fibrin and Aortic-Diseases

Fibrin is a major component of many atherosclerotic plaques. Within the intima there is continuous formation of fibrin, and continuous fibrinolysis. In aortic lesions, a lipoprotein bound to fibrin can be released by incubation with plasmin. Most of this lipoprotein is accounted for by Lp(a). The atherogenicity of Lp(a) may be more associated with lipid deposition than with inhibition of fibrinolysis. Fibrin degradation products may be chemotactic to monocyte-macrophages and stimulate smooth muscle cell proliferation.

Topics: Antigens; Aorta; Aortic Diseases; Arteriosclerosis; Binding Sites; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Humans; Lipoprotein(a); Lipoproteins

In trauma patients, resuscitation to endpoints below normal blood pressure (BP) levels may reduce further blood loss due to the rebleeding often caused by more aggressive resuscitation. However, patients whose BP is maintained at lower levels for extended periods are at increased risk for organ failure. The purpose of this study was to determine whether recombinant activated factor VII (rFVIIa) raises the BP level at which rebleeding occurs in a prospective, randomized, blinded study using a porcine model of uncontrolled hemorrhage and resuscitation. Thirty anesthetized 40-kg pigs were assigned to three groups (n = 10/group): control, low-dose rFVIIa (180 microg/kg), or high-dose (720 microg/kg). Vehicle or drug was infused 5 min before creating a 2.0-mm infrarenal aortotomy. Ten minutes later, resuscitation with lactated Ringer's (LR) solution at 100 mL/min was begun. Hemorrhage and LR volumes and BP were recorded continuously. We found that pretreatment with rFVIIa increased the mean arterial pressure at which rebleeding occurred during resuscitation (45 +/- 3, 69 +/- 5, and 66 +/- 6 mmHg in the control, low-dose, and high-dose groups, respectively, P = 0.003). Rebleed hemorrhage volume was reduced with rFVIIa (39 +/- 9, 22 +/- 7, and 26 +/- 5 mL/kg for control, and low and high dose, respectively; P = 0.055). This is the first study to show that rFVIIa increases the BP at which rebleeding occurs during resuscitation in an injury to a major artery, suggesting the formation of a tight, stronger fibrin plug in the presence of high concentrations of rFVIIa.

Topics: Animals; Antithrombins; Aorta; Aortic Diseases; Blood Pressure; Body Weight; Disease Models, Animal; Factor VII; Factor VIIa; Female; Fibrin; Hemorrhage; Pressure; Prospective Studies; Recombinant Proteins; Resuscitation; Secondary Prevention; Swine; Thrombin; Time Factors; Treatment Outcome

The incidence of infection following arterial reconstruction using synthetic graft materials varies from less than 1 to 5%. One of three mechanisms is thought to be responsible: 1. intraoperative contamination, 2. extension from adjacent infected or colonized tissue, or 3. hematogenous or lymphogenous seeding. We present ultrastructural data of a patient with a polymicrobial graft infection due to a prostheto-enteric fistula 16 years after reconstruction of an aortobifemoral graft. The polymer surface showed signs of biodegradation and was completely covered with a layer of plasma proteins. Disrupted fibroblasts on the intersegmental graft surface were surrounded by bundles of collagen. Gram-negative rods and grampositive cocci were embedded in an extracellular EPS matrix. Bacterial culture confirmed growth of Eikenella corrodens, Fusobacterium nucleatum and Peptostreptococcus species. Fibrin and granulation tissue from the neoadventitia started to mark off the inflammatory process. Transmission electron microscopy is a valuable tool for the investigation of alloplastic arterial devices. After 16 years of implantation the graft shows different signs of biodegradation.

Topics: Aorta, Abdominal; Aortic Diseases; Bacteriological Techniques; Biofilms; Blood Vessel Prosthesis; Coated Materials, Biocompatible; Collagen; Fibrin; Gram-Positive Cocci; Gram-Positive Rods; Granulation Tissue; Humans; Intestinal Fistula; Ischemia; Leg; Leriche Syndrome; Male; Microscopy, Electron; Middle Aged; Polyesters; Postoperative Complications; Prosthesis-Related Infections

Dissolution of the fibrin blood clot is regulated in large part by plasminogen activator inhibitor-1 (PAI-1). Elevated levels of plasma PAI-1 may be an important risk factor for atherosclerotic vascular disease and are associated with premature myocardial infarction. The role of the endogenous plasminogen activation system in limiting thrombus formation following atherosclerotic plaque disruption is unknown. This study found that genetic deficiency for PAI-1, the primary physiologic regulator of tissue-type plasminogen activator (tPA), prolonged the time to occlusive thrombosis following photochemical injury to carotid atherosclerotic plaque in apolipoprotein E-deficient (apoE(-/-)) mice. However, anatomic analysis revealed a striking difference in the extent of atherosclerosis at the carotid artery bifurcation between apoE(-/-) mice and mice doubly deficient for apoE and PAI-1 (PAI-1(-/-)/apoE(-/-)). Consistent with a previous report, PAI-1(+/+)/apoE(-/-)and PAI-1(-/-)/apoE(-/-) mice developed similar atherosclerosis in the aortic arch. The marked protection from atherosclerosis progression at the carotid bifurcation conferred by PAI-1 deficiency suggests a critical role for PAI-1 in the pathogenesis of atherosclerosis at sites of turbulent flow, potentially through the inhibition of fibrin clearance. Consistent with this hypothesis, intense fibrinogen/fibrin staining was observed in atherosclerotic lesions at the carotid bifurcation compared to the aortic arch. These observations identify significant differences in the pathogenesis of atherosclerosis at varying sites in the vascular tree and suggest a previously unappreciated role for the plasminogen activation system in atherosclerosis progression at sites of turbulent flow. (Blood. 2000;96:4212-4215)

Topics: Animals; Aorta, Thoracic; Aortic Diseases; Apolipoproteins E; Arteriosclerosis; Carotid Artery Diseases; Carotid Artery Injuries; Carotid Artery, Common; Carotid Stenosis; Disease Progression; Fibrin; Fibrinogen; Hemorheology; Male; Mice; Mice, Knockout; Photochemistry; Plasminogen; Plasminogen Activator Inhibitor 1

The acute platelet response and chronic smooth muscle cell (SMC) proliferation following aortic injury in apolipoprotein E-deficient mice was investigated. The purpose of this study was to evaluate whether thrombus formation would occur following plaque injury, to determine the type of thrombus that developed, and to evaluate SMC proliferation. Aortic injury was performed by squeezing the aorta between forceps. The response to injury reflects the findings primarily associated with plaque disruption. An attempt was made to exclude the use of injured vascular segments that showed marked injury to the media to minimize the effects that medial SMCs may have in thrombus formation. Acute and chronic experiments following injury were terminated at 30 min and at 2 weeks, respectively. Injury in normal and heterozygous mice and nonplaque injury in apolipoprotein E-deficient mice were accompanied by endothelial denudation. In apolipoprotein E-deficient mice, plaque injury, which released plaque contents, foam cells and fragments of foam cells, was followed by thrombus formation that contained degranulating platelets mixed with fibrin. Large platelet-fibrin aggregates were in close contact with disrupted plaques and were mixed with foam cell debris. In addition, small thrombi were in nonplaque areas following plaque disruptions. These thrombi were not associated with injury to the media and most likely represent a heightened thrombogenicity associated with plaque disruption. At 2 weeks following injury, a thickened neointima was present in both wild type and mutant mice. Lipid filled cells were seen only in the media but not in the intima of apo E -/- vessels at 2 weeks. The results suggest that plaque injury in homozygous apolipoprotein E-deficient mice promotes platelet-fibrin thrombus formation and that these thrombi are primarily associated with disrupted plaque contents. The results also suggest that the platelet response and SMC proliferation induced by aortic injury are not altered by hyperlipidemia caused by apolipoprotein E deficiency.

Topics: Animals; Aorta, Abdominal; Aortic Diseases; Apolipoproteins E; Arteriosclerosis; Blood Platelets; Cell Division; Disease Models, Animal; Endothelium, Vascular; Female; Fibrin; Genotype; Male; Mice; Mice, Inbred C57BL; Muscle, Smooth, Vascular; Thrombosis

Soluble fibrin/fibrinogen-related antigens and insoluble fibrin are present in virtually all samples of human aortic intima. Components of the soluble fraction were identified by SDS-PAGE and immunoblotting with specific antisera. The fibrinogen was characterized by increased proportions of low molecular mass (Mr) species (300 and 280 kD), the FDP by fragments DY and DD derived from crosslinked fibrin, and by fragment E that lacked fibrinopeptide A (FPA). Experiments suggest that fibrin is formed in situ, and free thrombin was present in all 10 samples analysed for prothrombin-related antigen (PtRA). Fibrin-derived fragment E is mitogenic, so fibrin degradation may provide continuing stimulation of smooth muscle cell (SMC) proliferation.

Topics: Aorta; Aortic Diseases; Arteriosclerosis; Electrophoresis, Polyacrylamide Gel; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinopeptide A; Humans; Muscle, Smooth, Vascular

Aortic aneurysms are characterized by the destruction of the extracellular matrix of the media, whereas occlusive disease involves excess matrix accumulation within the intima. Plasmin degrades extracellular matrix directly and indirectly by activation of latent metalloenzymes. To determine the expression of tissue- and urokinase-type plasminogen activators, immunoassay, fibrin autography, Northern analysis, and immunohistochemistry were performed on specimens of aneurysmal (n = 12), occlusive (n = 8), and healthy (n = 6) aorta.. Immunoassay of tissue-type plasminogen activator revealed 8.7 +/- 0.9 ng tissue-type plasminogen activator/mg extracted protein in aneurysmal aorta, 5.7 +/- 0.3 ng/mg in normal aorta, and 2.5 +/- 0.3 ng/mg in occlusive aorta (p < 0.05 for comparisons between all groups). No urokinase-type plasminogen activator antigen was detected by urokinase-type plasminogen activator immunoassay. Fibrin autography exhibited lytic activity at 64 kDa and 54 kDa attributable to tissue-type plasminogen activator and urokinase-type plasminogen activator. The vast majority of fibrinolysis was secondary to free tissue-type plasminogen activator and was greatest in aneurysmal disease and least in occlusive disease. There was only a small amount of lysis secondary to urokinase-type plasminogen activator. Expression of tissue-type plasminogen activator and urokinase-type plasminogen activators mRNA was comparable in aneurysmal and occlusive aortas. In contrast to occlusive disease, aneurysms had an inflammatory cell infiltrate characterized by the expression of urokinase-type plasminogen activator by specific mononuclear cells. Tissue-type plasminogen activator expression was evident in the intima of normal and diseased aorta and in the media of diseased aorta.. Differential expression of plasminogen activators within the arterial wall may contribute to the unique pathogenesis of aneurysmal and occlusive aortic disease.

Topics: Adult; Aged; Aorta, Abdominal; Aortic Aneurysm, Abdominal; Aortic Diseases; Arterial Occlusive Diseases; Autoradiography; Blotting, Northern; DNA Probes; Electrophoresis, Polyacrylamide Gel; Fibrin; Humans; Immunohistochemistry; Middle Aged; Plasminogen Activators

Fifteen patients (9 male, 6 female) undergoing peripheral vascular surgery were monitored during surgery for evidence of subclinical anticoagulation using the activated coagulation time (ACT), thromboelastography (TEG), and heparin titration monitoring. Assessments were made at 30-minute intervals before and after the occlusion clamp. Mean (+/- SD) ACT values preoperatively were 111 (17) seconds, and 10 minutes after 5,000 IU of heparin, the ACT was 264 (57) seconds (P < 0.001). Intraoperatively, there was a significant decline in ACT values at 30 minutes (ACT 228 [50] sec, P < 0.005) and 60 minutes (200 [46] sec, P < 0.001) postheparin. No significant difference in ACT was observed between samples drawn distally and proximally to the clamp. TEG profiles were abolished in all patients immediately following heparinization. However, in 2 patients nearly complete return of the TEG coagulation profile was observed prior to the termination of the procedure and was associated with ACT values less than 160 seconds. The heparin device was unable to accurately monitor heparin elimination at these low doses. Variability of patient response to heparinization necessitates the use of intraoperative monitoring of anticoagulation during peripheral vascular surgery.

Topics: Aged; Aged, 80 and over; Aortic Diseases; Arterial Occlusive Diseases; Blood Coagulation; Blood Vessel Prosthesis; Female; Femoral Artery; Fibrin; Heparin; Humans; Iliac Artery; Male; Middle Aged; Monitoring, Intraoperative; Peripheral Vascular Diseases; Thrombelastography; Titrimetry; Whole Blood Coagulation Time

Thrombotic occlusion is the major cause of myocardial infarction (MI), and fibrin accumulation appears to play a significant role in development of atherosclerotic lesions. Any factor that reduces the lysis of fibrin may thus increase the risk of MI, and it has been suggested that this accounts for the atherogenicity of the lipoprotein variant Lp(a). The characteristic feature of Lp(a) is an apoprotein which is homologous with part of the plasminogen molecule, and experiments in vitro suggest that it interferes with uptake and activation of plasminogen on cell surfaces and fibrin. The presence of Lp(a) also seemed to offer an explanation for the apparent absence of plasminogen from 70-80% of intimal samples. We have compared the levels of Lp(a) and plasminogen in normal intima and atherosclerotic lesions. In aortic intima there was no relation between Lp(a) and plasminogen, which was absent in some samples with no Lp(a), and present in others with high levels. In intravascular thrombi plasminogen was present at a rather constant concentration (16.3 +/- 4.6 micrograms/100 mg wet tissue), whereas Lp(a) varied over a 100 fold range (0-104 micrograms/100 mg). Plasminogen binds to fibrin and is activated on the fibrin clot, so levels in extracts may not fully represent Lp(a)/plasminogen interactions. After extraction the residual tissues and thrombi were treated with 1 M epsilon-aminocaproic acid (epsilon-aca) to elute lysine-bound components. Lp(a) was eluted from all but one intimal sample, confirming previous findings on its binding to fibrin in lesions, but there was no relation between the amounts of Lp(a) and plasminogen in the tissue eluates. Paradoxically, in the thrombi there was a weak positive correlation between Lp(a) and plasminogen in epsilon-aca eluates (r = 0.504, P = 0.05). These results do not support the hypothesis that Lp(a) displaces plasminogen in vivo, but the large amount of Lp(a) eluted by epsilon-aca suggests that its atherogenicity resides in preferential binding to fibrin, leading to increased lipid accumulation in lesions.

Topics: Adult; Aged; Aorta; Aortic Diseases; Arteriosclerosis; Binding, Competitive; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Humans; Lipoprotein(a); Lipoproteins; Lipoproteins, LDL; Male; Middle Aged; Myocardial Infarction; Plasminogen; Thrombosis

Experimental atherosclerosis was induced in a rabbit model by intimal damage of the infrarenal aorta followed by two months cholesterol feeding. The influence of four different antiplatelet drug regimens on acute platelet and fibrin deposition after transluminal angioplasty of the atherosclerotic abdominal aorta was then evaluated. The study group consisted of 32 New Zealand rabbits: 7 controls, 7 treated with prostacyclin (10 mg/kg/min i.v.), 5 treated with low-dose acetylsalicylic acid (2 mg/kg i.v.), 7 treated with acetyl-salicylic acid (5 mg/kg i.v.) and dipyridamole (2 mg/kg i.v.), and 6 treated with low molecular dextran (5 ml/kg). By 2 hours after angioplasty, there was a significant increase of the deposition of platelets (P less than 0.001) as well as fibrin (P less than 0.01) when comparing dilated to non-dilated segments in the control animals. There was no significant difference in the amount of platelets and fibrin deposition among the control and drug treated groups. Thus, in this animal model there appears to be no immediate benefit in using antiplatelet drugs during transluminal angioplasty. Although, this study did not address the potential long-term effects of antiplatelet drug therapy, future evaluation of the clinical benefits of these drugs in conjunction with transluminal angioplasty seems warranted.

Topics: Angioplasty, Balloon; Animals; Aorta, Abdominal; Aortic Diseases; Aortography; Arteriosclerosis; Cholesterol; Female; Fibrin; Male; Platelet Aggregation Inhibitors; Platelet Count; Rabbits; Thrombosis

Using cultured bovine aortic endothelial cells (BAEC), the authors attempted to determine whether prior irradiation would alter the susceptibility of these cells to three known injurious stimuli and, if so, whether the alteration would be related to radiation dose. BAEC were irradiated with 0, 5, or 10 Gy of gamma rays and, on the third postirradiation day, exposed to fibrin, nicotine, or bacterial endotoxin (lipopolysaccharide, LPS). Release of prelabeled 51Cr, representing cell lysis, cell detachment, or a combination of the two, was determined. Significant differences between irradiated and control cells were determined by using paired Student's t-tests. Irradiation did not appear to have altered the sensitivity of BAEC to fibrin-induced injury. Cells irradiated with 10 Gy of gamma rays, but generally not those irradiated with half this dose, showed a heightened susceptibility to nicotine. Contrary to the nicotine results, irradiated cells showed less cell detachment and lysis after exposure to LPS. These results suggest that the susceptibility of irradiated BAEC to harmful stimuli depends largely on the nature of the stimulus as well as the radiation dose.

Topics: Animals; Aorta; Aortic Diseases; Cattle; Disease Susceptibility; DNA; Endothelium, Vascular; Fibrin; Lipopolysaccharides; Male; Nicotine; Proteins

The aim of the present study was to evaluate the sequence of the immediate and the mid/long-term organization of the blood interface of a collagenous membrane used as vascular substitute in rats. The implants were prepared from calf skin type I insoluble collagen, obtained after acidic dispersion, in absence of chemical or tanning treatment. They were used to patch an aortic defect by means of microsurgical techniques. The animals were sequentially sacrificed for immediate hemocompatibility studies at 10 s, 30 s, 10 min, 3 h, and 6 h, for long-term analyses of the organization of the blood material interface at the 7th, 15th, 45th, 60th, 90th day following the surgery and each month until 14 months after aortic replacement. The superficial immediate events at the blood patch interface demonstrated erythrocytes heavily engulfed in a thin but dense fibrin mesh both at the patch and at the adjacent aortic wall surfaces. Neither adherent platelet nor platelet aggregate were detectable on the collagen patch surface. This fibrinoerythrocytic membrane covered the patch completely at 60 s and at 3 h the deposit was limited to 5-6 erythrocyte layers as confirmed by histology. It did not further develop on the 7th day. At the blood-collagen interface there progressively developed a tissue composed of active myofibroblasts, collagen bundles, and elastic fibers. After 4 months, nests of fibroendothelial cells were present, and between 6 and 14 months surface cell differentiation, although complete on the adjacent aorta was still incomplete on the bovine collagen patch, amorphous fibers, and fibroendothelial cells coexisting. Heterologous patch debris were still present 14 months after implantation and were associated with macroscopic and ultrastructural calcification, which need further investigations concerning the exact nature and mechanism of mineralization of vascular substitutes of biological nature.

Topics: Animals; Aorta; Aortic Diseases; Biocompatible Materials; Blood Vessel Prosthesis; Cattle; Collagen; Erythrocytes; Fibrin; Microscopy, Electron; Microscopy, Electron, Scanning; Rats; Rats, Inbred Strains; Skin; Time Factors

Arterial thrombi were induced in rat aorta by a new microsurgical procedure. These thrombi, originally platelet-fibrin masses, got progressively infiltrated by various cell types. Both the importance of mononuclear cells in organization and investment and the origins of foamy cells, smooth muscle-like cells and macrophages, are discussed. Rethrombosis is regularly found at all time intervals. Thrombus volume and its position with respect to the flap are calculated.

Topics: Animals; Aortic Diseases; Blood Platelets; Disease Models, Animal; Fibrin; Male; Rats; Rats, Inbred Strains; Thrombosis; Time Factors

Topics: Animals; Aortic Diseases; Aortography; Blood Coagulation; Cats; Collateral Circulation; Fibrin; Indomethacin; Partial Thromboplastin Time; Platelet Count; Prothrombin Time; Thrombosis

In the soft, gelatinous thickenings that appear to be the precursors of fibrous plaques, concentrations of plasma low-density lipoproteins (LP) and fibrinogen were three to four times higher than that in normal intima, but their concentrations of fibrin was not significantly higher. By contrast, in 60% of cholesterol-rich areas from more advanced plaques, fibrin (mean concentration 22.7 mg/100 mg lipid-extracted dry weight) was ten times higher than normal, and this was associated with a twelve-fold increase in a bound LP fraction that was released by incubation with fibrinolytic enzymes. The origin of this fibrin is uncertain, and to test similarity of fibrin in the lesion with that of mural thrombus free and bound LP, fibrinogen, and cholesterol were measured in thrombi and pseudo-intimas from prosthesis grafts. In the pseudo-intimas and the thrombi that were not covered with endothelium the concentrations of all these substances were very low, but in thrombi covered with endothelium the concentrations of free and bound LP were similar to those in intimal lesions. Thus, endothelialisation appears to promote accumulation of LP in mural thrombi.

Topics: Aged; Aorta; Aortic Diseases; Blood Vessel Prosthesis; Cholesterol; Endothelium; Female; Fibrin; Fibrinogen; Humans; Lipoproteins, LDL; Male; Middle Aged; Thrombosis

A prospective study was performed on 32 consecutive patients undergoing elective operations on the abdominal aorta. Dacron prosthetic grafts were used to replace resected abdominal aortic aneurysms or to bypass aorta-iliac occlusive disease. Complete coagulation studies were performed preoperatively, immediately postoperatively and 24 hours postoperatively. Twenty to 30 per cent of the patients had significant postoperative alterations in prothrombin time, partial thromboplastin time and platelet count. Fibrin monomer, fibrin split products and plasminogen were abnormal in 40 to 80 per cent of the patients postoperatively. Results of preoperative studies showed no significant abnormalities. One of the 32 patients had mild clinical evidence of disseminated intravascular coagulation postoperatively, which was treated with 5 units of heparin per kilogram per hour. Results of the study indicate that aortic grafting procedures frequently produce intravascular coagulation, either local or disseminated. In most patients, this is offset by activation of the fibrinolytic system. However, clinically significant sequelae may result, requiring prompt recognition and treatment.

Topics: Aged; Aorta, Abdominal; Aortic Aneurysm; Aortic Diseases; Arterial Occlusive Diseases; Blood Cell Count; Blood Coagulation Tests; Blood Platelets; Blood Vessel Prosthesis; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Humans; Male; Middle Aged; Postoperative Complications; Prospective Studies; Prothrombin Time; Thromboplastin

Following the administration of cholesterol for a period of 6-7 weeks, Scanning Electron Microscopic (S.E.M.) observations revealed mono-cellular, crater-like and dome-shaped endothelial changes on top of the large intimal plaques in the rabbit aortas. Finger-like and other shaped cell protrusions were observed at the edges of these crater-like and dome-shaped endothelial changes, giving the intimal plaques a rough appearance. At other sites, normal, smooth, although irregularly arranged, endothelial cells covered the lesions. By impregnating the cell borders with silver-nitrate or silver proteinate containing perfusates, it was possible in most cases to ascertain that the lesions were derived from changes in one cell or from changes in a small collection of cells. S.E.M.-observations further revealed crater-like and dome-shaped endothelial changes to be present in large fields or as isolated cell changes in normal areas at sites where no gross lesions were observed with the light microscope. In addition large, multi-cellular, crate-like endothelial changes were observed at the edges of the large intimal plaques. At these sites several endothelial cells were lacking, leaving behind a crater in which sometimes cells and a few fibrin threads were found. Following the administration of cholesterol for periods of 4-5 and 2-3 weeks similar monocellular changes were observed, some extending over large areas, other as single cells in apparently normal surroundings. Quantitatively the number of lesions was less than when the cholesterol was administered for a longer period. Transmission electron microscopic studies revealed the presence of large amounts of membrane-bound lipid globules in the subendothelial spaces and within some endothelial cells, structures which were assumed to be cross-sections of the crater-like or dome-shaped endothelial cell protrusions, visible with the S.E.M.

Topics: Animals; Aortic Diseases; Arteriosclerosis; Cholesterol; Diet, Atherogenic; Endothelium; Female; Fibrin; Histocytochemistry; Microscopy, Electron, Scanning; Rabbits; Time Factors

Topics: Animals; Aorta; Aortic Diseases; Blood Flow Velocity; Cell Membrane; Dietary Fats; Endothelium; Fatty Liver; Female; Fibrin; Mice; Microscopy, Electron; Organoids; Platelet Adhesiveness; Pregnancy; Thrombosis; Time Factors

Topics: Adolescent; Adult; Aged; Aorta; Aortic Diseases; Arteriosclerosis; Child; Child, Preschool; Fibrin; Fluorescent Antibody Technique; Humans; Infant; Middle Aged

Topics: Animals; Aorta; Aortic Diseases; Arteriosclerosis; Cholesterol; Diet, Atherogenic; Fibrin; Guinea Pigs; Lipoproteins; Male; Microscopy, Electron, Scanning

Topics: Adolescent; Adult; Aged; Aorta; Aortic Diseases; Arteriosclerosis; Autopsy; Child; Child, Preschool; Female; Fibrin; Histocytochemistry; Humans; India; Infant; Male; Middle Aged; Staining and Labeling

Topics: Aortic Diseases; Brain; Cholesterol; Embolism; Female; Fibrin; Heart Atria; Heart Neoplasms; Humans; Kidney; Male; Middle Aged; Myxoma; Paresis; Spinal Cord; Spinal Cord Diseases; Vertebral Artery

Topics: Animals; Aorta; Aortic Diseases; Fibrin; Histological Techniques; Mesenteric Arteries; Microscopy, Electron; Necrosis; Rats

Topics: Aminocaproates; Animals; Aorta, Abdominal; Aorta, Thoracic; Aortic Diseases; Arteriosclerosis; Fibrin; Rabbits; Thrombin; Thrombosis

Topics: Animals; Antibodies; Aortic Diseases; Arteriosclerosis; Atherosclerosis; Fibrin; Fluorescent Antibody Technique; Freund's Adjuvant; Immune Sera; Immunoelectrophoresis; Rabbits; Research; Serum Albumin; Serum Globulins

Topics: Aorta; Aortic Diseases; Arteriosclerosis; Fibrin; Fluorescent Antibody Technique; Humans

Topics: Aorta; Aorta, Thoracic; Aortic Diseases; Disease; Fibrin; Heart Diseases; Humans; Thrombosis