(1/247) Histological changes in the rat common carotid artery induced by aneurysmal wrapping and coating materials.

Histological changes in and around the arterial walls of rats were investigated following topical application of aneurysmal wrapping and coating materials, including a fibrin glue, a cyanoacrylate glue (Biobond), and cotton fibers (Bemsheet). Bilateral common carotid arteries were exposed using sterile techniques, and one of the test materials was applied to the right artery. The left artery was used as the control. Changes in arterial histology were evaluated at 2 weeks, 1 month, 2 months, and 3 months after surgery. The fibrin glue was surrounded by intense inflammation at 2 weeks after surgery. Both the fibrin glue and inflammation had disappeared at 2 months, but the glue had induced mild inflammation in the adventitia. Biobond caused chronic inflammation, necrosis of the media, and thickening of the arterial wall due to fibrosis in both the media and adventitia. Bemsheet produced chronic inflammation, progressive fibrosis, and granuloma. Connective tissue increased in the adventitia, but no major changes were observed in the media. The Bemsheet fibers remained unchanged, and adhered to the arterial wall. Although arterial stenoses were not observed in the present study, the results suggest that cyanoacrylate glue can cause the arterial occlusive lesions observed following aneurysm surgery.  (+info)

(2/247) Postoperative magnetic resonance imaging after acoustic neuroma surgery: influence of packing materials in the drilled internal auditory canal on assessment of residual tumor.

Serial magnetic resonance (MR) images taken after acoustic neuroma surgery were analyzed to evaluate the pattern and timing of postoperative contrast enhancement in 22 patients who underwent acoustic neuroma removal via the suboccipital transmeatal approach. The opened internal auditory canal (IAC) was covered with a muscle piece in nine patients and with fibrin glue in 13. A total of 56 MR imaging examinations were obtained between days 1 and 930 after surgery. MR imaging showed linear enhancement at the IAC within the first 2 days after surgery, and revealed nodular enhancement on day 3 or later in patients with a muscle piece. MR imaging tended to show linear enhancement at the IAC, irrespective of the timing of the examination in the patients with fibrin glue. Postoperative MR imaging on day 3 or later showed the incidence of nodular enhancement in patients with muscle was significantly higher than in patients with fibrin glue. The results illustrate the difficulty in differentiating nodular enhancement on a muscle piece from tumor by a single postoperative MR imaging study. Therefore, fibrin glue is generally advocated as a packing material of the IAC because it rarely shows masslike enhancement on postoperative MR imaging. When a muscle piece is used in patients at high risk for postoperative cerebrospinal fluid leaks, MR imaging should be obtained within the first 2 days after surgery, since benign enhancement of muscle will not occur and obscure the precise extent of tumor resection.  (+info)

(3/247) Modulation of vascular cell growth kinetics by local cytokine delivery from fibrin glue suspensions.

PURPOSE: Fibrin glue (FG) has been used as a delivery system for bioactive agents on grafts and angioplasty sites. Reports from two different institutions suggest that heparin concentrations of 500 U/mL in FG inhibit smooth muscle cell (SMC) proliferation, but do not effect endothelial cell (EC) proliferation. The purposes of this study were to (1) quantify the diffusive release of fibroblast growth factor-1 (FGF-1) and heparin from FG; (2) determine the effect of heparin and FGF-1 on SMC proliferation when the cells are immediately plated on the FG; and (3) by means of the diffusive release data, design a new in vitro model that may differentiate the effect of FG-incorporated FGF-1 and heparin, rather than the released, solubilized components of these two factors, on SMC and EC proliferation. METHODS: 125I-FGF-1 or 3H-heparin release from FG into the overlying media was measured serially in a 96-hour period, either with or without cells. SMCs were immediately plated on FG containing various concentrations of FGF-1 and heparin. SMCs or ECs were plated on identical groups of FG containing FGF-1 and heparin 24 hours after the FG was made to exclude the effect on cell growth of the initial release of FGF-1 into the media. RESULTS: In the first 24 hours, 70% +/- 1% of the FGF-1 and 59% +/- 2% of the heparin in the FG was released into the overlying media, with minimal release occurring thereafter. The cell type or absence of cells did not affect release, but there was five times more FGF-1 and four times more heparin in the media at 72 hours for the immediate plating versus the delayed plating because of a diffusive release primarily in the first 24 hours. A heparin concentration of 500 U/mL inhibited SMC proliferation, as compared with 5 U/mL heparin, only when immediate plating of SMCs was used. Comparing immediate versus delayed SMC plating, at equivalent FGF-1 and heparin doses, immediate plating induced greater proliferation than delayed plating; this was likely caused by the higher soluble FGF-1 concentration. Heparin doses as high as 500 U/mL had little effect on SMC proliferation. In contrast, ECs died with delayed plating on FG containing 500 U/mL heparin, and their growth was inhibited at 50 U/mL heparin, as compared with 5 U/mL heparin. CONCLUSION: The differences in SMC proliferation when comparing immediate versus delayed plating are likely caused by diffusive release of heparin and FGF-1 into the media. Our ongoing work uses an optimized in vitro FG system that minimizes the effects of soluble factors. This is an important distinction, because the cytokines that are released in vivo will be removed by blood flow and, thus, may not exert an effect unless they are contained within the FG.  (+info)

(4/247) Mesh-and-glue technique to prevent leakage of cerebrospinal fluid after implantation of expanded polytetrafluoroethylene dura substitute--technical note.

Expanded polytetrafluoroethylene (ePTFE) can be used as a dura substitute but is associated with leakage of cerebrospinal fluid (CSF) through the suture line. Fibrin glue alone may not prevent this problem. This new method for sealing the suture line in ePTFE membrane uses an absorbable polyglycoic acid mesh soaked with fibrinogen fluid placed on the suture line. Thrombin fluid is then slowly applied to the wet mesh, forming a large fibrin membrane reinforced by the mesh over the suture line. Only one of 33 patients in whom this technique was used had CSF leakage, whereas 12 of 59 patients in whom a dural defect was closed with ePTFE alone showed postoperative subcutaneous CSF collection (p < 0.05). Our clinical experiences clearly show the efficacy of the mesh-and-glue technique to prevent CSF leakage after artificial dural substitution. Mesh and glue can provide an adequate repair for small dural defect. The mesh-and-glue technique may also be used for arachnoid sealing in spinal surgery.  (+info)

(5/247) Hemostatic efficacy of fibrin sealant (human) on expanded poly-tetrafluoroethylene carotid patch angioplasty: a randomized clinical trial.

PURPOSE: The efficacy of solvent-detergent-treated fibrin sealant (human [FSH]) for controlling anastomotic bleeding from expanded polytetrafluoroethylene (ePTFE) patch angioplasty during carotid endarterectomy was evaluated, and FSH was compared with thrombin-soaked gelatin sponge (Gelfoam; TSG). METHODS: The study was of a randomized, open-label, single-site, single-treatment, parallel design that took place in a referral center with hospitalized patients. Forty-seven adult patients (33 men, 14 women) underwent elective carotid endarterectomy. Patients were randomized to receive either FSH (N = 24) or TSG (N = 23). FSH was obtained as an investigational new drug. FSH was applied as a liquid by means of a dual-syringe technique. Heparin anticoagulation, patch thickness, and suture type were standardized. Two different needle sizes were used (CV-6, PT-13: N = 21 [FSH: N = 10, TSG: N = 11]; CV-6, PT-9: N = 26 [FSH: N = 14, TSG: N = 13]). The FSH or TSG was applied to the ePTFE patch, and then blood flow was restored through the carotid artery. Degree of anticoagulation was assessed by anti-factor Xa activity. The time from restoration of carotid blood flow until achieving hemostasis was recorded. The blood loss from patch suture hole bleeding was measured. Completion intraoperative duplex ultrasound scanning was performed in all cases. Heparin was reversed with protamine sulfate. The primary end point was successful hemostasis within 15 minutes of restoration of carotid blood flow. The secondary end points were the amount of blood loss caused by suture line bleeding and the time to achieve hemostasis. RESULTS: There was no difference in the number of patients with complete hemostasis at 15 minutes (TSG, 13 of 23; FSH, 12 of 24; P =.77). The measured blood loss was 99.0 +/- 119.9 (SD) mL for TSG, and 105.0 +/- 107.9 mL for FSH (P =.86). The time to hemostasis was the same for both groups (TSG, 16.5 +/- 16.5 minutes; FSH, 16.6 +/- 14.2 minutes; P =.97). Within both treatment groups, the use of larger needles (PT-13) was associated with greater blood loss (FSH, 169.7 +/- 124.2 mL; TSG, 172.7 +/- 151.5 mL) than was the use of smaller needles (PT-9; FSH, 58.8 +/- 66.3 mL; TSG, 34.1 +/- 25.6 mL; P =.036, P =.001, respectively). There were no postoperative strokes or bleeding complications in either group. No abnormalities were shown in either group by means of completion carotid duplex ultrasound scanning. CONCLUSION: FSH was equivalent, but not superior to, TSG in achieving hemostasis during carotid endarterectomy performed with ePTFE patch angioplasty. Adhesion properties of FSH to ePTFE are possibly different than those to native tissue and warrant additional investigation.  (+info)

(6/247) Preoperative embolization of intracranial meningiomas with a fibrin glue preparation.

BACKGROUND AND PURPOSE: Preoperative embolization expands the spectrum of meningioma that can be operated on safely. Our goal was to achieve the distalmost loading of the vascular bed and confluent tumor necrosis with a fibrin glue preparation in the preoperative embolization of meningiomas. METHODS: Between 1992 and 1997, 80 patients with a meningioma had diagnostic angiography with a standard transfemoral Seldinger technique, performed with a 6F guiding catheter and digital subtraction angiography. Preoperative embolization was carried out in the same session with an additional microcatheter system. Fibrin glue was the only component used. In all cases, CT was performed immediately after embolization; in nine patients, MR imaging was also performed. RESULTS: Angiography verified the elimination of tumor blush in all patients. The high-density areas seen on postembolization CT scans, caused by the fibrin glue dispersed in the embolized supply area, were found to be necrotic at surgery and were easily removed by suction. Two (2.5%) of the 80 patients had complications associated with embolization that resulted in neurologic deficits. CONCLUSION: The most effective preoperative embolization of tumors requires a distalmost loading of the vascular bed. Fibrin glue, which is easy to use and safe to handle, causes confluent tumor necrosis within the injected vascular territory.  (+info)

(7/247) The S130K fibroblast growth factor-1 mutant induces heparin-independent proliferation and is resistant to thrombin degradation in fibrin glue.

OBJECTIVE: Site-directed mutagenesis is an important technique that can alter cytokine function, thereby eliciting desired responses. S130K is a mutation of fibroblast growth factor-1 (FGF-1), with lysine replacing serine in the heparin-binding site. We measured molecular stability and mitogenic activity of FGF-1 and S130K, both in the media and when suspended in fibrin glue (FG), on smooth muscle cells (SMCs) and endothelial cells (ECs) to determine if the mutation altered the function and potential clinical applicability. METHODS: EC and SMC proliferation of soluble FGF-1 or S130K at 0, 0. 1, 1, 10, or 100 ng/mL with heparin at 0, 5, 50, or 500 units (U)/mL was measured on growth-arrested cells in serum-free media. EC and SMC proliferation assays with cells on FG containing either FGF-1 or S130K at 0, 1, 10, 100, or 1000 ng/mL in combination with heparin at 0, 5, 50 or 500 U/mL were also performed during the exponential growth phase. Molecular degradation by thrombin was measured by sodium dodecylsulfate-polyacrylamide gel electrophoresis. RESULTS: S130K induces greater EC and SMC proliferation in the absence of heparin than FGF-1 does (P <.0001 for both the 10 and 100 ng/mL doses). S130K is also significantly more potent than FGF-1 in the presence of heparin. Heparin in the media enhances cytokine-induced SMC and EC proliferation at doses of 5 U/mL, but inhibits SMC proliferation at concentrations of 500 U/mL. For the FG data, unlike FGF-1, S130K induces EC and SMC proliferation in the absence of heparin. The addition of 5 U/mL of heparin enhances the proliferation induced by S130K. For ECs, as the heparin dose increases to 50 U/mL, proliferation decreases, as compared with the 5 U/mL concentration when either FGF-1 or S130K in the FG was compared at concentrations of 10, 100, and 1000 ng/mL (P <.01). S130K is more potent in FG than is FGF-1 both with and without heparin and exhibits maximal EC and SMC proliferation at 10 ng/mL, whereas FGF-1 activity is maximal at 100 ng/mL. Gel electrophoresis demonstrated that S130K was relatively more resistant to thrombin degradation than FGF-1. CONCLUSIONS: Site-directed mutagenesis changed the potency and the heparin dependency on cellular proliferation of FGF-1 in vitro. These techniques should allow the delivery of mutant growth factors to areas of vascular intervention to induce specific, desired responses. We believe that these studies will enhance our knowledge of the function of various regions of the FGF-1 molecule, allowing us to more precisely design increasingly more useful FGF-1 mutants.  (+info)

(8/247) Oozing type cardiac rupture repaired with percutaneous injection of fibrin-glue into the pericardial space: case report.

Two patients, a 56-year-old man and an 81-year-old woman who were admitted to hospital because of anteroseptal acute myocardial infarction, were initially treated successfully with direct percutaneous transluminal coronary angioplasty. However, both patients later developed sudden cardiogenic shock due to cardiac tamponade caused by left ventricular free wall rupture (LVFWR). Prompt, life-saving pericardiocentesis was performed, then fibrin-glue was percutaneously injected into the pericardial space. After the procedure, there was no detectable pericardial effusion on echocardiography and the hemodynamic state became stable. The surgical treatment was the standard procedure for LVFWR, but percutaneous fibrin-glue therapy can also be considered for oozing type LVFWR.  (+info)