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  • 1
    Electronic Resource
    Electronic Resource
    NSAID-induced delay in gastric ulcer healing is not associated with decreased epithelial cell proliferation in rats (1995)
    Springer
    Digestive diseases and sciences 40 (1995), S. 2684-2693 
    Details
    ISSN: 1573-2568
    Keywords: aspirin ; indomethacin ; gastric ulcer ; ulcer healing ; cell proliferation ; regeneration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Nonsteriodal antiinflammatory drugs initiate gastric ulceration and delay gastric ulcer healing. This study aimed to investigate the role of epithelial cell proliferation in delayed ulcer healing and to identify the most reproducible technique for measuring cell proliferation. Rats with acetic acid-induced gastric ulcers were treated for two weeks with indomethacin (1 mg/kg), aspirin (200 mg/kg), or vehicle control. Ulcers were assessed by macroscopic measurement of ulcer area, quantitative histological measurement of mucosal regeneration, and 5-bromo-2′-deoxyuridine immunohistochemistry to assess epithelial cell proliferation. Indomethacin and aspirin significantly delayed ulcer healing and inhibited mucosal regeneration. Three techniques for assessing cell proliferation were compared, and a scoring system, designed to take into account the entire tissue, was shown to be the most reproducible technique. Indomethacin significantly enhanced cell proliferation in the fundic area of ulcer and aspirin had no effect on cell proliferation. We conclude that aspirin and indomethacin delay ulcer healing by an inhibition of mucosal regeneration, but they do not inhibit epithelial cell proliferation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02220461
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  • 2
    Electronic Resource
    Electronic Resource
    Influence of age on natural and delayed healing of experimentally-induced gastric ulcers in rats (1996)
    Springer
    Digestive diseases and sciences 41 (1996), S. 1838-1844 
    Details
    ISSN: 1573-2568
    Keywords: aging ; gastric ulcer ; ulcer healing ; indomethacin ; acetic acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study aimed to investigate the effect of age on natural ulcer healing and delayed ulcer healing induced by nonsteroidal antiinflammatory drugs, using a rat model. Gastric ulcers were induced in young, adult, and aged rats using serosal or mucosal (kissing ulcers) application of acetic acid. Rats were treated with indomethacin 1 mg/kg/day subcutaneously or vehicle for two weeks. Ulcers were assessed by macroscopic and histological measurements of ulcer size. Ulcer induction was affected by age. Aged rats developed significantly smaller ulcers when induced by serosal application of acetic acid and significantly larger ulcers from mucosal application of acetic acid. However, measurements of ulcer size from both models showed no age-related differences in natural ulcer healing. Similarly, indomethacin-induced delayed gastric ulcer healing was not effected by age. We conclude that there are age-related differences in the development of gastric ulcers but there are no age-related differences in natural or delayed ulcer healing in rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02088755
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  • 3
    Electronic Resource
    Electronic Resource
    Misoprostol hepatoprotection against ischemia-reperfusion-induced liver injury in the rat (1992)
    Springer
    Digestive diseases and sciences 37 (1992), S. 1275-1281 
    Details
    ISSN: 1573-2568
    Keywords: misoprostol ; ischemia ; reperfusion ; hepatoprotection ; reactive oxygen metabolites
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The hepatoprotective effects of misoprostol, a PGE1 analog, against ischemiareperfusion liver injury were studied using a rat partial liver ischemia model. Serum ornithine carbamoyltransferase (OCT) and alanine aminotransferase (ALT) levels were determined as biochemical indices of injury. Hepatic cell necrosis was assessed histologically using tetranitroblue tetrazolium (TNBT) and hematoxylin and eosin (H&E) staining. With placebo treatment, 90 min of partial hepatic ischemia followed by 24 hr of reperfusion resulted in increased levels of serum OCT (760±521IU/liter) and ALT (4327 ±1982 IU/liter), while extensive hepatic necrosis was evident by TNBT and H&E staining. Treatment with two doses of 25 μg misoprostol/kg body weight at 1 min before ischemia and 1 min before reperfusion significantly reduced the serum levels of OCT and ALT (207±189 IU/liter, P〈0.01 and 2075±1217 IU/liter, P〈0.01, respectively) and hepatic necrosis. When a single dose of misoprostol was administered 1 min before reperfusion, similar protective effects were observed. However, when the treatment of misoprostol was delayed to 1 min after reperfusion, significantly less hepatoprotection was seen. Misoprostol exerted no hepatoprotection at all when it was administered at 5 min or later after reperfusion. These results demonstrate that misoprostol partially protects the liver against ischemia-reperfusion injury in the rat. The observation that the protective effect of misoprostol occurs only within the first minute of reperfusion suggests that its mechanism of action involves an early event in reperfusion injury, such as modifying the effects of reactive oxygen metabolites.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01296572
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  • 4
    Electronic Resource
    Electronic Resource
    Effects of misoprostol on delayed ulcer healing induced by aspirin (1994)
    Springer
    Digestive diseases and sciences 39 (1994), S. 934-939 
    Details
    ISSN: 1573-2568
    Keywords: aspirin ; prostaglandin E1 ; misoprostol ; ulcer healing
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Clinical studies have suggested that treatment with the prostaglandin E1 analog, misoprostol, leads to significant healing of ulcers in patients taking regular nonsteroidal antiinflammatory therapy. This study aimed to investigate mechanisms involved in this healing using a rat model. Gastric ulcers were induced by application of acetic acid using a standard technique. Rats were treated with 200 mg/kg aspirin, 100 µg/kg misoprostol, a combination of both treatments, or methylcellulose vehicle for up to two weeks, starting two days after ulcer induction. Ulcers were assessed by macroscopic measurements of area and by quantitative histological measurements. Aspirin delayed ulcer healing compared with controls, while misoprostol significantly reversed this effect. Quantitative histology revealed that misoprostol cotreatment significantly increased mucosal regeneration compared with aspirin treatment alone. However, misoprostol did not reverse the effects of aspirin on an index of wound contraction. We conclude that treatment with misoprostol significantly reverses the delayed healing effect of aspirin, and this may occur via an effect on epithelial regeneration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02087540
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  • 5
    Electronic Resource
    Electronic Resource
    Expression of Adhesion Molecules and Leukocyte Recruitment into Gastric Mucosa Following Ischemia-Reperfusion (1997)
    Springer
    Digestive diseases and sciences 42 (1997), S. 326-332 
    Details
    ISSN: 1573-2568
    Keywords: GASTRIC MUCOSA ; ISCHEMIA-REPERFUSION ; LEUKOCYTE ; ENDOTHELIUM ; ADHESION
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Leukocyte infiltration is an important step inpostischemic tissue damage. This study aimed todetermine the expression of adhesion molecules and theirrelationship with leukocyte infiltration in thepostischemic gastric mucosa. Gastric tissue was obtainedfrom rats subjected to 30 min gastric ischemia followedby reperfusion. Sections were stained with specificantibodies against (1) L-selectin and (2) LFA-1 on leukocytes, (3) ICAM-1 on endothelial cells,(4) PMNs, and (5) monocytes. Stained cells or bloodvessels in mucosal tissue were counted using imageanalysis. Results showed that from 5 min of reperfusion, numbers of L-selectin-positive cells decreased,whereas LFA-1-positive cells and PMNs increased comparedwith controls. ICAM-1 expression did not increase until60 min of reperfusion. Monocyte numbers were unaffected by reperfusion. We conclude thatgastric ischemiareperfusion results in a rapid influx ofLFA-1-positive cells, the majority of which are PMN.L-Selectin is shed from these cells allowing them to adhere to the microvasculature viaconstitutively expressed ICAM-1.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018813902094
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  • 6
    Electronic Resource
    Electronic Resource
    Microvascular changes in liver after ischemia-reperfusion injury (1994)
    Springer
    Digestive diseases and sciences 39 (1994), S. 1683-1690 
    Details
    ISSN: 1573-2568
    Keywords: liver ; microvasculature ; ischemia ; reperfusion ; misoprostol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Morphological changes in the hepatic microvasculature were studied in experimentally induced ischemia-reperfusion injury in the rat using a vascular casting technique. Partial hepatic ischemia was induced for 90 min followed by 24 hr of reperfusion. Microvascular casting was performed after 24 hr reperfusion by either intraarterial or intravenous infusion of acrylic resin (Mercox). After corrosion of the tissue, the cast was examined by scanning electron microscopy. Casts of normal livers showed good patency with no evidence of unfilled areas. The mean diameter of sinusoids was 14±3 µm with those in zone 1 slightly smaller than those in zone 3. Liver casts from rats subjected to ischemia and reperfusion resulted in gross disruption of normal architecture. The common characteristics seen in both prograde and retrograde casts were clusters of closed sinusoids around zones 2 and 3 of the liver acini, which resulted in cavities of various sizes. Varicosities were observed in some areas. The mean diameter of sinusoids in areas of patent microvascular structure (10±2 µm) was significantly smaller compared to those in normal livers (P〈0.001). Misoprostol given at 1 min before reperfusion markedly reduced the microvascular injury. The hepatic microvasculature was generally intact with mild focal unfilled areas. The majority of the sinusoids were of normal size and no clusters of blind ending sinusoids were detected. The present study shows that hepatic ischemia-reperfusion results in extensive microvascular injury in the liver. The protective effects of misoprostol against this injury may occur at the vascular level.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02087776
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  • 7
    Electronic Resource
    Electronic Resource
    Microvascular structure of benign and malignant tumors of the colon in humans (1995)
    Springer
    Digestive diseases and sciences 40 (1995), S. 373-384 
    Details
    ISSN: 1573-2568
    Keywords: carcinoma ; colon ; human ; microvasculature ; microvessels
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Studies of experimental tumors in rodents indicate that there are morphological abnormalities of the tumor microcirculation compared to normal tissues. The aim of this study was to examine the structure of the microvasculature in benign and malignant colonic tumors in humans using microvascular casting techniques. There were 15 adenocarcinomas, four benign sporadic adenomas, and three specimens from patients with familial adenomatous polyposis (FAP). A cast of the microvessels of these tumors was prepared by intraarterial administration of acrylic resin (Mercox) and the cast examined by scanning electron microscopy. Quantitative measures of the microvasculature were obtained from histological sections using stereological techniques in four carcinomas, two sporadic adenomas, and 12 adenomas from patients with FAP. Vascular casts of benign colonic adenomas showed that the microvasculature had a similar organization to normal colon. However, capillaries and venules were elongated and had increased diameters compared to normal. In adenomas greater than 3 mm in diameter, there was an increased density of microvessels in the spaces between tumor cells. Vascular casts of colonic carcinomas were characterized by a disorganized structure and increased density of microvessels. The organization of microvessels within carcinomas had a similar overall pattern to normal colon. However, the increased number and density of microvessels resulted in formation of nodular clusters of capillaries, formation of “sheets” of frequently anastomosing capillaries, or almost complete packing of the interstitial spaces of the tumor by capillaries in places. Most capillaries had a long and tortuous course and numerous capillary sprouts were identified. Tumor microvessels had greater mean diameters than normal. Extravasation of resin from microvessels in carcinomas was frequently seen. The vascular volume of carcinomas (23.1%±12.2), sporadic adenomas (16.3%±3.4), and adenomas 〉3 mm diameter in patients with FAP (17.7%±3.0) were significantly greater than in normal colon (11.0%±4.2). This study indicates that there is an increased vascular density in benign and malignant tumors of the colon compared to normal colon. The presence of profusely anastomotic microvessels and frequent capillary sprouts is evidence of active neovascularization and suggests control of tumor growth could be achieved by modifiers of angiogenesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02065424
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  • 8
    Electronic Resource
    Electronic Resource
    Restoring control (2000)
    Springer
    Diseases of the colon & rectum 43 (2000), S. 1213-1216 
    Details
    ISSN: 1530-0358
    Keywords: Anal incontinence ; Fecal incontinence ; Artificial bowel sphincter ; ABS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract PURPOSE: Anal incontinence is a socially disabling problem affecting 1 to 2 percent of the population. Anal sphincter replacement is a treatment option if the problem is severe and not amenable to direct repair. The artificial bowel sphincter is an innovative approach. We report the technique for placement and the outcomes which have occurred in an initial series of 13 patients. METHODS: The Acticon Neosphincter® artificial bowel sphincter consists of an inflatable cuff of silicone elastomer placed around the anal canal and connected to a pressure-regulating balloon in the iliac fossavia a control pump placed in the labium or scrotum. Thirteen patients with severe anal incontinence not amenable to other methods were treated. Causes of incontinence included obstetric damage in eight patients, surgical damage in two patients, imperforate anus in two patients, and spina bifida in one patient. RESULTS: Surgical placement of the device was straightforward, mean operating time was 65 minutes, and median length of stay was 3.6 days. One infection of the perineal wound occurred in the early postoperative period necessitating removal of the device. In two further patients the artificial bowel sphincter was removed because of late infection in one at seven months and because of erosion through the skin in another at three months. The artificial bowel sphincter has been activated in ten patients resulting in full continence to solids and liquids except in one patient with postvagotomy diarrhea who had some leakage of liquids during episodes of diarrhea. The mean (± standard deviation) continence score (Cleveland Clinic system; maximal incontinence = 20) changed from 18.7 ± 1.6 preoperatively to 2.1 ± 2.6 after activation (P〈0.0001). Quality of life measured using a continence-specific series of up to 39 questions changed from 77 ± 16 percent of maximal reduction of quality preoperatively to 12 ± 19 percent postoperatively (P〈0.001). CONCLUSIONS: The artificial bowel sphincter can be placed without technical difficulty and with low morbidity. Preliminary experience shows full restoration of continence in most patients and ease of use. Longer follow-up is needed to determine the extent of problems with infection, erosion, and mechanical failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02237423
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  • 9
    Electronic Resource
    Electronic Resource
    Misoprostol protection against acetaminophen-induced hepatotoxicity in the rat (1994)
    Springer
    Digestive diseases and sciences 39 (1994), S. 1249-1256 
    Details
    ISSN: 1573-2568
    Keywords: acetaminophen ; hepatotoxicity ; misoprostol ; hepatoprotection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The hepatoprotective effects of misoprostol on acetaminophen (APAP)-induced toxicity were studied in the rat. Liver injury was evaluated at 36 hr after APAP administration by measuring serum ornithine carbamoyltransferase (OCT) and alanine aminotransferase (ALT) levels, by using tetranitroblue tetrazolium (TNBT) staining and by histological analysis. After APAP administration, peak serum levels of the drug were detected at 15 min. Liver GSH was depleted from control levels of 448±48 µg/g to 82±2 µg/g (P〈0.01) within 3 hr. Serum ALT levels increased significantly after 16 hr and H&E staining revealed significant hepatic necrosis after 12 hr. Rats treated with misoprostol before and after APAP administration showed reduced OCT and ALT levels at 36 hr of overdose (454±446 IU/liter and 2571±2944 IU/liter, respectively) compared to those without misoprostol treatment (1348±480 IU/liter and 6077±3025 IU/liter, respectively,P〈0.01). TNBT staining showed a reduced area of damage from 28.6±22.3% to 7.3±8.9% (P〈0.01), and H&E staining also showed less extensive hepatic necrosis in rats treated with misoprostol before and after the overdose. In a time sequence study, misoprostol treatment starting within 10 hr of overdose showed the same protective effect as when it was given before and after APAP ingestion. No protection was detected when the treatment was started during the development of hepatic injury. However, misoprostol given when injury was established seemed to be protective. Our results show that misoprostol protects the liver against APAP-induced injury if given within 10 hr of overdose. Late administration of misoprostol may also be beneficial and thus may be considered in treating patients with APAP toxicity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02093790
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  • 10
    Electronic Resource
    Electronic Resource
    5-Aminosalicylic Acid and Olsalazine Inhibit Tumor Growth in a Rodent Model of Colorectal Cancer (2000)
    Springer
    Digestive diseases and sciences 45 (2000), S. 1578-1584 
    Details
    ISSN: 1573-2568
    Keywords: chemoprevention ; colorectal cancer ; 5-aminosalicylic acid ; olsalazine ; apoptosis ; bromdeoxyuridine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The ability of 5-aminosalicylic acid and olsalazine to inhibit colonic aberrant crypts and tumors was investigated in 1,2-dimethylhydrazine-treated rats. The effect of these drugs on the rates of tumor apoptosis and proliferation was studied as potential mechanisms for their action. 5-Aminosalicylic acid reduced the number of aberrant crypt foci by over one third, while olsalazine had no effect on this parameter. However, both agents effectively reduced tumor number and load, increased the rate of tumor apoptosis, and reduced the rate of tumor cell proliferation. In conclusion, 5-aminosalicylic acid and olsalazine are both ultimately effective chemopreventive agents in this model; however, only 5-aminosalicylic acid inhibited the formation of aberrant crypt foci. The inhibitory effect of these agents in tumors is related to the inhibition of proliferation and the induction of apoptosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005517112039
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