Search PubMed⌕ Search

Biomedical subjects

S Szabo

Publications and source records attributed to S Szabo.

At least 109 records · Page 6Linked to original sources

From cysteamine to MPTP: structure-activity studies with duodenal ulcerogens.

Cysteamine is the first chemical identified that induces acute and chronic duodenal ulcers in rodents. Structure-activity studies with cysteamine, propionitrile and their derivatives, as well as with analogues of toluene, revealed numerous alkyl and aryl duodenal ulcerogens. Among these, one of the most interesting from an etiologic and pathogenetic point of view is the dopaminergic neurotoxin MPTP, which shows structural similarities with toluene. The chemically-induced duodenal ulcers are similar and localized on the anterior and posterior wall of the duodenal bulb. Both cysteamine and MPTP affect endogenous dopamine; MPTP is especially potent in depleting central dopamine and inducing lesions in the substantia nigra. MPTP given in high doses induces Parkinson's disease-like syndrome and gastric ulcers. Cysteamine and propionitrile also cause dyskinesia in large and multiple doses. The motility disorders and duodenal ulcers are abolished by dopamine agonists. Cysteamine and MPTP have been known to increase and decrease gastric acid secretion, respectively. However, both compounds induced duodenal dysmotility, decreased bicarbonate production, and reduced its delivery from distal to proximal duodenum. These factors decrease acid neutralization in the duodenal bulb and contribute to duodenal ulceration. Thus, studies with animal models may reveal endogenous mediators and specific receptors which might be involved in the pathogenesis of duodenal ulceration. Specific structure-activity studies in toxicology may lead to new insights in the pathogenesis and pharmacology of a poorly understood human disorder such as duodenal ulceration.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

Alternatives to the acid-oriented approach to ulcer disease: does 'cytoprotection' exist in man? A new classification of antiulcer agents.

This review summarizes the historical contradictions and inconsistencies that form the labile arguments advocating neutralization or inhibition of secretion of gastric acid for the prevention or treatment of gastroduodenal ulcers. Re-evaluation of old concepts is needed in the wake of recognition that even the most potent antisecretory agents do not change the natural history of ulcer disease; that is, the recurrence is high after termination of treatment. New biochemical, functional, and structural targets are listed for pharmacologic intervention in ulcer disease. As a supplement or alternative to the antisecretory agents, we should now consider prosecretory agents (for example, for bicarbonate and mucus secretion) and antioxidants (for example, free radical scavengers). Gastroduodenal motility, smooth muscle, the vascular endothelial cell, and the basement membrane seem to represent additional pharmacologic targets toward which new gastroprotective drugs can be directed even though the biochemical mechanism of action of these new agents may not be fully understood. New results suggest that these elements have a role in the pathogenesis of ulcer disease, and their modulations seem to exert a beneficial effect without inhibiting gastric secretion in rodents. In man, the acid antisecretory and cytoprotective doses seem to overlap, but arguments are presented to shift defining gastric 'cytoprotection' by the dose of drugs to the characterization of the phenomenon (for example, events such as the ethanol-induced hemorrhagic erosions which cannot be decreased by antisecretory agents). Furthermore, non-prostaglandin and non-H2-receptor antagonist drugs are available that exert acid-independent gastroprotection both in animals and humans. The future is thus bright for the development of new antiulcer agents.

Anti-Inflammatory Agents, Non-Steroidal↗

Effects of thyrotropin-releasing hormone and its analogue L-6-ketopiperidine-2-carbonyl-leucyl-L-prolin-amide on behaviour and electroencephalogram.

A comparative dose-response investigation of thyrotropin-releasing hormone (TRH) and L-6-ketopiperidine-2-carbonyl-leucyl-L-proline-amide (RGH-2202) was carried out on rats and cats. RGH-2202 reduced the occurrence of photically evoked after-discharge in rats more significantly than TRH. Neither of the two compounds influenced the parameters of visually evoked potentials. Both compounds desynchronized the background electrocortical activity in rats. The amplitude of the acoustic startle reflex in rats was decreased dose-dependently only by RGH-2202, and this effect was nearly 3 times more potent than that of TRH. Both compounds increased the time spent awake, the latency to light sleep and the proportion of light sleep in a dose-dependent manner. The higher doses of TRH equalled the effects of the lower doses of RGH-2202. In cats the latency increasing effect of TRH on paradoxical sleep was about 30% less than that of RGH-2202; furthermore, the relative increase in the proportion of light sleep coupled with a corresponding decrease of deep sleep and paradoxical sleep was significant only in the case of RGH-2202. In a complex conditioned reflex situation in cats, the dose-dependent motivation decreasing effect on food intake and, as a consequence, on spontaneous motor activity was more pronounced in the case of TRH. The effective doses of RGH-2202 and TRH in rats were nearly equal, while in cats RGH-2202 showed about 1/10 of the potency of TRH. This finding suggests a considerably lower species variability of the effects of RGH-2202.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Extrahepatic obstructive jaundice due to colorectal cancer.

A prospective registry of patients with obstructive jaundice referred for percutaneous bile duct drainage found six patients with extrahepatic obstruction due to colorectal cancer in a 21-month period. This cause of jaundice in patients with colorectal cancer is not uncommon, and deserves routine diagnostic consideration, even in the presence of intrahepatic metastases. Percutaneous biliary drainage was beneficial for four of the six patients.

Adenocarcinoma↗

Gastric mucosal protection by acetazolamide derivatives: role of carbonic anhydrase and sulfhydryls.

Acetazolamide, a carbonic anhydrase inhibitor, prevents acute gastric hemorrhagic lesions induced by ethanol. We used acetazolamide and other carbonic anhydrase inhibitors to correlate their gastroprotective effects with the degree of inhibition of carbonic anhydrase. Since acetazolamide is a thiadiazole, we also investigated structurally related thiadiazoles that contain sulfhydryls to test the hypothesis that the protection against ethanol-induced gastric erosions is related to the presence of sulfhydryls. Dose-response studies with acetazolamide revealed that the protection did not correlate with the inhibition of carbonic anhydrase in the rat gastric mucosa. The carbonic anhydrase inhibitors sulfanilamide and ethoxzolamide, did not offer protection. Bismuthiol I, a thiadiazole with two sulfhydryls, was twice as protective as 2-amino-5-mercapto-1,3,4-thiadiazole with only one sulfhydryl group. We conclude that the protection by acetazolamide against ethanol-induced lesions is not related to the inhibition of carbonic anhydrase in the gastric mucosa. The gastroprotective effect of acetazolamide and its derivatives may be related to their content of sulfhydryls in an oxidized or reduced state.

Acetazolamide↗

Time-course studies of the distribution of [1-14C]acrylonitrile in rats after intravenous administration.

Intravenous injection of acrylonitrile (ACN) causes adrenal hemorrhagic necrosis. ACN and its metabolites react with glutathione and bind covalently with macromolecules. Hence the purpose of this investigation was to measure the distribution and covalent binding of radiolabel derived from [1-14C]ACN in order to determine whether binding of ACN or its metabolites may be implicated in the pathogenesis of ACN-induced adrenal injury. Following intravenous injections of ACN, concentrations of total radiolabel were highest in the blood, liver, duodenum, kidneys, and adrenals. Except for blood, there was a time-dependent decrease in total radiolabel in these tissues. Compared with other major organ systems, the levels of covalently bound radiolabel were lower in the adrenal glands. These results do not support a role of covalent binding of ACN or its metabolites in the adrenal toxicity of ACN, but suggest that the initial high concentrations of total radiolabelled compounds derived from ACN could play a role in the action of ACN on the adrenal glands.

Acrylonitrile↗

Free radicals and lipid peroxidation in ethanol- or aspirin-induced gastric mucosal injury.

In this study the role of free radicals and lipid peroxidation as mediators of chemically induced mucosal damage was investigated. Two enzymatic antioxidants, superoxide dismutase or catalase injected intravenously, reduced mucosal damage either by ethanol or aspirin. Of six nonenzymatic antioxidants, given in a wide dose range subcutaneously 30 min before intragastric administration of absolute ethanol, only propyl gallate decreased mucosal damage, while four of the antioxidants tested against aspirin were protective. These nonenzymatic antioxidants were antisecretory in the pylorus-ligated rat. The concentration of conjugated dienes and malondialdehyde measured in the gastric mucosa shortly after ethanol or aspirin administration remained unchanged or slightly decreased. These results indicate that free radicals may be involved in the pathogenesis of acute gastric mucosal injury caused by chemicals, but their mechanisms of action probably does not involve lipid peroxidation.

Animals↗

Infections associated with transhepatic biliary drainage devices.

To determine the infectious complications associated with transhepatic biliary drainage devices, an analysis of the records of 38 patients who underwent placement of a pigtail catheter (n = 11), a Ring catheter/feeding tube (n = 13), or a Carey-Coons endoprosthesis (n = 15) was carried out. Nineteen infectious events occurred in 38 patients with 39 biliary devices. Infections consisted of bacteremia, cholangitis with and without documented bacteribilia, and intrahepatic abscesses and were frequently associated with obstruction (66.7 percent of infectious episodes). The most frequent organisms isolated from blood were Escherichia coli and Pseudomonas aeruginosa, and the most frequent organisms isolated from bile were P. aeruginosa, Klebsiella pneumoniae and Streptococcus faecalis. Trends for more frequent occurrence of neoplasms involving the gallbladder or biliary tract, recent surgical procedures and catheter manipulations in infected as compared with noninfected patients, and a delayed time to infection were noted in patients with an endoprosthesis.

Adult↗

Early ultrastructural changes in rat duodenal mucosa associated with cysteamine-induced ulcer.

The early morphologic sequelae induced by the duodenal ulcerogen, cysteamine, have been studied in rats by transmission electron microscopy. Cysteamine was administered per os at 70 mg/100 g body wt to groups of female rats sacrificed at 30 min, 1, 2, 4, 8, 12, 20, and 24 hr after chemical treatment, and duodenal tissue sampled from the antimesenteric side of the proximal duodenum, where ulcers develop, was studied. Emphasis was placed on early times as our previous scanning electron microscopic data had demonstrated enhanced in situ cellular necrosis and surface cavitation at 2-4 hr after cysteamine treatment. Results indicated intracellular changes as early as 30 min after treatment and prior to damage of the columnar cell microvilli or epithelial tight junctions. A staging of observed cellular degenerative changes suggested early apical endoplasmic reticular swelling and loss of cytoplasmic ground substance, followed later by moderate internal disruption of mitochondria. Through these stages the cell surface microvilli remained morphologically normal. Subsequently, microvilli degenerated and mitochondrial fine structure became severely disrupted and cell contents were expelled. Deeper villous changes such as separation of columnar cells from the lamina propria and alterations of selected elements within the lamina propria were observed. These data suggest that intracellular cytotoxic reactions at the villous tips occur early and may precede the influence of intraluminal damaging factors induced by cysteamine.

Animals↗

Ethanol-induced damage to mucosal capillaries of rat stomach. Ultrastructural features and effects of prostaglandin F2 beta and cysteamine.

Impairment of the mucosal microcirculation may contribute to ethanol-induced gastric mucosal damage. In this report, we describe diffuse and severe ultrastructural damage to the capillaries of the gastric glandular mucosa of the rat that occurred within 1 min after intragastric instillation of 100% ethanol. There was a gradient of damage in that endothelial cell structure was most severely disrupted in profiles of capillaries located close to the luminal surface but some morphologic evidence of damage was evident in the wall of capillary profiles to a mean depth of 256 micron. Capillary structure was generally normal in the deeper regions of the mucosa. Pretreatment with intragastric cysteamine, 30 mg/100 g, or intragastric prostaglandin F2 beta, 0.5 mg/100 g, significantly reduced the depth in the mucosa to which damage to capillaries extended. Pretreatment with intragastric prostaglandin F2 beta, 0.2 mg/100 g, afforded no significant protection. We conclude that a 1-min exposure to 100% ethanol induces striking damage to the microcirculation of glandular mucosa of the rat stomach with severe damage to capillary profiles near the lumen and sparing of capillary profiles near the muscularis mucosa, and pretreatment with the sulfhydryl agent, cysteamine, or with a large dose of prostaglandin F2 beta reduces the extent of but does not abolish ethanol-induced damage to gastric mucosal capillaries.

Animals↗

Development and significance of cysteamine and propionitrile models of duodenal ulcer.

Cysteamine is widely used in rodents to induce duodenal ulcer. Herein, the pathogenesis of duodenal ulceration in its earliest stages was reviewed using findings from cysteamine- and propionitrile-induced duodenal ulcer in rodent models, especially taking into account changes in the secretion of gastric acid, duodenal and pancreatic bicarbonate as well as gastroduodenal motility. The effect of cysteamine-HCl in inducing ulcers in rats is circadian rhythm-dependent. The effect is greatest from just before the end of diurnal rest to just after the start of nocturnal activity. The chronobiologic effect may be in part due to the circadian rhythm-dependent increased gastric acid production from cysteamine. Titratable acidity was found to be twice as great in the gastric juice of rodents when cysteamine was given by injection at 2000 (just after the start of nocturnal activity) in comparison to when given at 0800 or 1200 (at the beginning or middle span of daily rest). Further studies have shown that adrenalectomy of rats 7 days before cysteamine administration obliterated the observed circadian susceptibility to ulcer formation. Duodenal ulceration, at least in the cysteamine model, appears to be under chronobiologic neuroendocrine control or influence, seemingly mediated by the adrenal glands.

Animals↗

Mechanisms of gastric cytoprotection.

Gastric cytoprotection is a real but relative phenomenon that is induced by both endogenous and exogenous compounds. The key element in acute mucosal protection is the preservation of vascular integrity and the resulting maintenance of blood flow. The critical factors in chronic mucosal protection include the stimulation of bicarbonate and mucus secretion, and the proliferation of epithelial, endothelial, and mesenchymal cells. Investigations are currently underway to identify the biochemical targets of cytoprotection.

Animals↗

Role of lipid peroxidation in gastric mucosal lesions induced by HCl, NaOH, or ischemia.

We investigated whether lipid peroxidation is an important biochemical mechanism in acute gastric mucosal injury induced by acid, base, or postischemic reperfusion. Lipid peroxidation products, i.e., the concentration of conjugated dienes (absorbance at 242 nm), products absorbing at 270 nm, and malondialdehyde were measured in the gastric mucosa of rats killed 30 s or 1, 3, or 6 min after intragastric (ig) administration of 0.6 N HCl or 0.2 N NaOH. No increase in any of the lipid peroxidation products was detected at any of the time intervals. Mucosal lesions, however, were already visible at 30 s. Cumene hydroperoxide (1 ml, 100 mM ig) induced neither mucosal lesions nor lipid peroxidation. In vitro incubation of mucosal homogenates with cumene hydroperoxide (1 or 10 mM) however, rapidly induced elevation of the three parameters of lipid peroxidation. Ischemia induced by clamping the blood vessels of the stomach for 20, 30, and 40 min followed by reperfusion for 10, 30, and 40 min did not induce lipid peroxidation, despite the development of hemorrhagic mucosal lesions. Similarly, in gastric mucosal lesions induced by hemorrhagic shock no lipid peroxidation products were detected. In the small intestine, however, prolonged ischemia (2 h) followed by reperfusion (30 min) resulted in mucosal necrosis and elevation of malondialdehyde levels. These results suggest that lipid peroxidation is not a major pathogenetic mechanism in rapidly developing acute gastric mucosal injury caused by 0.6 N HCl or 0.2 N NaOH, or in the more slowly developing mucosal injury caused by postischemic reperfusion.

Animals↗

Mechanisms of mucosal injury in the stomach and duodenum: time-sequence analysis of morphologic, functional, biochemical and histochemical studies.

This review is based on results from our laboratory and those published by others, and is focused on the early stages of pathogenesis that can be studied mostly in animals. Gastric mucosal injury is analysed on the examples of ethanol- and aspirin-induced lesions. Ethanol (50-100%) rapidly penetrates the mucosa, causes directly and/or indirectly (e.g., release of vasoactive products) endothelial damage in superficial and deep capillaries and venules. The vascular damage results in increased vascular permeability and decrease in blood flow leading to complete circulatory standstill in superficial capillaries 1-2 min after intragastric administration of concentrated ethanol. The direct chemical damage to surface mucosal epithelium is then followed by hypoxia and deep hemorrhagic necrosis in 1-5 min (erosion or ulcer). Unionized aspirin initiates a similar and complex yet slower progressing and less extensive erosion than alcohol. Duodenal erosion and ulcer produced by cysteamine, mepirizole or MPTP are preceded by excess acid in the proximal duodenum. This could be due to increased gastric acid output (1-4 hr), decreased bicarbonate secretion or duodenal dysmotility (0.5-8 hr) preventing the proper mix of acid and base in duodenal bulb. Necrosis and desquamation of absorptive cells in duodenal villi are evident 2-4 hr, followed by villus amputation (4-8 hr), erosion and ulcer (8-24 hr). The pathogenesis of gastroduodenal mucosal injury can thus be reconstructed from results obtained with animal models and from human studies. The results should serve as a basis to design protective drugs that are active on the basis of pathogenetic events.

Animals↗

Prevention of ethanol-induced vascular injury and gastric mucosal lesions by sucralfate and its components: possible role of endogenous sulfhydryls.

We tested the hypothesis that sucralfate, which contains eight sulfate and aluminum molecules on a sucrose and its other components might decrease ethanol-induced vascular injury and hemorrhagic mucosal lesions through a sulfhydryl (SH)-sensitive process. Experiments performed in rats revealed that the entire sucralfate molecule is not a prerequisite for protection against ethanol-induced mucosal vascular injury and erosions. It appears that sulfate and sucrose octasulfate are potent components of sucralfate, although an equimolar amount of sucralfate is at least twice as effective in gastroprotection than its components. The SH alkylator N-ethylmaleimide abolished the gastroprotection by sucralfate, suggesting SH-sensitive process in the mucosal protection which seems to be associated with the prevention of rapidly developing vascular injury in the stomach of rats given ethanol.

Aluminum↗

Gastric mucosal protection by agents altering gastric mucosal sulfhydryls. Role of endogenous prostaglandins.

Intragastric administration of sulfhydryl-containing cysteamine or sulfhydryl-oxidizing diethylmaleate caused a dose-dependent reduction in the mean area of gastric lesions induced by absolute ethanol. The protective effects of these agents are abolished by the sulfhydryl blocker N-ethylmaleimide, while indomethacin, a potent inhibitor of cyclooxygenase, caused only about 50% reduction in this protection. This study indicates that mucosal generation of prostaglandins contributes to the gastric cytoprotection by these agents administered intragastrically, but endogenous sulfhydryls are also involved in the gastric mucosal protection by sulfhydryl-containing or sulfhydryl-oxidizing compounds.

Animals↗

Biochemical changes in tissue catecholamines and serotonin in duodenal ulceration caused by cysteamine or propionitrile in the rat.

Previous structure-activity and pharmacologic studies with duodenal ulcerogens cysteamine and propionitrile implicating catecholamines in the pathogenesis of duodenal ulceration have now been followed up by dose- and time-response biochemical investigations to assess the importance of monoamines in the development of duodenal ulcers. The concentrations of norepinephrine (noradrenaline), dopamine, serotonin and their metabolites were measured in total brain, brain regions, stomach, duodenum, pancreas and adrenals in the rat. Turnover of catecholamines was determined in rats pretreated with the inhibitor of tyrosine hydroxylase alpha-methyl-p-tyrosine. The duodenal ulcerogens caused a dose- and time-dependent depletion of norepinephrine in virtually all the tissues examined. The effect was maximal 4 or 7 hr after cysteamine or propionitrile, and norepinephrine levels returned to normal in 24 hr. Dopamine changes were selective and often biphasic, e.g., elevation in adrenals, biphasic in brain cortex, hippocampus and midbrain, but uniformly decreasing in glandular stomach and duodenum. In the median eminence dopamine levels decreased by 181 and 324% at 15 and 30 min, respectively, after cysteamine, but neither dopamine nor 3,4-dihydroxyphenylacetic acid was modified in the periventricular nucleus. Serotonin levels were relatively stable, revealing slight elevations or no changes in most of the tissues. The turnover of norepinephrine was accelerated by both chemicals in virtually all brain regions, but dopamine turnover was affected only in a few areas, e.g., in the corpus striatum and medulla oblongata cysteamine decreased dopamine turnover, whereas propionitrile first (at 1 hr) accelerated then (at 8 hr) significantly suppressed it.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗