elastin and Necrosis

Topics: Animals; Arteriosclerosis; Blood Platelets; Blood Vessels; Calcium; Cell Division; Cell Membrane Permeability; Collagen; Disease Models, Animal; Elastin; Endothelium; Fibrin; Glycosaminoglycans; Histocytochemistry; Humans; Lipid Metabolism; Microscopy, Electron; Necrosis; Platelet Adhesiveness

Topics: Arteries; Arteriosclerosis; Cholesterol; Collagen; Elastin; Glycosaminoglycans; Humans; Hypertension; L-Lactate Dehydrogenase; Macromolecular Substances; Metabolic Diseases; Necrosis; Oxidoreductases; Sclerosis; Thrombosis; Time Factors; Vasa Vasorum

Management of encephaloceles is challenging when massive brain herniation is present. In such instances, an expansile cranioplasty may be attempted so as to preserve some herniated brain tissue. Complications such as wound dehiscence, cerebrospinal fluid leak, and scalp necrosis are postoperative concerns. The treatment of scalp necrosis with dural and brain exposure is certainly a challenge due to the complexity of flap techniques in such a young age. Herein we describe the use of a novel technique for the management of a scalp necrosis and dehiscence in an infant.. A patient with a giant parietal encephalocele and massive brain herniation underwent an expansile cranioplasty. A large scalp necrosis ensued as a complication and later progressed to a suture dehiscence despite a new surgical intervention, with resultant brain exposure. A scalp reconstruction was subsequently performed using an artificial dermal substitute, laid directly onto the brain, followed by a split-thickness skin graft. We observed a rapid engraftment, without any further complications, with an acceptable cosmetic result in the long-term follow-up.. A simple technique, such as the use of an artificial dermal matrix with simultaneous split-thickness skin graft, may be an effective treatment for the repair of scalp defects, even when coverage of exposed brain tissue is necessary, when no other techniques are found to be suitable.

Topics: Collagen; Elastin; Encephalocele; Female; Humans; Infant; Magnetic Resonance Angiography; Magnetic Resonance Imaging; Necrosis; Plastic Surgery Procedures; Postoperative Complications; Prenatal Diagnosis; Scalp

Abdominal aortic aneurysm (AAA) is a common aortic disease with a progressive nature. There is no approved pharmacological treatment to effectively slow aneurysm growth or prevent rupture. Necroptosis is a form of programmed necrosis that is regulated by receptor-interacting protein kinases (RIPs). We have recently demonstrated that the lack of RIP3 in mice prevented aneurysm formation. The goal of the current study is to test whether perturbing necroptosis affects progression of existing aneurysm using the RIP1 inhibitors Necrostatin-1 (Nec-1) and an optimized form of Nec-1, 7-Cl-O-Nec-1 (Nec-1s). Seven days after aneurysm induction by elastase perfusion, mice were randomly administered DMSO, Nec-1 (3.2 mg/kg/day) and Nec-1s (1.6 mg/kg/day) via intraperitoneal injection. Upon sacrifice on day 14 postaneurysm induction, the aortic expansion in the Nec-1s group (64.12 ± 4.80%) was significantly smaller than that of the DMSO group (172.80 ± 13.68%) (P < 0.05). The mean aortic diameter of Nec-1 treated mice appeared to be smaller (121.60 ± 10.40%) than the DMSO group, though the difference was not statistically significant (P = 0.1). Histologically, the aortic structure of Nec-1s-treated mice appeared normal, with continuous and organized elastin laminae and abundant αActin-expressing SMCs. Moreover, Nect-1s treatment diminished macrophage infiltration and MMP9 accumulation and increased aortic levels of tropoelastin and lysyl oxidase. Together, our data suggest that pharmacological inhibition of necroptosis with Nec-1s stabilizes pre-existing aneurysms by diminishing inflammation and promoting connective tissue repair.

Topics: Animals; Anti-Inflammatory Agents; Aortic Aneurysm, Abdominal; Apoptosis; Cardiovascular Agents; Cell Movement; Disease Models, Animal; Elastin; Gene Expression Regulation; GTPase-Activating Proteins; Humans; Imidazoles; Indoles; Injections, Intraperitoneal; Macrophages; Male; Matrix Metalloproteinase 9; Mice; Mice, Inbred C57BL; Myocytes, Smooth Muscle; Necrosis; Pancreatic Elastase; Protein-Lysine 6-Oxidase; Tropoelastin

Topics: Accidents, Traffic; Adult; Aged, 80 and over; Burns; Cellulitis; Chondroitin Sulfates; Collagen; Debridement; Diabetic Foot; Elastin; Female; Foot Injuries; Humans; Leg Injuries; Male; Middle Aged; Necrosis; Skin, Artificial

Collagens in the atherosclerotic plaque signal regulation of cell behavior and provide tensile strength to the fibrous cap. Type VIII collagen, a short-chain collagen, is up-regulated in atherosclerosis; however, little is known about its functions in vivo. We studied the response to arterial injury and the development of atherosclerosis in type VIII collagen knockout mice (Col8(-/-) mice). After wire injury of the femoral artery, Col8(-/-) mice had decreased vessel wall thickening and outward remodeling when compared with Col8(+/+) mice. We discovered that apolipoprotein E (ApoE) is an endogenous repressor of the Col8a1 chain, and, therefore, in ApoE knockout mice, type VIII collagen was up-regulated. Deficiency of type VIII collagen in ApoE(-/-) mice (Col8(-/-);ApoE(-/-)) resulted in development of plaques with thin fibrous caps because of decreased smooth muscle cell migration and proliferation and reduced accumulation of fibrillar type I collagen. In contrast, macrophage accumulation was not affected, and the plaques had large lipid-rich necrotic cores. We conclude that in atherosclerosis, type VIII collagen is up-regulated in the absence of ApoE and functions to increase smooth muscle cell proliferation and migration. This is an important mechanism for formation of a thick fibrous cap to protect the atherosclerotic plaque from rupture.

Topics: Animals; Apolipoproteins E; Atherosclerosis; Cell Movement; Cell Proliferation; Cells, Cultured; Collagen; Collagen Type VIII; Elastin; Female; Femoral Artery; Gelatinases; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Muscle, Smooth, Vascular; Necrosis; Plaque, Atherosclerotic; RNA, Messenger; Signal Transduction; Up-Regulation

Extremely preterm infants often receive mechanical ventilation (MV), which can contribute to bronchopulmonary dysplasia (BPD). However, the effects of MV alone on the extremely preterm lung and the lung's capacity for repair are poorly understood.. To characterise lung injury induced by MV alone, and mechanisms of injury and repair, in extremely preterm lungs and to compare them with very preterm lungs.. Extremely preterm lambs (0.75 of term) were transiently exposed by hysterotomy and underwent 2 h of injurious MV. Lungs were collected 24 h and at 15 d after MV. Immunohistochemistry and morphometry were used to characterise injury and repair processes. qRT-PCR was performed on extremely and very preterm (0.85 of term) lungs 24 h after MV to assess molecular injury and repair responses.. 24 h after MV at 0.75 of term, lung parenchyma and bronchioles were severely injured; tissue space and myofibroblast density were increased, collagen and elastin fibres were deformed and secondary crest density was reduced. Bronchioles contained debris and their epithelium was injured and thickened. 24 h after MV at 0.75 and 0.85 of term, mRNA expression of potential mediators of lung repair were significantly increased. By 15 days after MV, most lung injury had resolved without treatment.. Extremely immature lungs, particularly bronchioles, are severely injured by 2 h of MV. In the absence of continued ventilation these injured lungs are capable of repair. At 24 h after MV, genes associated with injurious MV are unaltered, while potential repair genes are activated in both extremely and very preterm lungs.

Topics: Animals; Blood Gas Analysis; Body Weight; Bronchioles; Cell Proliferation; Collagen; DNA; Elastin; Electrolytes; Fetal Blood; Gene Expression Regulation, Developmental; Lung; Myofibroblasts; Necrosis; Organ Size; Premature Birth; Respiration, Artificial; RNA, Messenger; Ventilator-Induced Lung Injury; Wound Healing

Necrotic death of macrophages has long been known to be present in atherosclerotic lesions but has not been studied. We examined the role of receptor interacting protein (RIP) 3, a mediator of necrotic cell death, in atherosclerosis and found that RIP3(-/-);Ldlr(-/-) mice were no different from RIP3(+/+);Ldlr(-/-) mice in early atherosclerosis but had significant reduction in advanced atherosclerotic lesions. Similar results were observed in Apoe(-/-) background mice. Bone marrow transplantation revealed that loss of RIP3 expression from bone-marrow-derived cells is responsible for the reduced disease progression. While no difference was found in apoptosis between RIP3(-/-);Ldlr(-/-) and RIP3(+/+);Ldlr(-/-) mice, electron microscopy revealed a significant reduction of macrophage primary necrosis in the advanced lesions of RIP3(-/-) mice. In vitro cellular studies showed that RIP3 deletion had no effect on oxidized low-density lipoprotein (LDL)-induced macrophage apoptosis, but prevented macrophage primary necrosis occurring in response to oxidized LDL under caspase inhibition or RIP3 overexpression conditions. RIP3-dependent necrosis is not postapoptotic, and the increased primary necrosis in advanced atherosclerotic lesions most likely resulted from the increase of RIP3 expression. Our data demonstrate that primary necrosis of macrophages is proatherogenic during advanced atherosclerosis development.

Topics: Animals; Apolipoproteins E; Apoptosis; Atherosclerosis; Biomarkers; Body Weight; Bone Marrow Cells; Bone Marrow Transplantation; Caspase 8; Caspase Inhibitors; Cell Shape; Cholesterol; Collagen; Cytokines; Elastin; Female; Inflammation; Lipoproteins, LDL; Macrophages; Mice; Microdissection; Necrosis; Receptor-Interacting Protein Serine-Threonine Kinases; Receptors, LDL; RNA, Messenger; Up-Regulation

Acute aortic dissection is a life-threatening disease with a high rate of mortality. At the Institute of Legal Medicine of the Hanover Medical School, 30 cases with aortic dissections were found during autopsy and examined histologically between 2006 and 2009. The grade of medial alterations in the form of cystic medial necrosis, elastin fragmentation, fibrosis and medionecrosis were estimated semi-quantitatively. In order to assess the normal aging process, samples of the aortic wall of 25 decedents without dissecting aneurysms were analyzed histologically. This study demonstrates that there are partly quantitative differences, particularly with a statistically significant increase in cystic medial necrosis (p<0.001) and elastin fragmentation (p<0.001), between aortas from dissecting aneurysms and the normal aging aorta, which may help to identify genetically predisposed relatives of patients with a dissection of the aorta.

Topics: Adult; Aged; Aged, 80 and over; Aging; Aorta; Aortic Aneurysm; Aortic Dissection; Arteriosclerosis; Case-Control Studies; Elastin; Female; Fibrosis; Forensic Pathology; Humans; Male; Middle Aged; Necrosis; Tunica Media

The aim of our case report was to analyse the results obtained with the Matriderm® system and autologous skin grafting for the surgical treatment of skin necrosis of scrotum as a result of endovascular embolisation. We recruited one patient with scrotum skin necrosis as a result of endovascular embolisation admitted at the department of Plastic and Reconstructive Surgery, University of Rome 'Tor Vergata'. The patient underwent Matriderm® system and autologous skin grafting for skin necrosis treatment. After a single treatment, reduction of the skin necrosis was obtained, after 30 days from the surgical treatment. Patient experienced a reduction in pain and a complete restoration of the loss in volume and quality of skin was noticed. Matriderm® system and autologous skin grafting is a simple, safe and feasible technique. When comparing this treatment with others, Matriderm® is a simpler, more economic and less time-consuming method, and does not require sophisticated laboratory facilities.

Topics: Adult; Collagen; Dermatologic Surgical Procedures; Elastin; Embolization, Therapeutic; Endovascular Procedures; Humans; Male; Necrosis; Plastic Surgery Procedures; Scrotum; Skin; Skin Transplantation; Skin, Artificial; Transplantation, Autologous; Vascular Malformations

Plaque with dense inflammatory cells, including macrophages, thin fibrous cap and superficial necrotic/lipid core is thought to be prone-to-rupture. We report a time-resolved laser-induced fluorescence spectroscopy (TR-LIFS) technique for detection of such markers of plaque vulnerability in human plaques.. The autofluorescence of carotid plaques (65 endarterectomy patients) induced by a pulsed laser (337 nm, 0.7 ns) was measured from 831 distinct areas. The emission was resolved spectrally (360-550 nm range) and temporally (0.3 ns resolution) using a prototype fiber-optic TR-LIFS apparatus. Lesions were evaluated microscopically and quantified as to the % of different components (fibrous cap, necrotic core, inflammatory cells, foam cells, mature and degraded collagen, elastic fibers, calcification, and smooth muscle cell of the vessel wall).. We determined that the spectral intensities and time-dependent parameters at discrete emission wavelengths (1) allow for discrimination (sensitivity >81%, specificity >94%) of various compositional and pathological features associated with plaque vulnerability including infiltration of macrophages into intima and necrotic/lipid core under a thin fibrous cap, and (2) show a linear correlation with plaque biochemical content: elastin (P<0.008), collagen (P<0.02), inflammatory cells (P<0.003), necrosis (P<0.004).. Our results demonstrate the feasibility of TR-LIFS as a method for the identification of markers of plaque vulnerability. Current findings enable future development of TR-LIFS-based clinical devices for rapid investigation of atherosclerotic plaques and detection of those at high-risk.

Topics: Calcinosis; Carotid Artery Diseases; Carotid Artery, Common; Collagen; Elastin; Endarterectomy, Carotid; Feasibility Studies; Fiber Optic Technology; Fibrosis; Foam Cells; Humans; Lasers; Lipids; Necrosis; Predictive Value of Tests; Reproducibility of Results; Rupture; Sensitivity and Specificity; Spectrometry, Fluorescence; Time Factors

Thrombospondin (TSP)1 is implicated in various inflammatory processes, but its role in atherosclerotic plaque formation and progression is unclear. Therefore, the development of atherosclerosis was compared in ApoE(-/-) and Tsp1(-/-)ApoE(-/-) mice kept on a normocholesterolemic diet. At 6 months, morphometric analysis of the aortic root of both mouse genotypes showed comparable lesion areas. Even when plaque burden increased approximately 5-fold in ApoE(-/-) and 10-fold in Tsp1(-/-)ApoE(-/-) mice, during the subsequent 3 months, total plaque areas were comparable at 9 months. In contrast, plaque composition differed substantially between genotypes: smooth muscle cell areas, mostly located in the fibrous cap of ApoE(-/-) plaques, both at 6 and 9 months, were 3-fold smaller in Tsp1(-/-)ApoE(-/-) plaques, which, in addition, were also more fibrotic. Moreover, inflammation by macrophages was twice as high in Tsp1(-/-)ApoE(-/-) plaques. This correlated with a 30-fold elevated incidence of elastic lamina degradation, with matrix metalloproteinase-9 accumulation, underneath plaques and manifestation of ectasia, exclusively in Tsp1(-/-)ApoE(-/-) mice. At 9 months, the necrotic core was 1.4-fold larger and 4-fold higher numbers of undigested disintegrated apoptotic cells were found in Tsp1(-/-)ApoE(-/-) plaques. Phagocytosis of platelets by cultured Tsp1(-/-) macrophages revealed the instrumental role of TSP1 in phagocytosis, corroborating the defective intraplaque phagocytosis of apoptotic cells. Hence, the altered smooth muscle cell phenotype in Tsp1(-/-)ApoE(-/-) mice has limited quantitative impact on atherosclerosis, but defective TSP1-mediated phagocytosis enhanced plaque necrotic core formation, accelerating inflammation and macrophage-induced elastin degradation by metalloproteinases, speeding up plaque maturation and vessel wall degeneration.

Topics: Animals; Apolipoproteins E; Apoptosis; Atherosclerosis; Blood Platelets; Elastin; Genotype; Macrophages, Peritoneal; Mice; Mice, Knockout; Myocytes, Smooth Muscle; Necrosis; Phagocytosis; Thrombospondin 1

Topics: Animals; Apolipoproteins E; Apoptosis; Atherosclerosis; Blood Platelets; Elastin; Genotype; Macrophages, Peritoneal; Mice; Mice, Knockout; Myocytes, Smooth Muscle; Necrosis; Phagocytosis; Thrombospondin 1

Arterial vein grafts (AVGs) often fail due to intimal hyperplasia, thrombosis, or accelerated atherosclerosis. Various approaches have been proposed to address AVG failure, including delivery of temporary mechanical support, many of which could be facilitated by perivascular placement of a biodegradable polymer wrap. The purpose of this work was to demonstrate that a polymer wrap can be applied to vein segments without compromising viability/function, and to demonstrate one potential application, i.e., gradually imposing the mid-wall circumferential wall stress (CWS) in wrapped veins exposed to arterial levels of pressure. Poly(ester urethane)urea, collagen, and elastin were combined in solution, and then electrospun onto freshly-excised porcine internal jugular vein segments. Tissue viability was assessed via Live/Dead staining for necrosis, and vasomotor challenge with epinephrine and sodium nitroprusside for functionality. Wrapped vein segments were also perfused for 24h within an ex vivo vascular perfusion system under arterial conditions (pressure = 120/80 mmHg; flow = 100 mL/min), and CWS was calculated every hour. Our results showed that the electrospinning process had no deleterious effects on tissue viability, and that the mid-wall CWS vs. time profile could be dictated through the composition and degradation of the electrospun wrap. This may have important clinical applications by enabling the engineering of an improved AVG.

Topics: Algorithms; Animals; Blood Vessel Prosthesis; Collagen; Elasticity; Elastin; Epinephrine; In Vitro Techniques; Jugular Veins; Microscopy, Electron, Scanning; Necrosis; Nitroprusside; Polyesters; Polymers; Saphenous Vein; Stress, Mechanical; Swine; Tissue Survival; Tunica Intima

Elastin fibres in sputum have been described as a more sensitive marker of pulmonary necrosis than plain chest X-rays. This study aimed to determine the prevalence of elastin fibres using non-directed non-protected mini-bronchoalveolar lavage (BM-BAL) in mechanically ventilated patients in the intensive care unit. Patients admitted to the general intensive care unit of a tertiary referral hospital requiring more than 48 hours of mechanical ventilation had surveillance BM-BAL performed on admission and were then examined weekly using potassium hydroxide wet preparations for the presence of elastin fibres. All positive and a random selection of 16 negative preparations from patients with acute respiratory distress syndrome or pneumonia were fixed and examined using Weigert's staining method for elastin. Of 412 patients enrolled, 130 (32%) had pneumonia on admission, 50 (12%) developed 58 episodes of ventilator-associated pneumonia and acute respiratory distress syndrome was diagnosed in 86 patients (21%). No chest X-ray showed cavitating infiltrates. Of 985 specimens examined, only seven had elastin fibres. Elastin fibres are uncommonly found using BM-BAL in general screening, acute respiratory distress syndrome or pneumonia in the intensive care unit, the incidence too low to be a useful indicator of pulmonary necrosis.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Biomarkers; Bronchoalveolar Lavage; Bronchoalveolar Lavage Fluid; Elastin; Female; Humans; Intensive Care Units; Lung Diseases; Male; Middle Aged; Necrosis; Pneumonia; Pneumonia, Ventilator-Associated; Respiration, Artificial; Respiratory Distress Syndrome

Tissue necrosis following spider bites is a widespread problem. In the continental United States, the brown recluse (Loxosceles reclusa), hobo spider (Tegenaria agrestis), garden spider (Argiope aurantia) and Chiracanthium species, among others, reportedly cause such lesions. The exact mechanism producing such lesions is controversial. There is evidence for both venom sphingomyelinase and spider digestive collagenases. We have examined the role of spider digestive proteases in spider bite necrosis. The digestive fluid of A. aurantia was assayed for its ability to cleave a variety of connective tissue proteins, including collagen. Having confirmed that the fluid has collagenases, the digestive fluid was injected into the skin of rabbits to observe whether it would cause necrotic lesions. It did not. The data do not support the suggestions that spider digestive collagenases have a primary role in spider bite necrosis.

Topics: Animals; Collagen; Collagenases; Connective Tissue; Elastin; Endopeptidases; Extracellular Matrix Proteins; Female; Fibrin; Hemolymph; Molecular Weight; Necrosis; Rabbits; Skin; Spider Bites; Spider Venoms; Spiders

Skin ultrastructure was examined in patients undergoing CO2 laser resurfacing for facial rejuvenation. The lasers used in this study were the Coherent Ultrapulse CO2 laser with computerized pattern generator, the Sharplan Feathertouch laser, and the Laserscope Paragon-70 pulsed CO2 laser with computerized pattern generator. Results showed that the epidermis was totally removed with one pass of the CO2 laser. After one laser pass, there was little compaction of collagen in the dermis, but after two and three passes, there were sequential graded increases in collagen compaction with loss of the intervening extracellular gel matrix. There was no "collagen shrinkage," and the collagen itself was marginally affected, except for occasional losses in striations at the surface of the specimens. Elastin was very much affected by the laser such that with only one pass, the elastin was abnormal, presenting with a mottled heterogeneous structure. This elastin aberrancy was present in both the papillary and reticular dermis. After one laser pass, fibroblast necrosis was present in the papillary dermis and the reticular dermis (depending on which laser was used), and the extent and depth of necrosis increased with multiple laser passes.

Topics: Collagen; Elastin; Equipment Design; Fibroblasts; Humans; Laser Therapy; Microscopy, Electron; Necrosis; Rhytidoplasty; Skin

Intravascular ultrasound imaging is a new method in which high resolution images of the arterial wall are obtained with use of a catheter placed within an artery. An in vitro Plexiglas well model was used to validate measurements of the luminal area, and an excellent correlation was obtained. One hundred thirty segments of fresh peripheral arteries underwent ultrasound imaging and the findings were compared with the corresponding histopathologic sections. Luminal areas determined with ultrasound imaging correlated well with those calculated from microscopic slides (r = 0.98). Three patterns were identified on the ultrasound images: 1) distinct interface between media and adventitia, 2) indistinct interface between media and adventitia but different echo density layers, and 3) diffuse homogeneous appearance. The types of patterns depended on the relative composition of the media and adventitia. Calcification of intimal plaque obscured underlying structures. Atherosclerotic plaque was readily visualized but could not always be differentiated from the underlying media.

Topics: Adult; Aged; Aged, 80 and over; Arteries; Arteriosclerosis; Calcinosis; Collagen; Elasticity; Elastin; Humans; Middle Aged; Models, Structural; Muscle, Smooth, Vascular; Necrosis; Reference Values; Ultrasonography

We studied the histologic and histometric features of the aortic media in cases of dissecting aneurysm in order to clarify the pathologic background of this condition. The results were then compared with cases of true aneurysm and control specimens of "normal" aging aorta. Most cases of dissecting aneurysm and true aneurysm, as well as a number of control specimens, showed severe cystic medial necrosis, and therefore this feature does not appear to be specific to dissecting aneurysm. Fibrosis was noted in the process of repair of medionecrosis in dissecting aneurysm, true aneurysm, and controls. The main pathologic features of the aortic media in dissecting aneurysm included a higher grade of elastin fragmentation (offensive factor) and less fibrosis (defensive factor). Our findings indicate that the pathologic balance between these offensive and defensive factors is an important consideration when evaluating the pathogenesis of dissecting aneurysm.

Topics: Aged; Aging; Aortic Aneurysm; Aortic Dissection; Elastin; Female; Fibrosis; Humans; Male; Necrosis; Reference Values; Retrospective Studies

Topics: Animals; Autoantibodies; Elastin; Fluorescent Antibody Technique; Hindlimb; Ischemia; Muscle, Smooth, Vascular; Necrosis; Peptides; Rabbits; Thromboangiitis Obliterans

Groups of Fischer-344 rats were exposed to either filtered air, 0.4, 1.4, or 4.0 ppm acrolein for 62 days (6 h/day, 5 days/week). Mortality was observed only in the 4.0 ppm chamber, where 32 of 57 male rats died, but none of the 8 exposed females died. The lungs of the 4.0 ppm group were heavier than those of the larger control animals. Relative to controls, there was a 20% increase in total dry lung weight while the percent dry weight decreased 1.5% in the high dose group. This increased dry weight and the absence of significant changes in the DNA and protein content per unit dry weight indicated that the greater lung weight observed in this group was in part due to increased cellularity. Lung connective tissue content was increased as a result of subchronic acrolein exposure. The amount of elastin per unit dry weight was 173% of control values in the animals exposed to 4.0 ppm acrolein. Collagen levels were elevated in both the 1.4 and 4.0 ppm groups, 113 and 137%, respectively, of control values. Histologically, the 4.0 ppm animals demonstrated bronchiolar epithelial necrosis and sloughing, bronchiolar edema with macrophages, and focal pulmonary edema. Exposure related lesions were observed in only 3 of the 31 rats examined from the 1.4 ppm chamber and in none of the animals exposed to 0.4 ppm acrolein.

Topics: Acrolein; Aldehydes; Animals; Body Weight; Collagen; DNA; Edema; Elastin; Female; Kinetics; Lung; Lung Diseases; Male; Necrosis; Organ Size; Proteins; Rats; Rats, Inbred F344

Potassium hydroxide (KOH) preparations for elastin fibers on sputum obtained from 80 patients seen over a four-month period at two Cleveland hospitals were performed. The results were compared with roentgenographic evidence of necrosis and case diagnosis. Sixty-one patients had neither elastin in sputum nor roentgenographic evidence of cavitation; 11 had positive results using both methods. Two patients had no elastin fibers in sputum but had parenchymal pulmonary cavities on chest x-ray film. Six patients had elastin observed in KOH preparations of sputum, but no cavitation roentgenographically. The presence of elastin in sputum was strongly correlated with roentgenographic evidence of pulmonary necrosis (p = 5.7 X 10(-8]. Including patients seen before, after, and during the prospective study, we have observed a total of nine with positive sputum preparations for elastin and no cavitation on chest x-ray film for whom tissue was available for study. All had pulmonary necrosis histologically. Our observations suggest that the KOH preparation of sputum for elastin fibers may be more sensitive than the chest roentgenogram in the detection of pulmonary necrosis and may be a useful adjunct in the diagnosis of necrotizing disease.

Topics: Diagnosis, Differential; Elastin; Humans; Lung; Necrosis; Pneumonia; Prospective Studies; Radiography; Sputum

We have observed five patients for whom the presence of fibers of elastin in potassium hydroxide (KOH) preparations of sputum represented the first evidence of necrotizing pulmonary disease. In four cases, the discovery of elastin fibers in sputum provided additional evidence supporting initiation or modification of antibiotic therapy. Necrotizing disease was confirmed in all cases by autopsy or by the development of cavitation on chest x-ray film. Cytochemical staining, electron microscopy, and elastase digestion all suggest that the refractile fibers seen on KOH wet mount of sputum are elastin. The test, first described in 1846, is simple to perform, requires little experience to read, and may be a valuable adjunct to the chest roentgenogram in the diagnosis of pulmonary parenchymal destruction.

Topics: Adult; Aged; Bronchopneumonia; Elastin; Female; Humans; Hydroxides; Male; Middle Aged; Necrosis; Pneumonia; Potassium; Potassium Compounds; Sputum

Partial ligation of the rabbit abdominal aorta with fine silk suture for 48 hours produced a circular band of transmural necrosis. On release of the ligature, blood cells from the lumen and from adventitial vasa vasorum, as well as cells derived by mitosis from the adjacent surviving endothelium and media, participated in the restitution of a continuous endothelial lining and an intact media containing well-differentiated smooth muscle cells within normal medial lamellar units. Initial deposition of a layer of blood platelets on the fibrillar material coating the denuded lumenal surface was followed by ingress from the lumen of polymorphonuclear granulocytes and mononuclear cells. These changes preceded the appearance of mitoses in surviving endothelial and medial smooth muscle cells at the margin of injury. By 24 hours, poorly differentiated cells had accumulated in the central portion of the intima and inner media. Similar cells formed a more extensive, nearly complete lumenal layer which was eventually continuous with and indistinguishable from the adjacent uninjured endothelium. By 7 days, smooth muscle cells repopulated the media, and a collection of less differentiated cells persisted between the restored endothelium and media. By 28 days, the only deviation from normal arterial structure was the persistence at the point of ligature of intimal thickening, consisting of smooth muscle cells and collagen and elastin fibers. Though still present at 6 weeks, this zone became increasingly compact and layered. There was no evidence that fibrin thrombus formation was a consistent feature of the initial reaction or that it played a role in the healing process or in the formation of the intimal lesion. Despite complete circumferential necrosis at the site of ligature, there was no evidence of medial rupture or intramural hemorrhage.

Topics: Animals; Aorta, Abdominal; Blood Platelets; Collagen; Elastin; Endoplasmic Reticulum; Endothelium; Female; Granulocytes; Ligation; Male; Mitosis; Muscle, Smooth; Necrosis; Rabbits; Ribosomes; Thrombosis; Time Factors; Wound Healing

Topics: Aging; Animals; Aorta; Aorta, Abdominal; Aorta, Thoracic; Arteries; Arteriosclerosis; Collagen; DNA; Elastic Tissue; Elastin; Humans; Muscle, Smooth; Necrosis; Pulmonary Artery; Rats; Sutures; Swine; Wound Healing

Topics: Animals; Aortic Valve; Aortic Valve Insufficiency; Cartilage; Cattle; Collagen; Connective Tissue; Elastin; Formaldehyde; Humans; Lymphocytes; Necrosis; Rupture, Spontaneous; Swine; Transplantation, Heterologous

Topics: Adrenal Glands; Age Factors; Animals; Aortic Diseases; Arteriosclerosis; Blood Vessels; Calcinosis; Cholesterol; Elastin; Endarteritis; Epinephrine; Female; Freund's Adjuvant; Glycoproteins; Glycosaminoglycans; Glycoside Hydrolases; Humans; Injections, Intravenous; Lipase; Lipid Metabolism; Male; Necrosis; Pancreatic Elastase; Rabbits; Sex Factors; Stress, Physiological; Thyroxine; Time Factors; Transplantation, Homologous