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  • 1
    Electronic Resource
    Electronic Resource
    Evaluation of putative cytoprotective properties of antiulcer drugs using quantitative histological techniques (1990)
    Springer
    Digestive diseases and sciences 35 (1990), S. 1130-1139 
    Details
    ISSN: 1573-2568
    Keywords: cytoprotection ; histology ; ethanol ; prostaglandin ; antiulcer drugs
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The capacity for cytoprotection has been claimed for a number of drugs that may have a place in the treatment of peptic ulcer disease. In this study we have used quantitative histological criteria to evaluate the ability of these drugs to be cytoprotective and have compared their effects with that of natural prostaglandin E2 (PG). The standard rat model, with injury by instillation of 1 ml of absolute ethanol, has been used. Putative cytoprotective agents were administered 15 min prior to ethanol. Each animal was sacrificed 15 min after ethanol exposure. The stomach was removed and studied using an established quantitative histological technique. This technique provides a measure of the surface area of mucosa damaged and of the volume of mucosa damaged. Ethanol alone caused damage to 76% of the area of the rat stomach and 14% of the volume of the rat gastric mucosa. Pretreatment by PG (25 μg/ml) resulted in reduction of the area of damage to 45% and reduction of the percentage volume damage to 2.2%. The synthetic analog of PGE2, Enprostil (1 μg/ml) achieved similar protective effects. With pretreatment with colloidal bismuth subcitrate (10 mg/kg) or sucralfate (25 mg/kg), no protection against the surface area damaged by ethanol was seen, but there was a marked reduction of the volume of mucosa damaged. Indomethacin pretreatment augmented the damage caused by ethanol. The protective effects of colloidal bismuth subcitrate and sucralfate were not blocked by pretreatment with indomethacin. The histamine H2-receptor antagonists cimetidine and ranitidine, the substituted benzimadazole compound omeprazole, and the antimuscarinic drug pirenzepine did not exhibit any cytoprotective effect in this study.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01537586
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  • 2
    Electronic Resource
    Electronic Resource
    Inability of cytoprotection to occur during a period of gastric ischemia (1991)
    Springer
    Digestive diseases and sciences 36 (1991), S. 1353-1360 
    Details
    ISSN: 1573-2568
    Keywords: cytoprotection ; microcirculation ; sucralfate ; prostaglandin E2 ; colloidal bismuth subcitrate ; ischemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Prostaglandin E2 (PGE2), colloidal bismuth subcitrate (CBS), and sucralfate (SUC) are known to protect the gastric mucosa from ethanol injury. The proposed central role for the microcirculation in gastric mucosal defense and as a site for the expression of the protective effects of these agents was investigated in the rat stomach. Animals were pretreated with either PGE2, CBS, or SUC. Control rats were given normal saline. After allowing 15 min for expression of the pretreatment, ethanol was administered as a 10%, 25%, 50% or 100% solution to groups of rats with normally perfused stomach and to other groups of rats in whom the stomach was made ischemic by cross-clamping the supracoeliac aorta immediately prior to the instillation of ethanol. The extent of gastric mucosal damage was measured using quantitative histological techniques and expressed as a percentage of surface area and volume of mucosa damaged. In the presence of ischemia, the extent of damage by ethanol was markedly increased, with total destruction of the mucosa by the 50% and 100% solutions. With 25% ethanol, the volume of mucosal damage was increased from 0.5% in the normally perfused stomach to 53.5% with ischemia. When 10% ethanol was instilled into the ischemic stomach, only 0.8% of the volume of the mucosa was damaged, which was not different from the volume of mucosa damaged after the ischemic stomach was exposed to normal saline alone (1.0%). Pretreatment with PGE2, CBS, or SUC did not significantly change the extent of damage seen with exposure of the ischemic stomach to 25% or 50% ethanol. These results show that the absence of normal mucosal microvascular perfusion markedly increases the extent of damage by ethanol and that, in the absence of microvascular flow, the protective effects of PGE2, CBS, and SUC are not expressed. These findings support the proposal that a primary component of the protective action of these agents is the, maintenance of the integrity of the mucosal microvasculature.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01296799
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  • 3
    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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  • 4
    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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  • 5
    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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  • 6
    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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