (Wiman and Wallen, 1977) are probably involved in this selective accumulation on fibrin. This accumulation assures that plasmin is primarily involved in the proteolysis of fibrin. In the absence of fibrin, plasmin is rapidly inactivated by inhibitors in plasma, so that other proteolytic effects are reduced. Otherwise, plasmin has a remarkably broad specificity (reviewed by Christman et al., 1977). The a2-antiplasmin is the most effective plasmin inhibitor, with «a-macroglobulin as a powerful second (Collen, 1976; Aoki et al., 1977). PLASMINOGEN ACTIVATORS AND PROACTIVATORS IN PLASMA Plasminogen activators are widely distributed in the organism. They are presently pragmatically subdivided into groups according to their source of origin: circulating plasminogen activators (blood), tissue plasminogen acti­ vators, urinary plasminogen activators (urokinase) and tissue culture plasmin­ ogen activators. Knowledge of their molecular biology is still fragmentary and the possible structural identities of several of the activators in these arbitrary groups are still mostly undetermined. The circulating plasminogen activators (restricted to cell-free plasma of blood) can be divided into activators of intrinsic or of extrinsic origin. Activators generated in the plasma from circulating proactivators are design­ ated as intrinsic activators to distinguish them from the extrinsic activators released into the blood plasma from cells, presumably mainly the vascular endothelial cells. The significance of this classification is substantiated by the recent finding that it parallels the functional division of activator ac­ tivity in plasma into a part which is susceptible to inhibition by Cl-inacti- vator and a part which is resistant to this inhibitor (Kluft, 1977a, 1978). a) INTRINSIC activation by a factor Xll-dependent pathway The occurrence of Hageman factor (factor XII)-dependent fibrinolysis in plasma was recognized in 1959 by Niewiarowski and Prou-Wartelle. The fibrin­ olytic activity produced by surface exposure was assumed to result from an interaction of surface activated Hageman factor with a hypothetical precursor of a plasminogen activator (latridis and Ferguson, 1962). The corresponding cascade type of mechanism is shown in figure 2. The early steps in this cas­ cade, which concern the activation and participation of factor XII, have been 11 FACTOR XII FACTOR XIlA PLASMINOGEN PUSMINOGEN PROACTIVATOR ACTIVATOR PLASMINOGEN PUSHIN Fig. 2. Tentative scheme for the factor Xll-dependent pathway of fibrinolysis. the subject of many studies in recent years (reviews by Griffin et al., 1976 and Kaplan et al., 1976). The formation of surface-bound agglomarates of several proteins appeared to be involved. Solid surfaces like that of glass, kaolin, collagen or celite or soluble high molecular weight acid polysaccha­ rides such as dextran sulphate serve as a rendezvous. The adsorbed factor XII and a
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