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

Fibrin adhesives have been advocated as a protective sealant in high-risk colonic anastomoses to prevent leakage. To assess the effect of fibrin glue sealing on the healing ischemic anastomosis, we compared the healing of sutured colonic anastomoses in the rat, with and without fibrin adhesive (Groups IA and IB), and ischemic anastomoses with and without fibrin adhesive (Groups IIA and IIB). On days two, four, and seven, 10 animals in each group were sacrificed. Adhesion formation was scored, and the in situ bursting pressure was measured. The collagen concentration and degradation were estimated by measuring hydroxyproline. Adhesion formation was more prominent in Groups IB, IIA, and IIB on day four only; abscesses were noted in the ischemic group in four rats. Anastomotic bursting pressure was significantly lower in sealed (IB) and ischemic anastomoses (IIA) than in normal anastomoses (IA) on day four. Sealing of ischemic anastomoses did not change bursting pressures on days two, four, and seven. The relative decrease of collagen in the sealed anastomoses is significantly higher on day four only. It is concluded that sealing of normal colonic anastomoses in the rat has a negative effect on wound healing. Ischemia at the anastomotic site results in weaker anastomotic strength on day four postoperatively. Also in ischemic anastomoses, fibrin sealant does not improve wound healing during the first seven days. Adhesion formation on ischemic intestinal anastomoses was not prevented by fibrin sealing.
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PMID:Healing of ischemic colonic anastomosis: fibrin sealant does not improve wound healing. 151 51

Thirty-one mongrel female dogs were submitted to a standard lesion on the right uterine horn, consisting of crushing, scratching, and ischemia of the segment. Three groups were formed for the study: control group (GC), experimental group I (G1), and experimental group II (G2). In GC, continuous washing with simple ringer solution was applied during surgery. In G1, heparin was added to the ringer solution at a doses of 100 IU/kg. In G2, in addition to the heparin diluted in the ringer solution, subcutaneous heparin was given at 12 hours intervals for three days, at a doses of 100 IU/kg/doses. The percentage of dogs with pelvic adhesions was determined by laparotomy. Adhesion intensity in the incision and in the pelvis was determined. 100% of dogs in G2 had adhesions in the incision, whereas 66.66% had incision adhesion in GC. There was no statistical difference. All groups presented around 50% of pelvic adhesions. Intensity of pelvic adhesions was not different in the three groups, but G2 had more adhesions than GC, such difference being statistically significant.
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PMID:[Heparin effect on prevention of pelvic adhesions. Experimental study]. 182 May 98

During their life span, leukocytes adhere transiently to one another, to other cell types, such as vascular endothelial cells, and to extracellular matrix proteins. This adhesiveness is mediated by families of specific cell surface adhesion molecules, namely, integrins, immunoglobulin superfamily molecules, and selectins. Adhesion is required for leukocyte-mediated cytotoxicity, phagocytosis, chemotaxis, and induction of lymphocyte proliferation and maturation. It also participates in recirculation and homing of lymphocytes into lymphoid organs and in leukocyte migration from the vascular compartment to extravascular tissues. Adhesion underlies the beneficial or detrimental role of leukocytes in immune and inflammatory responses. In animals, blocking monoclonal antibodies to adhesion molecules dramatically reduce vascular and tissue injury in several organs following ischemia-reperfusion, and delay renal allograft rejection. Moreover, expression of particular adhesion molecules is induced or increased in cells which are targets for allergic or autoimmune reactions and in inflamed tissues. On the other hand, a congenital deficiency of the CD11/CD18 integrins (Leu-CAMs) leads to recurrent, and sometimes fatal, bacterial infections, and lack of particular cell-adhesion molecules on Burkitt's lymphoma cells may enable these cells to escape immunosurveillance.
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PMID:Leukocyte adhesion in host defense and tissue injury. 183 Aug 30

Activated leukocytes appear to be directly involved in potentiating ischemic central nervous system (CNS) injury. Adhesion of leukocytes to endothelium is essential for their migration and requires the binding of adhesion receptors of the leukocyte (CD 18) to an intercellular adhesion molecule (ICAM) on endothelium. Monoclonal antibodies to an ICAM can block leukocyte adhesion and transendothelial migration. To determine the efficacy of anti-ICAM antibody treatment in preserving neurological function after CNS ischemia, two animal models were used. A 1-mg/kg dose of anti-ICAM was given to rabbits 30 minutes before induction of ischemia either in the spinal cord using temporary aortic occlusion or in the brain using intra-arterial microspheres. In this study, treatment with anti-ICAM produced a significant reduction in neurological deficits in the reversible spinal cord ischemia model but not in the irreversible brain ischemia model. This protective effect supports the active role of leukocytes in CNS reperfusion ischemic injury and offers potential for future therapy.
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PMID:Reduction of central nervous system ischemic injury by monoclonal antibody to intercellular adhesion molecule. 188 80

An ischemic bowel model was used to stimulate adhesion formation in eight ponies. Heparin (40 USP u/kg) or saline was administered intravenously at surgery and was continued subcutaneously every 12 hours for 48 hours to evaluate the efficacy of heparin in preventing intraabdominal adhesions. Ponies were euthanatized after 6 weeks, and postmortem examinations were performed. A statistically significant difference was found between the heparin-treated and the control groups. Adhesions developed in three of four control ponies, and adhesions did not develop in three of four heparin-treated ponies. None of the adhesions resulted in clinical disease. In this study, heparin decreased the formation of adhesions in ponies after experimentally induced intestinal ischemia.
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PMID:Prevention of intraabdominal adhesions in ponies by low-dose heparin therapy. 350 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

An effective host response to infection or tissue damage requires focal accumulation of leukocytes. Leukocyte adhesion to the vessel wall, a key step in this process, depends on the ordered expression of specific endothelial cell surface molecules. The endothelial molecules that support adhesion include selectins that recognize leukocyte cell surface glycoconjugates as well as members of the immunoglobulin superfamily that interact with leukocyte integrins. Although inflammation can occur with minimal damage to the vessel wall and surrounding tissues, control mechanisms sometimes appear to fail, and the inflammatory response itself becomes a significant clinical problem. In this review, we discuss endothelial-leukocyte adhesion molecules with particular emphasis on their expression and function in human disease. Pathophysiological processes presented include atherosclerosis, ischemia-reperfusion injury, acute lung injury, rheumatoid arthritis, and graft rejection. A more detailed description of the discovery and characterization of the key molecules appears in the antecedent article entitled "Endothelial-Leukocyte Adhesion Molecules".
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PMID:Endothelial-leukocyte adhesion molecules in human disease. 751 20

Cytokine induction of intercellular adhesion molecule-1 (ICAM-1) in cardiac myocytes may be a critical step in inflammation associated with ischemia-reperfusion injury. We investigated the involvement of tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6), and interleukin 8 (IL-8) on neutrophil-myocyte adhesion; These cytokines are increased in plasma of patients with acute myocardial infarction (AMI). ICAM-1 expression on cultured neonatal rat cardiac myocytes was determined through immunohistochemical and enzyme-linked immunosorbent assay (ELISA) analysis. ICAM-1 mRNA expression in myocytes was investigated by Northern blot hybridization. Rat neutrophils isolated from peripheral blood (PB) were used for adherence assay. In immunohistochemical study, cultured neonatal rat cardiac myocytes constitutively expressed ICAM-1 molecules. In ELISA analysis, ICAM-1 molecule expression on myocytes was significantly stimulated by TNF-alpha (100 U/ml), but not by IL-6 (100 U/ml) or IL-8 (100 ng/ml) dose dependently. The effect of TNF-alpha was observed as early as 6 h after stimulation. Levels of ICAM-1 mRNA were very low or almost undetectable in unstimulated myocytes, but its expression was markedly induced after exposure to TNF-alpha for 3 h. IL-6 and IL-8 showed no effect on ICAM-1 mRNA accumulation. Adhesion of rat neutrophils to myocytes was stimulated by TNF-alpha, and the effect of TNF-alpha on adherence was significantly inhibited by an anti-ICAM-1 monoclonal antibody (MoAb). These results show that TNF-alpha, but not IL-6 and IL-8, promotes neutrophil-myocyte adhesion through ICAM-1 expression, suggesting involvement of TNF-alpha in inflammation associated with ischemia-reperfusion injury.
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PMID:Neutrophil adherence to rat cardiac myocyte by proinflammatory cytokines. 751 17

Adhesion molecules are responsible for PMN-endothelial cell interactions involved in both PMN-mediated endothelial injury (e.g., after ischemia-reperfusion injury) and PMN-mediated host defense against bacterial infection. Inhibition of PMN-endothelial adherence with CD18 and P-selectin mAb has been shown to ameliorate the tissue injury resulting from ischemia and reperfusion under a variety of experimental conditions. However, interference with PMN function may result in an increased risk of bacterial infection. Previous investigations suggest that CD18 blockade can lead to increased infectious risk. Little is known of the infectious risks associated with selectin blockade. We report the effects of P-selectin blockade (using mAb PB1.3) on bacteria-induced PMN emigration into the peritoneum and subcutaneous (s.c.) tissue in rabbits. Leukocyte and PMN emigration into the peritoneum 4 h after inoculation with 10 ml of 10(9) CFU/ml Escherichia coli was significant in saline-treated animals, and not different in animals pretreated with mAb PB1.3. Similarly, the incidence and severity of abscess formation 7 days after s.c. inoculation with Staphylococcus aureus (10(7), 10(8), or 10(9) CFU) was not increased in rabbits pretreated with mAb PB1.3 compared to saline. PMN emigration to the s.c. S. aureus was also similar in both saline and mAb PB1.3-treated animals, as determined by light microscopy. We conclude that P-selectin blockade with mAb PB1.3: 1) does not interfere with acute, E. coli-induced PMN emigration into the peritoneum, 2) does not increase the incidence or severity of S. aureus abscess formation in s.c. tissue, and 3) interferes less with PMN antibacterial host defense mechanisms than inhibition of CD18-mediated PMN adherence.
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PMID:P-selectin blockade does not impair leukocyte host defense against bacterial peritonitis and soft tissue infection in rabbits. 769 61

Adhesion of leukocytes to the endothelium can occur in a few hours after the onset of ischemia, and the actions of leukocytes have been suggested to aggravate reperfusion injury. Adhesion is a prerequisite for the harmful leukocyte actions. Rapid mediation of leukocyte adhesion and aggravation of reperfusion injury can occur through production of platelet-activating factor (PAF). The authors hypothesized that prevention of leukocyte adhesion during ischemia reperfusion would have beneficial effects and that these effects might be enhanced by a PAF antagonist. To test this hypothesis, rabbits were anesthetized with pentobarbital and subjected to severe spinal cord ischemia (25 minutes) followed by 30 minutes of reperfusion, at which time either vehicle, antibody against the CD11/CD18 (anti-CD) leukocyte adhesion molecule (1 mg/kg), or the anti-CD and PAF antagonist, WEB 2086 (3 mg/kg), was administered intravenously and the animals were monitored for 6.5 hours. Using a score from 0 to 5, recovery of motor function was improved at 5.5 hours by the CD antibody (2.0 +/- 0.5 versus 0.4 +/- 0.2 in the six animals in the vehicle group, p < 0.05). No further improvement was induced by WEB 2086 in the six anti-CD treated animals (1.6 +/- 0.7). Spinal cord blood flow (laser Doppler flowmetry) at 6 hours was at the preischemic level in the control animals (-7% +/- 20%), but clearly increased in the anti-CD group (+73% +/- 29%, p < 0.5). The severity of blood-brain barrier damage in the spinal cord gray matter was decreased by the treatments. Extravasation of intravenously injected Evans blue albumin (EBA), measured by detection of EBA fluorescence, was reduced by approximately 50% in both treated groups (p < 0.05). The number of morphologically normal motor neurons in the lumbar anterior horns of the infarcted spinal cord showed protection in the seven animals in the anti-CD treated group at 6.5 hours: 12.7 +/- 1.7 versus 5.3 +/- 1.6 (vehicle), p < 0.05 without an additional effect by PAF antagonist 12.2 +/- 2.6 (anti-CD + WEB 2086). Our results suggest that ultraacute treatment of reperfusion injury based on special inhibition of leukocyte effects may be beneficial. Platelet-activating factor antagonism failed to enhance this therapeutic effect, which may suggest dependency on a common mechanism.
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PMID:Antagonism of neutrophil adherence in the deteriorating stroke model in rabbits. 781 56


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