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PubMed1983

Effect of unilateral ureteral occlusion on fibrin deposition in the kidney and renal blood flow during intravascular coagulation in rat.

The effect of unilateral ureteral occlusion on fibrin deposition in the kidney and the interrelation of the fibrin deposition and the renal blood flow was studied in rat. Intravascular coagulation in the kidney was induced by infusion of thrombin and inhibition of fibrinolysis with tranexamic acid. The effects unilateral occlusion of the ureter for 1 and 24 h on fibrin deposition and renal blood flow were studied. Fibrin in the kidneys was quantitated by intravenous injection of 125I-labelled fibrinogen 24 h before the experiment. The renal blood flow was measured before and after infusion of thrombin by injection of 85Sr- and 141Ce-labelled microspheres into the left ventricle. After ureteral occlusion for 1 h the deposition of fibrin in the kidneys was unaffected. After 24 h substantially less fibrin deposition was found in the occluded than in the unoccluded kidney (0.3 +/- 0.2 and 5.7 +/- 1.6 mg, respectively; p less than 0.05). Before thrombin infusion the blood flow to the occluded kidney was less than that in the unoccluded kidney (2.1 +/- 0.8 and 3.7 +/- 1.2 ml/min, 100 g body weight, respectively; p less than 0.05). The blood flow after infusion of thrombin was equally reduced in both kidneys. The results contradict the hypothesis that vasoconstriction increases the amount of fibrin in the kidneys in thrombin-induced intravascular coagulation.

Animals↗
PubMedDate not supplied

The significance of red cell surface area to the permeability of fibrin network.

Thrombus formed under low shear conditions in the intravascular compartment consists of red cells enmeshed within a fibrin network framework. The permeability of the network determines the rate of molecular transport by convection. The effect of red cells on the permeability of the fibrin network was examined in networks developed from red cell suspensions in platelet-rich (PRP) and platelet-poor plasma (PPP). Red cell-rich networks developed in PRP were significantly more permeable than those developed in PPP. Network permeability decreased linearly with increase in hematocrit due to volume exclusion and cell surface hydraulic drag. The hydraulic resistance of the red cells was similar in order of magnitude to that of the fibrin fibers. The hydraulic resistance was calculated to be dependent on the surface area of the red cells, as well as on red cell concentration. Calculation of red cell surface area from permeability (45-90 microns2) was found to be lower than the known surface area (145 microns2). From these studies, it is suggested that red cells entrapped within the network are aggregated. Aggregation is promoted by low shear plasma conditions during fibrin polymerization and by fibrin polymerization intermediaries. The degree of red cell aggregation regulates the hydraulic resistivity of the red cells, and the fibrin fiber structure regulates the hydraulic resistivity of the fibrin network. Both are significant determinants of the network permeability and, therefore, of molecular transport in thrombi.

Blood Platelets↗
PubMed1999

Fibrin gel induces the migration of smooth muscle cells from rabbit aortic explants.

A major step in the pathogenesis of atherosclerosis is the vectorial migration of smooth muscle cells (SMCs) from the arterial media into the intima. Although subcultured SMCs usually show synthetic phenotype, the behaviour of contractile SMCs may be crucial for the subsequent migration of the cells. In the present study, we utilized an in vitro assay system to evaluate the effects of fibrin gels on the migration of SMCs from explants taken from rabbit aorta. After cultured for 5-7 days in a serum-free condition, SMCs appeared from explants covered with fibrin gel. The cells were positive on immunostaining for SMC specific alpha-actin. No migration of SMCs from the control explants without fibrin gel was observed. Then the percentage of explants showing cell migration and the number of migrating cells increased with time. The migration of SMCs into fibrin gels was not dependent on the concentration of fibrinogen used for the preparation of fibrin gel in the range of 1.5-3 mg/ml. Variations of thrombin concentration in the range of 0.25-1.25 U/ml had no significant effect. However, there was less migration of SMCs with higher concentrations of thrombin. Thrombin inhibitors, hirudin and PPACK had no significant effect on the migration of SMCs. An RGD-containing peptide, GRGDS inhibited the migration of SMCs although a control peptide GRGES at the same concentration had no significant effect. A monoclonal antibody to alphavbeta3, LM609, completely inhibited the migration of SMCs from the explants, suggesting that alphavbeta3 integrin is involved in the migration of SMCs into fibrin gels. SMCs which migrated from the explants showed the positive staining with the monoclonal antibodies against SMC myosin heavy chain isoforms, SMemb, SM1 and SM2, suggesting that they are in an intermediate state changing from contractile to synthetic state. In conclusion, the present study showed that fibrin gel induces the migration of SMCs from explants into itself and the process may not need other growth factors or cytokines.

Animals↗
PubMed1975

The role of granulocytes in the activation of intravascular coagulation and the precipitation of soluble fibrin by endotoxin.

This study examines the role of neutrophils (PMN) in the pathogenesis of endotoxin-induced microclot formation. It is intended to clarify whether granulocytes are involved in endotoxin-induced activation of intravascular coagulation (generation of soluble fibrin) and/or in endotoxin-induced precipitation of soluble fibrin. Precipitation of soluble fibrin was achieved by injection of endotoxin into ancrod-infused rabbits with circulating soluble fibrin (first model). Activation of intravascular coagulation was elicited by two intravenous injections of endotoxin into rabbits (second model). Seventy-two and ninety-six hours after injection of nitrogen mustard, leukopenic rabbits had PMN counts between 0 and 50 cells per mul. Neutropenia did not prevent the occurrence of glomerular microclots after infusion of ancrod and injection of endotoxin (first model). Neutropenia influenced neither the decrease in mean fibrinogen concentrations nor the drop in mean platelet counts after ancrod and endotoxin administration. In contrast to the first model, neutropenia prevented the occurrence of glomerular microclots and of circulating soluble fibrin after two injections of endotoxin (second model). It did not, however, protect rabbits from the decrease in mean platelet counts after endotoxin administration. These data indicate that granulocytes are involved in endotoxin-induced activation of intravascular coagulation and the production of soluble fibrin but are not essential to endotoxin-induced precipitation of soluble fibrin.

Animals↗
PubMed2000

Vascular endothelial growth factor binds to fibrinogen and fibrin and stimulates endothelial cell proliferation.

Vascular development and response to injury are regulated by several cytokines and growth factors including the members of the fibroblast growth factor and vascular endothelial cell growth factor (VEGF) families. Fibrinogen and fibrin are also important in these processes and affect many endothelial cell properties. Possible specific interactions between VEGF and fibrinogen that could play a role in coordinating vascular responses to injury are investigated. Binding studies using the 165 amino acid form of VEGF immobilized on Sepharose beads and soluble iodine 125 ((125)I)-labeled fibrinogen demonstrated saturable and specific binding. Scatchard analysis indicated 2 classes of binding sites with dissociation constants (K(d)s) of 5.9 and 462 nmol/L. The maximum molar binding ratio of VEGF:fibrinogen was 3.8:1. Further studies characterized binding to fibrin using (125)I-labeled VEGF- and Sepharose-immobilized fibrin monomer. These also demonstrated specific and saturable binding with 2 classes of sites having K(d)s of 0.13 and 97 nmol/L and a molar binding ratio of 3.6:1. Binding to polymerized fibrin demonstrated one binding site with a K(d) of 9.3 nmol/L. Binding of VEGF to fibrin(ogen) was independent of FGF-2, indicating that there are distinct binding sites for each angiogenic peptide. VEGF bound to soluble fibrinogen in medium and to surface immobilized fibrinogen or fibrin retained its capacity to support endothelial cell proliferation. VEGF binds specifically and saturably to fibrinogen and fibrin with high affinity, and this may affect the localization and activity of VEGF at sites of tissue injury. (Blood. 2000;96:3772-3778)

Binding Sites↗
PubMed1979

Interfering factors in the assay of plasminogen activators by the fibrin plate method. Occurrence of different inhibitors against tissue plasminogen activator and urokinase.

The assay of plasminogen activator activities on fibrin plates was re-evaluated with special reference to fibrinolysis inhibitors present in samples and in fibrin plates. The nature, action and stability of inhibiting material were studied in tissue with considerable differences in activator and inhibitor contents: human lung, liver and placenta. Extracts were tested for inhibitory capacity against purified human uterine tissue plasminogen activator, urokinase and plasmin of fibrin plates prepared from different grades of fibrinogen and fibrin. The tissue extracts inhibited fibrinolysis on fibrin plates to varying degrees, dependent on the sample medium, the type of fibrin plate and the kind of plasminogen activator. The influence of inhibitors in the sample and in the fibrin plate was partly abolished by the presence of 2 M KSCN in the sample. The procedure for preparing the samples as described by Astrup and Albrechtsen did not completely eliminate the inhibitory action against the added plasminogen activators. Comparison of urokinase inhibition with tissue activator inhibition by the tissue extracts as to the degree of denaturation in the Astrup and Albrechtsen procedure showed that they have much in common. Nevertheless, some differences were found which indicated the possible existence of separate urokinase and tissue activator inhibitors or of different inhibition mechanisms for these plasminogen activators.

Antifibrinolytic Agents↗
PubMed2002

Fibrinogen assembly and crosslinking on a fibrin fragment E template.

There is an ongoing controversy concerning whether crosslinked gamma chains in fibrin are oriented "transversely" between fibril strands or "end-to-end" along fibril strands. From the latter viewpoint, Veklich et al. [Proc Natl Acad Sci (USA) 95: 1438, 1998] observed that fibrinogen fibrils that had been assembled on a fibrin fragment E template, cross-linked with factor XIIIa, and then dissociated in acetic acid solution, were aligned end-to-end. This led to the conclusion that crosslinked gamma chains in fibrin under physiological conditions were also aligned end-to-end. To assess its validity we studied the assembly and organization of fibrinogen molecules on a des AB-fibrin fragment E (E-des AB) or a des A-fibrin fragment E (E-des A) template. We evaluated the roles of E polymerization sites E(A) and E(B), and D association sites gammaXL, Da, Db, betaC and alphaC in this process. E(A):Da interactions caused fibrinogen: E "DED" complexes to form, and markedly enhanced the gamma chain crosslinking rates of fibrinogen or des alphaC-fibrinogen. Fibrinogen crosslinking without added fibrin E was slower, and that of des alphaC-fibrinogen was still slower. These events showed that although alphaC domains promote fibrinogen fibril assembly and crosslinking, they contribute little to increasing the E(A):Da-dependent crosslinking rate. Electron microscopic (STEM) images of E-des AB and fibrinogen plus factor XIIIa showed single-, double-, and multistranded fibrils with interstrand DED complexes aligned side-to-side. This alignment was due to betaC:betaC contacts resulting from D subdomain rearrangements initiated by the E(B):Db interactions, and also occurred in mixtures of des alphaC-fibrinogen with E-des AB. In contrast, a mixture of fibrinogen and E-des A plus XIIIa revealed double-stranded fibrils with interstrand DED complexes in a half-staggered arrangement, an alignment that we attribute to crosslinking of gammaXL sites bridging between fibrils strands. These and other features of E-des A-based fibrinogen fibrils, including interstrand gamma chain bridges and early and extensive lateral fibril strand associations concomitant with accelerated gamma chain crosslinking, indicate that crosslinking of fibrin fibril strands takes place preferentially on transversely positioned gamma chains.

Biopolymers↗
PubMedDate not supplied

[Features of the structure of fibrin clots, connected with conditions of gel formation].

Fibrinogen to fibrin conversion and then fibrin clot three-dimensional network formation is one of the final steps in the coagulation system activation. Different factors, such as the environment temperature and pH, ions, so on, render an effect on the fibrin gel formation. Recently, the presence or absences of interface between two phases influence on the fibrin gel structure during its formation have been shown. Studies of fibrin gel structure peculiarities formed at different conditions (between two phases and without one phase) are demonstrated in this article. The plasmin enzymatic hydrolysis of fibrin clots both with surface film and without it was investigated. Experimental data allow to make a conclusion that the fibrin clot structure changes depend on its essential influence on the plasmin hydrolysis process of these clots.

Electrophoresis, Polyacrylamide Gel↗
PubMed2002

Fibrin glue treatment for epistaxis.

Our study was made to prove the second-generation surgical fibrin sealant Quixil to be an effective substitute for nasal packing, chemical coagulation and cautery in management of patients with epistaxis. Our series includes 204 patients with anterior epistaxis (186), and with posterior epistaxis (18) as results of trauma, clotting disorders, chronic and/or atrophic rhinitis and upper respiratory infections, and hypertension. Patients were randomly divided into four groups: with fibrin glue (67) (Quixil), with electric cautery (61), with silver nitrate coagulation (60), and with foam nasal packing (16). For the fibrin glue group, hemostasis was achieved by spraying with 0.3 ml Quixil fibrin glue to each bleeding nostril. The results were excellent in all of the 62 (92.5%) patients of the fibrin glue group with complete and immediate hemostasis. We found good healing of bleeding sites, no swelling and secondary bleeding, no inflammation, no plaque or crists. Three months monitoring of atrophic changes of the nasal mucosa proved absence of atrophy of the nasal mucosa. In this group, the bleeding time averaged 2 min 30 sec since the moment of admittance. In the groups where cautery, coagulation, or nasal packing was used, we found local swelling, pain, and slow healing of the bleeding site with accidental atrophy of the nasal mucosa. The rates of these side effects were significantly higher in comparison with the fibrin glue group. The bleeding time was also longer. We found that the fibrin glue is more effective hemostatic in comparison with foam nasal packing, cautery and coagulation, and provides no complications usual for these types of treatment of epistaxis.

Adolescent↗
PubMed2002

Closure of proximal colorectal fistulas using fibrin sealant.

Fibrin glue has been used in upper gastrointestinal and perianal fistula disease, but its success in proximal colorectal pathology has not been widely documented. This report describes the use of endoscopically injected fibrin glue as a successful adjunct to traditional methods in accelerating the closure of colorectal fistulas. A retrospective review was performed on cases of colon and rectal fistulas treated with fibrin glue using an endoscopic technique of injection. Fistulas were injected via a flexible fiberoptic endoscope with fluoroscopic guidance (three) or directly with a rigid proctoscope (one). Fibrin glue was mixed directly from cryoprecipitate, thrombin, and calcium (one) or using a Tisseel kit (three) (Baxter, Deerfield, IL). Four patients were identified and included: two J-pouch fistulas, a colocutaneous fistula, and a complex rectocutaneous fistula. The median duration of fistula was 33 days (range 4-365 days). Total parenteral nutrition and bowel rest were used in two patients and three required drainage of an abscess. All fistulas were obliterated and patients required a mean of one application of fibrin glue (range one to two). The mean time to resuming a regular diet postinjection was 2 days (range 1-5). No complications were identified. Fistula resolution was documented in all cases with a contrast enema and no patient has had a fistula recurrence at a median follow-up of 12 months (range 6-65). This preliminary series demonstrates that fibrin glue can be used to obliterate proximal rectal, colonic, and pouch fistulas. Endoscopy and fluoroscopy may aid in administering the fibrin glue. This adjunctive technique may shorten the time to fistula closure and may allow some patients to avoid further surgery.

Adult↗
PubMed1975

The comparative ultrastructure of fibrin induced by thrombin and by staphylocoagulase.

Fibrin induced by the action of thrombin and by staphylocoagulase was studied by transmission electron microscopy. Periodic striations were consistently observed in the negatively stained preparations of both fibrins. When 4200 major periods in the thrombin fibrin system were measured the mean length was 228 A. For 3666 major periods in the coagulase fibrin system the mean length was 223 A. While the T test analysis of these values gave a value of 10, it is noteworthy that the differences are well within the scatter of periodicity reported in the literature for thrombin-induced fibrin. Gross inspection of the preparations indicated that the coagulase-induced fibrin had a knottier appearance and was accompanied by a greater amount of background debris than the thrombin-induced fibrin.

Animals↗
PubMed2002

[Repair of anorectal fistulas using fibrin glue tissue adhesive--preliminary experience in 15 patients].

PURPOSE: The goal of this study was to evaluate whether commercially produced fibrin sealant can be used for the treatment of complex anorectal fistulae. METHODS: Fibrin glue was used for patients with primary and recurrent ano-rectal fistulae, but patients with Crohn's disease or AIDS were excluded. The procedure was performed under anesthesia in the operating room. The primary and secondary openings were identified using blue dye. The secondary opening and the tract of the fistula were curetted, and 4 ml of fibrin sealant were injected through the secondary opening until fibrin sealant was seen coming from the primary opening. The patients were discharged on the next day following the procedure, and were followed-up closely in the outpatient clinic. RESULTS: Fifteen consecutive patients underwent one trial of fibrin glue injections. The average follow-up period was 4 months. Overall, eleven of the 15 patients (73.3%) had successful closure of their fistulae. The healing rates for intersphincteric, transsphincteric and suprasphincteric were 50%, 77.7% and 100% respectively. Fibrin glue treatment was effective in five out of the 6 patients (83.3%) who were operated on for recurrent fistulae. Of the 4 patients in whom the treatment failed, the mean time for recurrent symptoms was 4 weeks. No patient suffered from fecal or gas incontinence and all of the patients returned promptly to routine life. CONCLUSION: Sealing the tracts with fibrin glue is a unique mode for the treatment of ano-rectal fistulae, and our preliminary results with this technique are promising. The procedure is safe and easy to perform, and can be offered as an alternative to conventional surgery. Most importantly, this method minimizes the risk of fecal incontinence and the discomfort of prolonged wound healing.

Adult↗
PubMed2003

Chemical crosslinking of urokinase to pulmonary surfactant protein B for targeting alveolar fibrin.

Intraalveolar fibrin formation is a consistent finding in acute inflammatory and chronic interstitial lung disease. Polymerization of fibrin in the presence of pulmonary surfactant results in far-reaching incorporation of the hydrophobic surfactant compounds into the growing fibrin matrix, with loss of surface activity, altered fibrin structure and reduced susceptibility of the clot to fibrinolysis. For specific targeting of such alveolar fibrin, we designed a hybrid molecule consisting of the catalytic domain of urokinase (B-chain) and the hydrophobic surfactant protein B (SP-B), termed SPUC. The urokinase B-chain, obtained by limited reduction of human two-chain-urokinase (u-PA) and subsequent affinity purification, was chemically coupled to SP-B in a semi-organic solvent system using a hetero-bifunctional crosslinker. Purification of the chimeric proteins included reversed phase and cation exchange chromatography. SDS-PAGE and Western Blotting with immunostaining were employed for biochemical characterization of the conjugate. Chromogenic substrate assays, (125)I-based fibrin plate assays, active site titration and surface tension measurements (pulsating bubble surfactometer) were performed to analyze the specific fibrinolytic activity of the conjugate and its surface activity. SPUC was found i) to be assembled stoichiometrically in a 1: 1 fashion (SP-B: u-PA), ii) to fully retain the biophysical activity as compared to native SP-B and iii) to also retain the fibrinolytic activity. SPUC was 2-3 fold more effective in lysis of surfactant containing clots and 5-fold more resistant against plasminogen activator 1 (PAI-1) as compared to the native u-PA. We conclude that urokinase and SP-B can be chemically crosslinked, thereby yielding a fibrinolytic enzyme suitable for targeting alveolar fibrin.

Chromogenic Compounds↗
PubMed1992

The effect of fibrin structure on fibrinolysis.

Fibrin structure contributes to the regulation of the fibrinolytic rate. As the fibrin fiber size is decreased, the fibrinolytic rate also decreases. Fibrin structure was altered by either changing the ratio of thrombin to fibrinogen, i.e. altering the assembly rate or by adding a fibrin assembly inhibitor, iopamidol. Changes in the fibrinolytic rate were followed by measuring the time dependence of the decrease in the fiber mass/length ratio during fibrinolysis. A measure of the overall fibrinolytic rate was determined from the decrease in the mass/length ratio versus time. An 8-fold reduction in the fibrinolytic rate was seen on decreasing the mass/length ratio from 2.7 x 10(12) daltons/cm to 0.5 x 10(12) daltons/cm. It is shown that thin fibrin fibers have a decreased rate of conversion of plasminogen to plasmin by tissue plasminogen activator and that thin fibrin fibers are lysed more slowly than thick fibrin fibers.

Amino Acid Sequence↗
PubMed1977

Fibrin and fibrinogen proteolysis products: comparison between gel filtration and SDS polyacrylamide electrophoresis analysis.

The proteolysis of purified human fibrinogen, stabilized and non-stabilized fibrin by plasmin were investigated by gel filtration analysis and SDS polyacrylamide electrophoresis of the reaction products. Plasmin proteolysis of fibrinogen followed the sequential steps previously reported and the two analytical methods yielded concordant results. Large molecular weight proteolysis products, of substantially greater molecular weight than native fibrinogen, were identified by gel filtration analysis following dissolution of stabilized and non-stabilized fibrin clots; with further incubation with plasmin, these proteolysis products gradually diminished in size. On the other hand, SDS polyacrylamide electrophoresis of these fibrin digests demonstrated that while non-stabilized fibrin yielded breakdown products similar in size to those obtained after proteolysis of fibrinogen, stabilized fibrin digests showed moieties of greater molecular size estimated to be of molecular weight 400,000 to 800,000. The final breakdown products of stabilized fibrin differed from those of fibrinogen and nonstabilized fibrin in that fragment D was present in the "double D" cross-linked form.

Antigens↗
PubMed2003

Effect of fibrin glue on air leak and length of hospital stay after pulmonary lobectomy.

AIM: Air leaks are a common cause of morbidity and prolonged hospital stay after pulmonary lobectomy. We reviewed our experience with intraoperative fibrin glue to determine if it reduced air leak and improved patient outcomes. METHODS: Records of patients undergoing pulmonary lobectomy for benign or malignant disease over a 4-year period (1998-2001) were reviewed. Data was collected on age, sex, pulmonary function, pulmonary pathology, use of fibrin glue, duration of chest tube drainage, length of hospital stay, and postoperative complications. RESULTS: Three hundred and sixty patients underwent lobectomy. Fibrin glue was used intraoperatively to seal air leaks in 102 of the 360 patients (study group: 102;control group: 258). Fibrin glue was used at the discretion of the surgeon, with some surgeons using it routinely. The groups did not differ in age (p=0.29), sex (p=0.42), FEV1 (p=0.57), or pathology (p=0.08). There were no differences in outcomes such as operative mortality (study: 2 of 102, control 6 of 258, p=0.85), empyema (study: 0 of 102, control: 3 of 258, p=0.55), prolonged (>7 days) air leaks (study: 10 of 20; control: 20 of 258, p=0.71), or length of hospital stay (study: 6.3+/-2.5 days, control:7.7+/-7.2 days, p=0.83). The use of fibrin glue was associated with a reduction in the duration of chest tube intubation (study: 4.1+/-3.2 days, control: 5.5+/-3.8 days, p=0.001). CONCLUSION: Patients treated intraoperatively with fibrin glue had a significantly shorter duration of chest tube intubation after pulmonary lobectomy than those treated conventionally. However, the use of fibrin glue did not significantly influence more clinically relevant outcomes such as length of hospital stay and incidence of prolonged (>7 days) air leaks.

Aged↗
PubMed1992

[Rupture of the Achilles tendon--fibrin gluing or suture?].

The rise of recreational sports activities and the incidence of ruptures of the Achilles tendons has increased simultaneously. Recently the use of fibrin sealing for surgical therapy of ruptured Achilles tendons has emerged as an alternative technique. Between 1982 and 1989 62 consecutive patients were operated for unilateral Achilles tendon rupture. Following causes for ruptures are known: 36 indirect traumas in sport (74%), 9 direct blunt injuries at occupational work (18%), 3 traffic-accidents (11%) and 1 rupture after operation of a Haglund exostosis. 25 patients (56%) were treated by suture technique and 20 patients (44%) with fibrin sealant. The mean long term follow-up of 49 months is known of 49 patients. There were 3 (12%) postoperative infections in the suture group and none in the fibrin group. After suturing the Achilles tendon 3 (12%) reruptures occurred 8-10 weeks after tendon repair and 1 (5%) rerupture after fibrin sealing. All reruptures are caused by a new adequate trauma. The time of return to social and recreational activities was 9 months in the suture group and 7 months in the fibrin group. The functional and cosmetic results after use of fibrin was significant better, and the long-term results were very satisfactory. We prefer fibrin sealing for the treatment of acute ruptures of Achilles tendons.

Achilles Tendon↗
PubMed1992

[Prevention and treatment of postoperative fistulae--new indications for fibrin gluing].

The additional sealing of bronchial and gastrointestinal sutures and anastomoses, respectively, by means of fibrin sealant helped to significantly reduce the postoperative dehiscence rate; this rate amounted to 3.6% for additionally sealed bronchus stump occlusions and to 4.2% in gastrointestinal operations, whereby naturally in emergency abdominal operations the rate was higher (7.7%) than in elective surgery (3.8%). Eight postoperative bronchus stump fistulae and eleven out of the twenty-five gastrointestinal anastomotic dehiscences could be closed using a fibrin clot. Furthermore, fibrin occlusion of the pancreatic duct following Whipple's operation for the protection of the pancreatic-digestive anastomosis (n = 67) has turned out to be a success, since no postoperative pancreatic fistulae occurred, which resulted in the very low mortality rate of 1.5%. One more indication for fibrin sealing was the prevention of postoperative lymph fistulae by additional wound sealing (n = 123) and the fibrin occlusion of these fistulae (n = 18); the postoperative lymph fistulae rate amounted to only 3.3%. All 4 cases, as well as 14 other cases of existing lymph fistulae were healed quickly by instillation of fibrin. These relatively new, partly endoscopic, procedures using fibrin sealing proved to be very successful, because on the one hand postoperative fistulae could be largely avoided and on the other hand they could be treated without further operation.

Bronchial Fistula↗