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Biomedical subjects

J Lonovics

Publications and source records attributed to J Lonovics.

107 records · Page 6Linked to original sources
PubMed1979

Investigation of cholecystokinin-octapeptide splitting enzyme in dog kidney.

In vitro experiments were carried out to examine the enzymatic activity in various organ homogenates of the dog, which inactivates the biological activity of the synthetic cholecystokinin-octapeptide (CCK-OP). The highest splitting activity was found in the renal cortex; substantially lower activities were registered in the lung, pancreas and small intestine. It seems interesting that neither the gallbladder nor the saliva and the serum contained measurable amount of the CCK-OP splitting activity. An effort was made to characterize the CCK-OP inactivating principle found in the renal cortex. It was ascertained that the CCK-OP was inactivated by a peptidase which is heat sensitive, has a pH optimum of 7,4 and could be inhibited by chelating agents (EDTA) and epsilon-aminocaproic acid. The fact that most of the enzyme function is associated with the sediment obtained at 12 000 g speaks in favour of its mitochondrial origin.

Animals↗
PubMed1975

Anaphylactoid-inflammation-promoting factor. An insulin-induced factor derived from non-sensitized lymphocytes increases anaphylactoid inflammation in rats.

The experiments reported here indicate that, when exposed to insulin, viable lymphocytes rapidly released into the incubation medium a factor capable of increasing the dextran-induced anaphylactoid reaction, but having no effect on the inflammatory response evoked by 5-HT. This pro-inflammatory factor was shown to be elaborated by cell suspensions derived from lymph nodes of rats, rabbits, pigs or calves as well as from human tonsils. Thymus cells showed no such activity. The pro-inflammatory factor was termed as anaphylactoid-inflammation-promoting factor (AIPF). Its production depended upon the dose of insulin, and the time of exposure. AIPF was found to have an elution pattern in Sephadex G-100 gels similar to that of BSA (67,000 daltons). The activity was abolished by heat or incubation with DNase or a-chymotrypsin, but was not influenced by RNase. AIPF by itself did not induce increased vascular permeability, and proved to be distinct from the permeability factors present in the lysate of lymph node cells.

Adrenalectomy↗
PubMedDate not supplied

Recovery of exocrine pancreas six months following pancreatitis induction with L-arginine in streptozotocin-diabetic rats.

The aim of the present work was to investigate the laboratory and morphologic alterations in the pancreas 6 months after pancreatitis induction with L-arginine (Arg) in normal and streptozotocin (STZ)-diabetic rats. The amylase content of the pancreas was significantly decreased in the Arg-treated groups vs. the control group. No significant changes were observed in the DNA, soluble protein and lipase contents of the pancreas. In the STZ-treated groups, the serum glucose level was significantly elevated, whereas the serum immunoreactive insulin (IRI) level was significantly decreased vs. the control group. In these treated groups, the amylase content of the pancreas was also significantly decreased, but that of trypsinogen was significantly elevated vs. the control group. Histologic sections revealed periductal fibroses, adipose tissue and tubular complexes in the Arg-treated rats, but centroacinar hyperplasia was not observed in these groups. No alterations were observed on histological examination in the diabetic rats vs. normal rats 6 months following pancreatitis induction. In conclusion, a major restitution of the pancreatic enzyme content, but moderate histologic alterations were detected 6 months following pancreatitis induction with Arg. The diabetic state appeared to shift the normal pancreatic enzyme content (decreased amylase and increased trypsinogen) in this long-term study, but not to modify the recovery of the exocrine pancreas 6 months following Arg-induced pancreatitis.

Amylases↗
PubMedDate not supplied

The pathogenesis of L-arginine-induced acute necrotizing pancreatitis: inflammatory mediators and endogenous cholecystokinin.

This study was aimed at an assessment of the role of oxygen-derived free radicals, cytokines and endogenous cholecystokinin (CCK) in the pathogenesis of L-arginine (Arg)-induced acute pancreatitis in rat. We measured the levels of malonyl dialdehyde (MDA), glutathione peroxidase (GPx), catalase and superoxide dismutase (Mn- and Cu, Zn-SOD) in pancreatic tissue, the serum levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and CCK, and evaluated the protective effect of the xanthine oxidase inhibitor allopurinol and a novel CCK receptor antagonist KSG-504. Acute pancreatitis was induced in male Wistar rats by injecting 2x 250 mg/100 g body weight of Arg intraperitoneally in an 1-h interval, as a 20% solution in 0.15 M NaCl. Control rats received the same quantity of glycine. 200 mg x kg(-1) allopurinol 30 min before the first Arg treatment or 50 mg x kg(-1) KSG-504 30 min before and 6, 18 and 36 h after the first Arg injection was administered subcutaneously. Rats were killed at 6, 12, 24 and 48 h following Arg administration, and acute pancreatitis was confirmed by a serum amylase level elevation and typical inflammatory features observed microscopically. The serum level of amylase reached the peak level at 24 h after the Arg injection (30,800 +/- 3,813 versus 6,382 +/- 184 U x L(-1) in the control) and normalized at 48 h. The tissue concentration of MDA was significantly elevated at 24 h, and reached the peak value at 48 h (5.00 +/- 1.75 versus 0.28 +/- 0.05 nM x mg(-1) protein in the control). The catalase and Mn-SOD activities were significantly decreased throughout the study, while the GPx activity was significantly reduced at 6 and 12 h, and the Cu, Zn-SOD activity was significantly lower at 12 h after the Arg injection as compared with the controls. Both the TNF-alpha and the IL-6 levels were already elevated significantly at 12 h and peak at 24 h versus the controls (19.1 +/- 7.9 U x mL(-1) and 57.6 +/- 11.2 pg x mL(-1) versus 3.1 +/- 0.8 U x mL(-1) and 15.2 +/- 3.1 pg x mL(-1), respectively). No significant changes in plasma CCK levels were observed. Allopurinol treatment markedly reduced the serum amylase elevation (12.631 +/- 2.257 U x L(-1) at 24 h), prevented the increase in tissue MDA concentration (0.55 +/- 0.09 nM x mg(-1) protein at 48 h) and significantly ameliorated the pancreatic edema, necrosis and inflammation at 48 h after Arg administration. KSG-504 administration did not exert any beneficial effect on the development of histopathological changes neither modified the serum amylase or cytokine levels. Oxygen-derived free radicals and cytokines are involved, while endogenous CCK does not seem to play a role in the pathogenesis of Arg-induced acute pancreatitis.

Allopurinol↗
PubMedDate not supplied

Water immersion pretreatment decreases pro-inflammatory cytokine production in cholecystokinin-octapeptide-induced acute pancreatitis in rats: possible role of HSP72.

Heat shock proteins (HSPs) are cytoprotective proteins that are expressed constitutively and/or at elevated levels upon the exposure of cells to stress. The aim of this study was to investigate the potential effects of HSP preinduction by cold- (CWI) or hot-water immersion (HWI) on pro-inflammatory cytokine production (IL-1, IL-6, TNF-alpha) in cholecystokinin-octapeptide(CCK)-induced acute pancreatitis. Rats were injected with 3 x 75 microg/kg CCK subcutaneously at intervals of 2 h at the peak level of HSP synthesis, as determined by Western blot analysis. The animals were killed by exsanguination through the abdominal aorta 2 h after the last CCK injection. The serum IL-1, IL-6, TNF-alpha, and amylase levels, the pancreatic weight/body weight ratio, and the pancreatic contents of DNA, protein, amylase, lipase and trypsinogen were measured; biopsy for histology was taken. HWI significantly elevated the HSP72 expression, while CWI significantly increased the HSP60 expression. HWI pretreatment decreased all of the measured serum cytokine levels in this acute pancreatitis model. CWI and HWI pretreatment ameliorated most of the examined laboratory and morphological parameters of CCK-induced pancreatitis. The findings suggest the possible roles of HSP60 and HSP72 in the protection against CCK-induced pancreatitis. HSP72 might also participate in the reduction of pro-inflammatory cytokine synthesis.

Acute Disease↗
PubMedDate not supplied

Opposite effects of acute and chronic administration of alcohol on gastric emptying and small bowel transit in rat.

The effects of acute and chronic administration of a large dose of alcohol on gastric emptying and small bowel transit were studied in rats. The development of tolerance to the acute effect of alcohol on gastrointestinal motility during chronic alcohol administration was also investigated. Gastric emptying and small intestinal transit were assessed by the Phenol Red recovery method. Acutely, ethanol was given in a dose of 2.5 g/kg body wt by gavage 30 min before the test meal. Chronically, ethanol was administered by two different methods: (1) a dose of 2.5 g/kg body wt was administered by gavage daily for 10 days; (2) animals received 15% ethanol in their drinking water for 30 days. A single large dose of alcohol inhibited gastric emptying and small bowel transit. Treatment with a large dose of alcohol for 10 days did not change the gastric emptying significantly, but inhibited the small intestinal transit. Alcohol consumption in drinking water for 30 days accelerated gastric emptying and small bowel transit. Tolerance to the acute inhibitory effect of a single large dose of alcohol on gastrointestinal motility did not develop during chronic alcohol treatment.

Animals↗
PubMedDate not supplied

Manometric assessment of impaired esophageal motor function in primary Sjögren's syndrome.

OBJECTIVE: To evaluate by manometry the esophageal motility changes in patients with primary Sjögren's syndrome (SS). METHODS: Esophageal manometry was carried out in 25 (F/M: 22/3) primary SS patients with systemic manifestations and in 42 control subjects. The primary SS patients also completed a dysphagia scoring questionnaire and underwent whole salivary flow measurements. RESULTS: As compared with the controls the primary SS patients exhibited a decreased lower esophageal sphincter (LES) pressure (P < 0.01) and a prolongation of LES relaxations (P < 0.02). In the esophageal body (EB) a decreased peristaltic velocity (p < 0.01), an increased duration of contractions (p < 0.01) and a higher occurrence of simultaneous waves (p < 0.01) were detected. Since decreased peristaltic velocity was the most frequent motor abnormality (11/25 cases), two groups of patients were formed for further analysis: patients with a decreased (group I, n = 11) and patients with a normal (group II, n = 14) peristaltic velocity. The SS patients with a decreased EB propagation velocity (< or = 2.7 cm/s, group I) displayed more significantly decreased pressures (p < 0.01) and more prolonged relaxation times (p < 0.05) in the LES, with higher rates of simultaneous contractions on dry swallows (p = 0.05) in the EB, as compared with those who had a normal peristaltic velocity (group II). Of the clinical parameters, the decreased EB peristaltic velocity was associated with a smaller whole saliva production both in the basal state and after stimulation. Furthermore, this group of patients had a significantly higher liquid requirement for swallowing than those who had normal peristaltic velocities (p = 0.05). CONCLUSIONS: Primary SS patients with systemic manifestations exhibit several esophageal motility abnormalities. In this study, a decreased EB peristaltic velocity was the most common manometric change, and showed an association with impaired saliva production and higher liquid requirement for swallowing, but not with the laboratory parameters or with the systemic manifestations of the disease.

Adult↗