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PubMed1999

Beta3 integrin activation improves alphavbeta3-mediated retraction of fibrin matrices.

BACKGROUND: Integrins are heterodimeric transmembrane glycoproteins that mediate cell interactions with the extracellular matrix. In vivo, integrin affinity can be modulated by intracellular signaling events. This can be simulated by a point mutation (D723R) in the cytoplasmic tail of the beta3 integrin subunit which results in constitutive activation. The effects of beta3 integrin activation on the function of alphavbeta3, an integrin which is important to the adhesive events of multiple cell types, were addressed using Chinese hamster ovary cells expressing either the wild-type alphavbeta3 integrin or the mutant alphavbeta3(D723R). The interactions of these cell lines with fibrin matrices were compared. METHODS: Receptor expression levels were confirmed by FACS analyses using a monoclonal anti-alphavbeta3 antibody. Cell attachment to fibrin-coated dishes was determined after 1 h by fixation and crystal violet staining followed by elution of the dye and OD measurement. Fibrin clot retraction was measured by culturing cells in fibrin clots for 24 h. The clots were detached from the dish and the surface area was calculated at individual time points. RESULTS: CHO alphavbeta3(D723R) cells displayed a greater than twofold increase in attachment to fibrinogen or to fibrin matrices when compared to wild-type transfectants. Further, CHO alphavbeta3(D723R) cell retraction of fibrin matrices was significantly greater at nearly all time points. CONCLUSION: Activation of the beta3 integrin subunit significantly improves the interaction of alphavbeta3 with fibrin and may play a role in the integrin-mediated signaling events which occur following vascular injury.

Animals↗

PubMed1996

The configuration of fibrin clots determines capillary morphogenesis and endothelial cell migration.

In the living organism, capillary growth frequently occurs in a fibrin-rich extracellular matrix. The structure and the mechanical properties of fibrin clots are influenced by various macromolecules (i.e., hyaluronic acid and thrombospondin) and also by pH, ionic strength, and thrombin concentrations of the milieu in which they polymerize. The configuration (three-dimensional architecture) and the rigidity of fibrin clots correlate with their opacity measured by spectrophotometric absorbance readings at 350 nm. By using bovine pulmonary artery endothelial cells and bovine fibrinogen, we show here that transparent fibrin clots (A(350) < 1.0), polymerized at > or = pH 7.5 or in the presence of increased thrombin or sodium chloride concentrations, strongly stimulated capillary morphogenesis in vitro. In contrast, opaque fibrin gels (A(350) > 1.5), polymerized at pH 7.2 or in the presence of dextran, stimulated only the migration of endothelial cells but not capillary morphogenesis. We demonstrate that the angiomorphogenic effects of basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) are strongly dependent on the structure of the fibrin clots. Our findings suggest that bFGF/VEGF primarily stimulate the proliferation of endothelial cells, whereas the three-dimensional architecture of the fibrin matrix is decisive for capillary morphogenesis.

Animals↗

PubMed1989

Influence of various structural domains of fibrinogen and fibrin on the potentiation of plasminogen activation by recombinant tissue plasminogen activator.

Fibrinogen, fibrin, and related fragments have varying stimulatory effects on the initial rate of the activation of human plasminogen ([ Glu1]Pg) by recombinant tissue plasminogen activator (rt-PA). A detailed analysis of this enhancement was undertaken using various purified and complexed forms of the known domains of fibrin(ogen) with a view to gaining additional knowledge regarding the substructures of fibrinogen and fibrin that are important for their stimulatory capacities. Both arvin-mediated fibrin, as well as fibrinogen fragments generated as a result of its cleavage with CNBr, stimulate the activation in a biphasic manner, most likely as a result of changes in the promoter molecule accompanying the denaturation processes that are normally employed to either solubilize or generate these particular promoters. Using purified fibrinogen and fibrin fragments, it was found that fragment E, which binds to [Glu1]Pg, does not enhance the activation reaction, while fragment D1 has a potentiating effect. This suggests that the binding of [Glu1]Pg to fibrin(ogen) alone is not, in itself, sufficient for stimulation of activation to occur, but that the rt-PA-fibrin(ogen) interaction is fundamental to this same process. All purified and mixtures of fragments containing the fragment D domain (e.g., D2E, X-oligomer, fragment X) stimulate the reaction to a greater degree than fibrinogen and fragment D1. It is concluded that the fibrinogen D domain is a sine qua non for the enhancement reaction, while structures containing the E domain had a symbiotic effect on enhancement.

Binding Sites↗

PubMed1999

Repair of fistulas-in-ano using autologous fibrin tissue adhesive.

PURPOSE: Our goal was to determine if autologous fibrin tissue adhesive derived from the precipitation of fibrinogen using a combination of ethanol and freezing, could be used to completely close both simple and complex fistulas-in-ano. METHODS: A 26-patient pilot study was performed in which 100 ml of a patient's blood was drawn 90 minutes before surgery. Autologous fibrin tissue adhesive was prepared. In the operating room the patient underwent an examination under anesthesia, and the primary and secondary fistula tract openings were attempted to be identified. The fistula tract was curetted, and autologous fibrin tissue adhesive was injected into the secondary fistula tract opening until fibrin glue was seen coming from the primary opening. A petroleum jelly gauze was then applied over the secondary opening, and the patient was sent home. Follow-up visits were scheduled for one week, one month, three months, and one year later. RESULTS: Twenty-six patients received autologous fibrin tissue adhesive fistula injections, with a mean follow-up of 3.5 months. Initial results were encouraging. Twenty-one of 26 patients (81 percent) had successful initial closure of their fistulas. Two of five failures were injected a second time, and one closed, giving an overall successful closure rate of 85 percent (22/26 patients). Of five patients who failed, mean time to failure was 3.8 weeks. In addition, there was no evidence of infection or complications related to the procedure. CONCLUSION: Our initial results are optimistic and require further support through longer follow-up data. Fibrin glue treatment of anorectal fistulas offers a unique mode of management that is safe, simple, and easy for the surgeon to perform. By using autologous fibrin tissue adhesive the patient avoids the risk of anal incontinence and the discomfort of prolonged wound healing which may be associated with fistulotomy.

Adult↗

PubMed1999

Technical manual for manufacturing autologous fibrin tissue adhesive.

PURPOSE: The aim of this article is to provide a concise and simple technical manual for manufacturing autologous fibrin tissue adhesive derived from the precipitation of fibrinogen using a combination of ethanol and freezing for surgery. METHODS: All materials and equipment needed to manufacture ethanol-based autologous fibrin tissue adhesive are listed. In addition, step-by-step instructions are provided to allow for easy and rapid fibrin adhesive production. RESULTS: Ethanol-based autologous fibrin tissue adhesive can be manufactured in under 60 minutes. Furthermore, at our institution the startup cost for manufacturing ethanol-based autologous fibrin tissue adhesive was under $2,500.00. CONCLUSION: Ethanol-based autologous fibrin tissue adhesive is a safe, reliable, and easily manufactured autologous fibrin tissue adhesive that can be made by a trained technician in any blood bank, pharmacy, or surgical laboratory.

Ethanol↗

PubMed1995

Effects of fibrin on the angiogenesis in vitro of bovine endothelial cells in collagen gel.

The effect of fibrin on angiogenesis in vitro was investigated using an experimental model of tube formation by bovine capillary endothelial cells (BCEs) in type I collagen gel. One milligram per milliliter of fibrin added into type I collagen gel significantly increased the length of the tubular structures formed by BCEs in the gel by about 180% compared with type I collagen only. The facilitating effect of fibrin on tube formation by BCEs was inhibited by either anti-basic fibroblast growth factor (bFGF) IgG (25 micrograms/ml) or anti-urokinase type plasminogen activator (uPA) IgG (10 micrograms/ml) added to the gel and culture medium, but not by anti-tissue type plasminogen activator (uPA) IgG (10 micrograms/ml) added to the gel and culture medium, but not by anti-tissue type plasminogen activator (10 micrograms/ml) or non-immune IgG. The Arg-Gly-Asp (RGD) containing peptides (100 micrograms/ml) added to the culture medium also suppressed tube formation by BCEs in fibrin-containing type I collagen gel, but not in type I collagen gel. These results suggest that the increased release of bFGF and uPA by BCEs therefore plays a role in the angiogenic effect of fibrin in vitro, and the angiogenic effect of fibrin is mediated by the RGD sequence in fibrin, probably via the function of integrin receptor of the BCEs.

Amino Acid Sequence↗

PubMed1996

Altered properties of the fibrin gel structure in patients with IDDM.

High plasma fibrinogen levels are associated with vascular complications in the general population. Fibrin, the structural element in a clot, is derived from fibrinogen by activation of thrombin. An abnormal fibrin gel structure has been demonstrated in patients with myocardial infarction and in diabetic patients during poor metabolic control. In the present study the properties of fibrin gel structure were investigated in 20 patients with insulin-dependent diabetes mellitus (IDDM): 10 patients without (age: 30 +/- 8; diabetes duration: 7 +/- 6 years), and 10 patients (age: 44 +/- 7; diabetes duration: 27 +/- 9 years) with microangiopathy. Fifteen healthy subjects served as controls (age: 40 +/- 8 years). The glycosylated haemoglobin level (HbA1c) was elevated (p < 0.001) in the patients: 6.5 +/- 1.5% in diabetic patients without, and 7.1 +/- 1.0% in diabetic patients with microangiopathy. C-reactive protein and plasma fibrinogen were similar as compared to healthy control subjects. The properties of the fibrin gel structure; i.e. the permeability coefficient (Ks) and the fibre mass length ratio (mu) formed in recalcified plasma on addition of thrombin were investigated. Ks was decreased in the diabetic patients, with (6.5 +/- 2.0 cm2; p < 0.01) and without microangiopathy (6.5 +/- 2.7 cm2; p < 0.05), as compared to healthy subjects (10.0 +/- 3.4 cm2), while mu was not significantly (p = 0.14) altered. The results indicate a lower fibrin gel porosity in patients with IDDM, despite normal plasma fibrinogen and irrespective of microangiopathy. The abnormal fibrin gel structure may be due to an increased glycosylation of the fibrin (-ogen) molecule caused by long-term hyperglycaemia and may be of importance for the development of angiopathy in diabetic patients.

Adult↗

PubMed2004

[Fibrin glue for closing conjunctival wounds in ophthalmic surgery].

BACKGROUND: Tissue adhesives offer the attractive prospect of sutureless surgery and provide a mechanism for repairing potentially difficult surgical wounds. We examined the ability of fibrin glue--instead of sutures--to close conjunctival wounds at the end of different ophthalmic surgeries. METHODS AND PATIENTS: Between 2002 and 2003 the fibrin glue Beriplast was used in our department to close the conjunctival wound in 100 eye muscle surgeries, 10 scleral buckling procedures in retinal detachment, and 20 pars plana vitrectomies. RESULTS: No patient showed postoperative adverse or allergic reactions, bacterial infections, inflammation, or delayed healing. The healing process of the conjunctiva takes a similar time course as in suture closure, but without disturbing suture ends and knots. In children with extensive Tenon's fascia, adaptation of the conjunctiva is safer using sutures. The necessary time using fibrin glue is reduced to one-fourth of the usual 4-8 min necessary for suturing the conjunctiva. The costs for fibrin glue are the same as for Vicryl 9/0, i.e., approximately 18-20 Euros per patient. CONCLUSIONS: Fibrin glue for closing conjunctival wounds results in good adaptation, is time saving, effective, and not more expensive than a suture with a high-end needle. Especially the thin atrophic conjunctiva in adults will tear using sutures in contrast to the very fast and effective adaptation with fibrin glue. Application of fibrin glue is limited in children with extensive Tenon's fascia: in these patients a suture is superior for good adaptation of the conjunctiva.

Adult↗

PubMed1997

[Effect of cataract technique and duration of surgery on fibrin reaction after IOL implantation].

BACKGROUND: Having changed our cataract operation technique from ECCE to phacoemulsification (PE) we had the impression of less fibrinous membranes postoperatively. METHOD: To ascertain whether our impression was correct, we examined the last 2056 IOL implanted cataract patients retrospectively. RESULTS: In the 2056 cataract cases we found 152 fibrinous reactions (7.4%). We observed after ECCE (n = 586) a 12.8% rate of fibrinous membranes, after phacoemulsification (PE) with sutured 6.5-mm corneoscleral incision (n = 546) 7.0%, and after PE with clear corneal self-sealing 4.1-mm incision (n = 924) only 3.9%. In 56% of these patients we found diabetes, in 13% former uveitis with posterior synechiae, in 11% glaucoma with rigid pupil, and in 10% pseudoexfoliation syndrome. In those cases with no diabetic retinopathy but known diabetes (n = 198), we found a 27% rate of fibrin reactions following ECCE (12 mm), 12% following PE (6.5 mm) and 8% following PE (4.1 mm). In non-proliferative diabetic retinopathy (n = 80) a 32% rate of fibrinous changes was observed after ECCE, 18% after PE (6.5 mm), and 9% after PE (4.1 mm). In cases of uncomplicated ECCE (n = 341) the rate of fibrinous reactions amounted to 22.4% following prolonged procedures (> 50 min) by residents, while it was as low as 9.5% following operations of short duration (< 30 min) by experienced surgeons. Intraocular injection of tPA (25 micrograms) was the most effective treatment. CONCLUSION: The self-sealing corneal small incision cataract technique guarantees a short duration of the surgical procedure and the last fibrinous reactions.

Cataract Extraction↗

PubMed2004

Endoscopic hemostasis using fibrin adhesive to treat hemorrhage in the upper digestive system.

PURPOSE: There are several methods of achieving endoscopic hemostasis of hemorrhage in the upper digestive system. We compared the therapeutic results and advantages of using a local injection of fibrin adhesive for endoscopic hemostasis, which we have found more effective than other hemostatic methods. METHODS: Between October 2000 and April 2002, 16 patients with hemorrhage in the upper digestive system underwent endoscopic hemostasis using fibrin adhesive. The hemorrhage was caused by a hemorrhagic tendency from liver disease, anticoagulant therapy, or failed hemostasis with clipping or local ethanol injection. The fibrin adhesive was injected through a standard 21-gauge endoscopic needle using the so-called sandwich method. RESULTS: Hemostasis was successfully achieved by a single local injection of fibrin adhesive, in all except one patient who had been on anticoagulant therapy for a long time and needed an additional local injection of fibrin adhesive. CONCLUSION: Fibrin adhesive does not cause any tissue injury, and a sufficient amount can be injected endoscopically even in patients with liver dysfunction and those on anticoagulant therapy. Thus, we think that endoscopic hemostasis with fibrin adhesive is safe and effective.

Aged↗

PubMed2006

Less chronic pain following mesh fixation using a fibrin sealant in TEP inguinal hernia repair.

Endoscopic hernia repair methods have become increasingly popular over the past 15 years. The postulated main advantages of the endoscopic technique are less postoperative pain, early recovery and lower recurrence rates. Fixation of the endoscopic mesh seems to be necessary to minimize the risk of recurrence. Stapling has been implicated to cause chronic inguinal pain syndromes. We performed a retrospective study on male patients who were endoscopically operated on primary inguinal hernias. Our aim was to clarify whether mesh fixation using a fibrin sealant is as safe and reliable as conventional stapling. Additionally, we compared the prevalence of chronic inguinal pain. A standardized population of 133 male patients (mean age 55.9 years) with 186 (80 unilateral; 53 bilateral) consecutive primary laparoscopic total extraperitoneal inguinal hernia repairs was assigned to two groups, depending on whether stapling or a fibrin sealant had been used for mesh fixation. A retrospective case control study was performed to conduct statistical analysis based on the following parameters: recurrence, complications, chronic inguinal pain, foreign body sensation and numbness. Hernia repairs numbering 173 (staples n=87; fibrin n=86) were followed up for a mean duration of 23.7 (11-47) months. The prevalence of chronic inguinal pain was significantly (P=0.002; Fisher exact test) higher in the stapled group-20.7% than in the fibrin sealant group with a prevalence of 4.7%. In terms of recurrence rate, complications and foreign body sensation, fewer patients were affected in the fibrin group than in the reference population, although the differences were not statistically significant. There were no major complications in either of the groups. The mean postoperative stay in hospital was 1.4 days. Fibrin sealing is as effective as stapling in providing secure mesh fixation. The fibrin group displayed a statistically significant lower prevalence of chronic pain syndromes. Mesh sealing provides adequate fixation and reduces the risk of chronic inguinal pain as a complication of the intervention.

Case-Control Studies↗

PubMed1995

Prevention of residual ventricular septal defects with fibrin sealant.

BACKGROUND: Modern echocardiography now allows for the detection of a substantial number of residual ventricular septal defects (VSDs) after surgical patch repair that remained hidden in the past. Mostly without hemodynamic significance, residual VSDs may have clinical consequences (progressive dehiscence, hemolysis, prophylactic antibiotic treatment, endocarditis). To reduce the number and size of residual VSDs we performed an experimental and a clinical study. METHODS: (1) In an experimental setup, burst pressure of 60 fibrin glue-sealed defects (calibrated between 1.0 and 5.0 mm in diameter) was determined using a computerized recording system and pressure loads up to 500 mm Hg. (2) In a prospective clinical trial with blinded postoperative echocardiographic controls VSD closure was performed in 36 consecutive patients (age, 37 +/- 40 months; range, 4 to 134 months) using a polytetrafluoroethylene patch and running sutures reinforced with pledgets (22 of 36 patients) or sealed with fibrin glue (14 of 36 patients) in accordance to the surgeon's preference. RESULTS: (1) Experimentally, mean pressure load achieved was more than 500 +/- 0 mm Hg for 1.0-mm defects, 413 +/- 52 mm Hg for 2.5-mm defects, 363 +/- 58 mm Hg for 4.0-mm defects, and 313 +/- 48 mm Hg for 5.0-mm defects (r 0.873, p < 0.001). (2) Clinically, all patients survived. Residual VSDs at echocardiography were observed in 16 of 22 patients (72%) for reinforced versus 5 of 14 patients (36%) for sealed with fibrin glue (p < 0.05). Diameter of residual VSDs accounted for 1.3 +/- 1.2 mm for reinforced versus 0.3 +/- 0.4 mm for sealed with fibrin glue (p < 0.01). Hemodynamically significant residual VSDs were fond in 2 of 22 patients (9%) for reinforced versus 0 of 14 patients (0%) for sealed with fibrin glue (p = not significant). CONCLUSIONS: Small defects sealed with fibrin glue resist physiologic pressure load. Fibrin glue sealing of prosthetic patches during intracardiac VSD repair allows for significant reduction of number and size of residual VSDs. Improved long-term outcome can be expected.

Anti-Bacterial Agents↗

PubMed1994

Polymorphic forms of Lp(a) with different structural and functional properties: cold-induced self-association and binding to fibrin and lysine-Sepharose.

Two different Lp(a) polymorphs were isolated from the same individual and shown to have important differences both in their solution properties and in interaction with lysine Sepharose and fibrin. One Lp(a) particle (d-Lp(a)) with a large apo(a) isoform had a density of 1.087 g/ml and a molecular weight of 3.17 million, while the other Lp(a) particle with a small apo(a) isoform having a mobility faster than that of apoB was larger and had a molecular weight of 3.75 million and a density of 1.054 g/ml. D-Lp(a) underwent cold-induced self-association and also had a higher affinity for lysine Sepharose, whereas the other Lp(a) polymorph did not. Both Lp(a) particles bound fibrin via two different binding sites, one of which involved fibrin lysine residues which are also recognized by plasminogen. Lysine-mediated binding of d-Lp(a) by fibrin was ten times stronger than that of the other Lp(a) particle, whereas non-lysine-mediated binding of either Lp(a) species by fibrin was of equal strength. At saturation, 80% of d-Lp(a) bound fibrin at sites that did not involve lysine residues, whereas only 33% of the other Lp(a) polymorph bound to these sites. These findings indicate that the binding of Lp(a) to fibrin is more complex than previously thought and imposes another layer of difficulty on our understanding of how Lp(a) regulates and/or impairs fibrinolysis.

Aminocaproic Acid↗

PubMed1984

Crosslinked fibrin derivatives and fibronectin in ascitic fluid from patients with ovarian cancer compared to ascitic fluid in liver cirrhosis.

Ascitic fluid from patients with ovarian cancer and from patients with alcohol induced liver cirrhosis were compared in respect to hematological and related parameters (content of fibrinogen and fibrin (ogen) degradation products, fibrinopeptide A, F-CB3 related antigen, ratio of crosslinked fibrin to non crosslinked fibrin (ogen), fibronectin and total protein). In tumor ascites all parameters except FPA were significantly elevated compared with cirrhosis ascites. Tumor ascites contains a six-fold higher level of fibrin (ogen) degradation products. A considerable portion of it constitute crosslinked (factor XIII induced) high molecular weight fibrin derivatives. Their content is approx. 10 times higher in tumor ascites than in cirrhosis ascites. Characterization of the crosslinked fibrin derivatives revealed the presence of fragments DD, DY, and some other fragments compatible with XY, DXD, DXY, YXY and DXX. The fibronectin content is also significantly higher in tumor ascites compared with cirrhosis ascites. The value ranges showed no overlap. The findings suggest a turnover of fibrinogen in both ascitic fluids via coagulation and fibrinolysis. In tumor ascites however, fibrinogen seems to be catabolized to a higher degree via the degradation of crosslinked fibrin.

Ascitic Fluid↗

PubMed1987

The resistance of fibrin-stimulated tissue plasminogen activator to inactivation by a class PAI-2 inhibitor (minactivin).

Solid phase fibrin was an efficient stimulator of the tissue-type plasminogen activator (t-PA), and the plasmin produced could be detected by colorimetric assay of the soluble phase above the fibrin. However the fibrin-stimulated activity of t-PA was not inhibited by minactivin. This result was in contrast to that obtained with poly-D-lysine (PL) stimulated t-PA, where minactivin was a potent inhibitor. However, if PL was added to fibrin-bound t-PA, the enzyme once again became susceptible to minactivin inhibition. This occurred without release of t-PA from the fibrin matrix. Minactivin alone did not bind to fibrin or to the t-PA fibrin complex. It was therefore concluded that minactivin normally has no significant role in the regulation of t-PA mediated fibrinolysis, but this effect can be induced by PL.

Drug Interactions↗

PubMed1989

Comparison of affinities of urokinase and tissue plasminogen activator for fibrin clots.

Affinities of low molecular weight two-chain urokinase (UK) and tissue plasminogen activator (t-PA) for fibrin clots were investigated by using clot lysis rates to estimate an affinity (Kd) between activator and fibrin clots. Lysis rates were obtained using a simple spectrophotometric based clot lysis assay which is described here. Fibrin clots, containing residual plasminogen, were suspended in a 1 ml cuvette and the increase in absorbance at 280 nm due to release of soluble fibrin peptides measured over a 150 to 250 minute time period. Lysis rates were obtained from plots of time squared vs absorbance change. Plots of activator concentration vs reciprocal rates yielded regression coefficients of 0.999 and Kd values of nM for the affinity of both activators for fibrin clots. Although both activators are known to differ in affinity for fibrin, they nonetheless had similar affinities and lysis rates for the insoluble fibrin clots. This assay also suggested possible synergism; rates over twice that expected by an additive effect were observed when the two activators were mixed at 0.3 to 7.6 nM each.

Drug Synergism↗

PubMed1990

Single chain-urokinase binds to oxidized fibrin(ogen) derivatives.

Single chain- urokinase (scu-PA), in contrast to two chain urokinase, is a physiological plasminogen activator of fibrin selectivity. The mechanism of selective fibrinolysis of scu- PA has not been clarified up to now. This study has shown that fibrin selectivity might involve oxidative processes. Binding studies with immobilized oxidized fibrinogen degradation products (FDP) demonstrated higher affinity of scu-PA to oxidized than to unmodified FDP. The fibrin(ogen) domain responsible for this oxidant mediated increase of scu-PA affinity is localized in the D-subunit of fibrin(ogen). Thus, experimental data upon the interaction of scu-PA with fibrin(ogen) using oxidized and I- labelled fibrin(ogen) might be interpreted with caution: the oxidized product may behave in a distinct manner than the unoxidized, native, one. Activated leukocytes release large amounts of scu-PA and of oxidants of the chloramine type. The oxidants could contribute significantly to fibrinolysis and proteolysis in areas of inflammation, preparing fibrin for its specific degradation. The present data support the concept of an involvement of oxidative processes in the fibrinolytic pathway.

Fibrin Fibrinogen Degradation Products↗

PubMed1991

Studies on fibrin network structure in human plasma. Part II--Clinical application: diabetes and antidiabetic drugs.

Using measurements of fibrin fibre thickness (microT) derived from turbidity and permeability (tau) of clotted plasma, it has been found that glucose in vitro added to plasma decreases permeability of the network despite unaltered fibrinogen conversion. Fibrin fibre thickness (microT) in uncontrolled diabetes is found significantly reduced. In diabetic plasma the degree of conversion to fibrin is similar to that in age and sex matched plasma from non-diabetics: the effect on fibrin network and fibre thickness probably arises from glycosylation of fibrinogen. Studies with Gliclazide, Metformin, Glibenclamide and insulin have shown that while all other drugs tested have no effect, Gliclazide increases fibrin fibre thickness (microT) significantly, diminishes tensile strength and reduces permeability. In separate experiments lysability of 125I-labelled fibrin networks developed in the presence of all four hypoglycaemic agents by tissue activator was tested. Networks developed in the presence of Metformin were found to lyse more quickly, followed by insulin and Gliclazide. Alterations induced in fibrin networks in diabetes may be nullified by some oral hypoglycaemic agents such as Gliclazide and not by others. Whether nullification of such changes has long-term effects in reducing the incidence of vascular disease in diabetics remains to be established.

Adult↗