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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epicardial adhesions are believed to form secondarily to impaired pericardial fibrinolytic activity. This activity was reconstituted in a rabbit pericardial adhesion model with single doses of the fibrinolytic agents tissue plasminogen activator (t-PA), t-PA analog (Fb-Fb-CF), and streptokinase (SK), resulting in reductions in the extent and tenacity of adhesion formation. Adhesions of the median strip of the anterior cardiac surface were reduced in area from 89% (n = 22) in controls, to 28% (n = 5) by treatment with Fb-Fb-CF (0.94 mg), and to 49% (n = 7) by treatment with SK (93,750 IU). A modified fabric of oxidized regenerated cellulose (mTC7) used to deliver the agent to the cardiac surface did not interfere with the activity of these agents (Fb-Fb-CF 19%, n = 14; SK 33%, n = 7). t-PA (0.94 mg) was also found to reduce adhesion formation in combination with mTC7 (4%, n = 4), although the appearance of significant postoperative bruising and bleeding resulted in a decision to terminate the treatment of further animals with t-PA with and without mTC7. Postoperative bruising, bleeding, and swelling, to a lesser extent, were associated with SK and Fb-Fb-CF. Despite the efficacy of the these fibrinolytic drugs further work is required to assess their safety before they are used clinically.
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PMID:Fibrinolytic drugs prevent pericardial adhesions in the rabbit. 140 17

The effect of pretreatment of metastatic B16 melanoma cells with 10(-6) M all trans-retinoic acid resulted in a significant inhibition of lung colonization following injection of 10(5) cells into the tail vein of syngeneic C57BL mice. Adhesion of melanoma cells to vascular endothelial cell monolayers, and subendothelial extracellular matrix was also inhibited by pretreatment with retinoic acid, as was tumour cell aggregation following seeding of pretreated cells on to 0.5% agar. Release of 35SO4 from radiolabelled subendothelial extracellular matrix by melanoma cells was essentially unaltered by retinoic acid pretreatment, as was the release of radiolabel from [3H]proline-labelled matrix, while plasminogen activator activity was enhanced in retinoic-acid-treated cells. These observed changes in adhesive properties may be responsible, at least in part, for the retinoic-acid-induced inhibition of lung colonization.
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PMID:Retinoic acid-induced inhibition of metastatic melanoma cell lung colonization and adhesion to endothelium and subendothelial extracellular matrix. 173 48

We investigated the ability of recombinant tissue plasminogen activator to inhibit post-radical pelvic surgery adhesions formation in 40 adult female canines undergoing radical hysterectomy, bilateral salpingo-oophorectomy, omentectomy, resection of pelvic and abdominal peritoneum, and placement of a peritoneal access catheter. Immediately after operation one half of animals received either recombinant tissue plasminogen activator, 1 mg/kg weight, diluted in 9 ml sterile normal saline solution per milligram of the plasminogen activator or 10 ml vehicle per kilogram intraperitoneally every 12 hours for a total of 10 doses. A single control animal died postoperatively of complications of intestinal obstruction. No bleeding abnormalities were noted in either group of animals. Four weeks after surgery, animals underwent reexploration and adhesions were quantified. Adhesion scores for the animals treated with recombinant tissue plasminogen activator (n = 20; mean score, 1.29 +/- 1.97; median, 0.6) were significantly less than for control animals (n = 19; mean score, 4.64 +/- 3.71; median, 3.86; p = 0.03). Whereas recombinant tissue plasminogen activator appears to effectively prevent post-radical pelvic surgery adhesions in this canine model, phase I and II trials in humans will be required to determine safety and clinical benefit.
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PMID:The ability of recombinant tissue plasminogen activator to inhibit post-radical pelvic surgery adhesions in the dog model. 195 91

Adhesions are the leading cause of small bowel obstruction and a frequent cause of failure of infertility operations. Fibrinolysis is involved in the formation and resolution of adhesions. Although intravenous dextran (Macrodex) is known to augment intravascular fibrinolysis, the effects of intraperitoneal dextran (Hyskon) on fibrinolysis have not been extensively studied. A fibrin plate assay system was used to assess plasminogen activator activity of rabbit peritoneum and plasma after treatment with intraperitoneal or intravenous dextran 70. Hyskon significantly reduced the ability of severe trauma to depress plasminogen activator activity of visceral peritoneum and was capable of direct plasminogen activation. Untraumatized or minimally traumatized peritoneum was not affected, nor was plasminogen activator activity of plasma. Pulmonary effusions and perioperative deaths were significantly associated with the use of Hyskon.
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PMID:Intravenous versus intraperitoneal administration of dextran in the rabbit: effects on fibrinolysis. 242 47

Recent work shows that a common pathway in adhesion production is a reduction in local plasminogen activator activity (PAA). This deficit permits deposited surface fibrin to become organized to fibrous adhesions. A rabbit model for adhesion formation was used to assess the effect of replacing the deficit with recombinant tissue plasminogen activator (rt-PA). Adhesions were produced by stripping peritoneum from corresponding parietal and visceral areas. One week later the adhesions were divided. Either rt-PA or placebo was applied to the divided adhesion. After a further week the animal was killed and the adhesions assessed. Sixty strips were performed. Fifty-five adhesions were produced (92%). Placebo gel was applied to 28 sides and rt-PA applied to 27. Twenty-two of the placebo group recurred (79%). Two of the rt-PA group reformed (7%, chi 2 = 20.883, P less than 0.001). Recombinant tissue plasminogen activator is an effective inhibitor of adhesion formation in the experimental animal.
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PMID:Intra-abdominal adhesions and their prevention by topical tissue plasminogen activator. 250 82

Postoperative abdominal adhesion formation can undo the reconstructive work of the infertility surgeon. Adhesions can form in as little as three hours after surgery. Most adhesions are transient and lyse spontaneously within 72 hours of surgery. Such factors as tissue trauma, anoxia and ischemia cause a reduction in plasminogen activator activity that is strongly correlated with the persistence and progression of postoperative adhesions. Adhesions can be prevented by a proper and meticulous surgical technique emphasizing preservation of tissue without abrasion, anoxia or ischemia. Dextran, antiprostaglandins, antibiotics, steroids, antihistamines, anticoagulants and enzymes have various roles. Our current regimen involves Hyskon, Motrin and deoxycycline.
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PMID:Formation and prevention of postoperative abdominal adhesions. 672 92

Recent laboratory and clinical studies concerning the pathogenesis and prophylaxis of postoperative peritoneal adhesions are reviewed. Since the late 19th century there have been several clinical and experimental observations demonstrating that peritoneal defects usually fail to heal with adhesion formation. Instead, mesothelization takes place, producing a surface indistinguishable from the original. This occurs from the base of the defect, meaning large defects heal as quickly as smaller defects. In a study conducted in rats (Ellis), it was noted that areas reperitonealized under tension developed adhesions while similar peritoneal defects left unrepaired and suture controls placed loosely in peritoneum usually healed without adhesions. These findings were confirmed by Buckman and coworkers who discovered that plasminogen activator activity was normally present in the mesothelium and submesothelial blood vessels of peritoneum. 2 other peritoneal insults known to induce adhesion formation are infection and foreign body contamination. Theoretically, it seems possible to reduce adhesion formation by taking the following steps: 1) reducing the initial inflammatory reaction and subsequent exudate release; 2) inhibiting coagulation of this exudate; 3) promoting the removal of fibrin deposition; 4) mechanically separating fibrin-covered surfaces; and 5) inhibiting fibroplastic proliferation. Adhesions continue to be a frequent sequelae of pelvic surgery despite the use of meticulous surgical technique. Although dextran solutions appear promising, their clinical value is unconfirmed.
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PMID:Prevention of postoperative adhesions. 698 92

To assess the effect of the removal of ovarian surface epithelium on repair, a standard injury was induced in the ovaries of 10 rabbits. In one ovary the surface cells were denuded, and in the other they were left intact. The effect on adhesion formation was assessed at 12 days. Adhesions were assessed by visual inspection at laparotomy and histological examination of adhesion formation, including a stereological assessment of scar volume. On visual assessment the overall adhesion scores for the denuded ovaries were greater than for the intact ovaries. Histology showed the adhesions were attached only to the site of injury. The Fallopian tube was adherent to 35 and 4% of the denuded and intact ovarian segments respectively (P = 0.003). The scar volumes for each side were similar. After 12 days there was only partial re-epithelialization on the denuded ovaries. Electron microscopy confirmed the slow healing, with much of the surface still covered by a fibrinous-like exudate. The findings of this small study lend further weight to the importance of the surface epithelium in the control of adhesion formation. Standard surgical procedures may generate adhesions by the inadvertent denuding of surface epithelium from adjacent healthy tissues, possibly by the loss of plasminogen activator activity that is found in the mesothelium of the peritoneum. This study highlights the importance of controlling for inadvertent cell loss whilst investigating methods for adhesion prevention.
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PMID:Removal of the ovarian surface epithelium from the rabbit ovary--a cause of adhesions following a standard injury. 800 41

The increased incidence of postoperative adhesions and their complications have refocused attention on our understanding of adhesions, their clinical consequences and prevention. Postsurgical adhesions have four major negative impacts on health care outcomes. First, adhesions cause significant morbidity, including intestinal obstruction, infertility and pelvic pain. Second, adhesions are associated with multiple surgical complications. Third, these complications lead to greater surgical workload and utilization of hospital and other health care resources. Fourth, all these negative impacts result in significant economic burden to society. The complexities of adhesion formation and limitations in their understanding and research have hampered the development of satisfactory preventive treatments. Adhesions are highly differentiated, formed through an intricate process and associated with a complex organ, the peritoneum. The surface lining of the peritoneum is the key site in adhesion formation and prevention. Two unique properties of the peritoneal surface play key roles in these processes: its delicacy and its uniform, relatively rapid rate of re-epithelialization, irrespective of the size of injury. A suitable barrier that separates damaged peritoneal surfaces for the entire five to seven days of re-epithelialization is likely to prove effective in reducing adhesion formation. Postsurgical peritoneal repair begins with coagulation, which releases a variety of chemical messengers that bring about a cascade of events. Some of the principal cellular elements in this cascade are leukocytes, including polymorphonuclear neutrophils and macrophages, mesothelial cells, and fibrin. Following surgical injury, macrophages exhibit increased phagocytic, respiratory burst and secretory activity, and after day 5, are the major component of the leukocyte population. Macrophages also recruit new mesothelial cells onto the surface of the injury. These cells form small islands throughout the injured area which proliferate into sheets of mesothelial cells and accomplish re-epithelialization, usually five to seven days after surgical injury. The progenitor to adhesions is the fibrin gel matrix which develops in several steps. These include the formation and insolubilization of fibrin polymer and its interaction with fibronectin and a series of amino acids. Protective fibrinolytic enzyme systems of the peritoneal mesothelium, such as the tissue plasminogen activator (tPA) system, can remove the fibrin gel matrix. However, surgery dramatically diminishes fibrinolytic activity. This occurs in at least two ways: first, by increasing levels of plasminogen activator inhibitors and second, by reducing tissue oxygenation. Peritoneal re-epithelialization and adhesion formation thus can be seen as alternative pathways following peritoneal injury. The pivotal events determining the pathway are the apposition of two damaged surfaces and the extent of fibrinolysis. Development of strategies to separate damaged peritoneal surfaces and to foster an appropriate degree of fibrinolysis appears to be among the most promising avenues of adhesion prevention research. Hopefully, these efforts will lead to adhesion-free peritoneal healing following abdominal surgery.
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PMID:Biochemical events in peritoneal tissue repair. 907 47

The aim of this study was to evaluate the bacterial adherence to biodegradable self-reinforced polyglycolic acid (SR-PGA) and self-reinforced poly-DL-lactic acid (SR-PLA 96) spiral stents in vitro. They are used as temporary urethral stents in urology. Gold-plated metal wire, polyurethane and latex were used as controls. Materials were incubated up to 28 days in artificial urine, after which a bacterial suspension was added. After detaching by sonication the adhesive bacteria were analysed as colony forming units (CFUs) and by scanning electron microscopy (SEM) analysis. Adhesion was more significantly correlated to stent bacterial type than to the tested material in both assays. No encrustation was seen on SR-PGA or SR-PLA 96. SR-PGA and SR-PLA 96 had no effect on the bacterial growth. In conclusion, the bacterial properties are equally or more important than the material properties in the adhesion process.
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PMID:Bacterial adherence to self-reinforced polyglycolic acid and self-reinforced polylactic acid 96 urological spiral stents in vitro. 966 40


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