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Biomedical subjects

C Wallin

Publications and source records attributed to C Wallin.

18 recordsLinked to original sources
PubMed2002

Effect of budesonide enema on remission and relapse rate in distal ulcerative colitis and proctitis.

BACKGROUND: Glucocorticosteroid enemas are equally effective as 5-ASA enemas in the treatment of active distal ulcerative colitis (UC). With the introduction of budesonide, the risk of systemic side effects may be reduced. We investigated whether budesonide enema, 2 mg/100 ml, administered twice daily (b.i.d.) could increase the remission rate in comparison with the once daily (o.d.) standard regimen. Furthermore, we evaluated whether 2 mg budesonide enema, given twice weekly, could have a relapse preventing effect. METHODS: 149 patients with active distal UC were treated in a controlled, double-blind multicentre study with two parallel groups: placebo enema in the morning and budesonide enema in the evening (i.e. 2 mg/day) or budesonide enema b.i.d. (i.e. 4 mg/day) until remission (absence of clinical symptoms and endoscopic healing) or at most 8 weeks. Patients in remission were randomized to either budesonide enema or placebo enema twice weekly for 24 weeks or until relapse. RESULTS: The remission rates at 4 weeks were 33% for o.d. and 41% for b.i.d. regimens (NS) and correspondingly 51% and 54% at 8 weeks (NS). The b.i.d. group had an increased frequency of impaired adrenal function, 32% versus 4.8% (P = 0.001). The relapse rates during maintenance treatment with budesonide enema and placebo were 15% versus 24% after 8 weeks, 31% versus 27% after 16 weeks and 41% versus 51% after 24 weeks (NS). CONCLUSION: Budesonide enema 2 mg o.d. appears to be the optimal dosage in active distal UC. We could not show that budesonide enema twice weekly is sufficient to maintain remission.

Adolescent↗
PubMed2000

Impairment of mitochondrial respiration after cerebral hypoxia-ischemia in immature rats: relationship to activation of caspase-3 and neuronal injury.

Mitochondrial damage may play a key role in the development of necrotic and apoptotic hypoxic-ischemic (HI) brain damage. It has previously been shown that mitochondrial respiration is depressed in the cerebral cortex after HI in neonatal animals. The aim of the present study was to further characterize the time course of the mitochondrial impairment during reperfusion and the correlation between the respiratory control ratio and brain injury and activation of caspase-3. Rat pups were subjected to unilateral carotid artery ligation and exposed to hypoxia (7.7% oxygen). Mitochondrial respiration was measured 0-72 h after HI in a mitochondrial fraction isolated from cerebral cortex. Microtubule associated protein-2 (MAP2) and caspase-3 were analyzed with immunoblotting in cerebral cortex homogenates. In addition, the time course of caspase-3 activation was measured as DEVD cleavage. The mitochondrial respiratory control ratio in cerebral cortex decreased immediately after HI followed by a partial recovery at 3-8 h. Thereafter, a secondary drop occurred with a minimum reached at 24 h of reperfusion. The secondary loss of respiratory function was accompanied by depletion of MAP2, cleavage of caspase-3 and an increased caspase-3 -like activity at 3-24 h after the insult. In conclusion, the primary phase of mitochondrial dysfunction was paralleled by a moderate decrease of MAP2 and a limited activation of caspase-3. The secondary mitochondrial impairment was associated with neuronal injury and pronounced activation of caspase-3.

Animals↗
PubMed2000

Alterations in glutathione and amino acid concentrations after hypoxia-ischemia in the immature rat brain.

Hypoxic-ischemic brain injury involves an increased formation of reactive oxygen species. Key factors in the cellular protection against such agents are the GSH-associated reactions. In the present study we examined alterations in total glutathione and GSSG concentrations in mitochondria-enriched fractions and tissue homogenates from the cerebral cortex of 7-day-old rats at 0, 1, 3, 8, 14, 24 and 72 h after hypoxia-ischemia. The concentration of total glutathione was transiently decreased immediately after hypoxia-ischemia in the mitochondrial fraction, but not in the tissue, recovered, and then decreased both in mitochondrial fraction and homogenate after 14 h, reaching a minimum at 24 h after hypoxia-ischemia. The level of GSSG was approximately 4% of total glutathione and increased selectively in the mitochondrial fraction immediately after hypoxia-ischemia. The decrease in glutathione may be important in the development of cell death via impaired free radical inactivation and/or redox related changes. The effects of hypoxia-ischemia on the concentrations of selected amino acids varied. The levels of phosphoethanolamine, an amine previously reported to be released in ischemia, mirrored the changes in glutathione. GABA concentrations initially increased (0-3 h) followed by a decrease at 72 h. Glutamine levels increased, whereas glutamate and aspartate were unchanged up to 24 h after the insult. The results on total glutathione and GSSG are discussed in relation to changes in mitochondrial respiration and microtubule associated protein-2 (MAP2) which are reported on in accompanying paper [64].

Age Factors↗
PubMed1999

Net efflux of cysteine, glutathione and related metabolites from rat hippocampal slices during oxygen/glucose deprivation: dependence on gamma-glutamyl transpeptidase.

Extracellular metabolism of the protective substance glutathione (gamma-glutamyl-cysteinyl-glycine) may generate cysteine, glycine, several gamma-glutamyl-containing dipeptides and possibly free glutamate, all of which could participate in neurotoxicity. In the present study, we have examined how blockage of gamma-glutamyl transpeptidase, the key enzyme in glutathione degradation, influences the extracellular concentrations of glutathione, cysteine and related metabolites during anoxia/aglycemia of rat hippocampal slices. The net efflux, i.e., the increase in extracellular concentration due to changes in release and/or uptake, of cysteine, cysteine sulfinate, gamma-glutamyl-glutamate, gamma-glutamyl-glutamine, glutathione, gamma-glutamyl-cysteine and glutamate increased as a result of anoxia/aglycemia. These increases in net efflux of cysteine, cysteine sulfinate, gamma-glutamyl-glutamate and gamma-glutamyl-glutamine were reduced or blocked by acivicin, an inhibitor of gamma-glutamyl transpeptidase. In contrast, acivicin caused an increase in both basal and anoxia/aglycemia-induced net efflux of glutathione whereas the basal and anoxia/aglycemia-induced efflux of glutamate was unchanged by acivicin treatment. The effect of acivicin on the efflux of gamma-glutamyl-cysteine was similar to that of glutathione although less pronounced. Addition of beta-mercaptoethanol to the incubation medium during and after 30 min of anoxia/aglycemia decreased the net efflux of cysteine sulfinate specifically, indicating that the increase in cysteine sulfinate during anoxia/aglycemia may be partly derived from the spontaneous oxidation of cysteine. The results suggest that gamma-glutamyl transpeptidase may be involved in the regulation of the extracellular concentrations of cysteine, several gamma-glutamyl-containing dipeptides and glutathione but not glutamate during ischemia.

Animals↗
PubMed1999

Glutathione efflux induced by NMDA and kainate: implications in neurotoxicity?

Neurotoxicity in acute as well as chronic neurological diseases may be partly mediated by oxidative stress caused by overactivation of glutamate receptors. A key component of the cellular defense against oxidative stress is reduced glutathione. In our earlier work, we have shown that ischemia in brain induces increased efflux, elevated metabolism, and decreased tissue concentrations of glutathione. In this study, we have evaluated the effect of glutamate receptor activation on the efflux of glutathione from hippocampus in vitro. NMDA and kainate induced a delayed increase in glutathione, taurine, and phosphoethanolamine efflux. Extracellular glutathione was recovered mainly in the reduced form (85-95%); the efflux was dependent on extracellular calcium but unrelated to dantrolene-sensitive intracellular calcium release and independent of glutathione or NO synthesis. The NMDA-induced efflux of glutathione was enhanced by blockage of gamma-glutamyl transpeptidase, indicating an increased transpeptidation of glutathione after NMDA receptor activation. Our results suggest that increased efflux of glutathione could be a factor in initiating nerve cell death via a change in intracellular redox potential and/or a decrease in the intracellular capacity for inactivation of reactive oxygen species.

Animals↗
PubMed1995

Release of somatostatin, neurotensin and vasoactive intestinal peptide upon inhibition of gastric acid secretion by duodenal acid and hyperosmolal solutions in the conscious rat.

The inhibitory effect of duodenal exposure to acid and hyperosmolal solutions on pentagastrin-stimulated gastric acid secretion was studied in conscious rats equipped with chronic gastric fistula and duodenal Thiry-Vella loop. The loop was challenged with saline, HCl or hyperosmolal polyethylene glycol. Gastric acid secretion was measured in samples from the gastric fistula. Gut peptide concentrations were measured in duodenal perfusates collected each 30 min, and in plasma samples collected both during stimulated acid secretion alone, and at the end of experiments in combination with luminal challenges of the loops. During pentagastrin-stimulated gastric acid secretion, luminal perfusion of the duodenal loop with acid caused inhibition of acid secretion (P < 0.001) and a prominent release of somatostatin both to the lumen (P < 0.001) and to the circulation (P < 0.05). Also, neurotensin (P < 0.01) and vasoactive intestinal peptide (P < 0.01) were released to the lumen, but not to the circulation. Upon perfusion of the duodenal loop with hyperosmolal polyethylene glycol, acid secretion was inhibited (P < 0.05) and somatostatin alone was released to the luminal side (P < 0.01). In conclusion, duodenal exposure to acid inhibits pentagastrin-stimulated gastric acid secretion and releases SOM to the circulation that may directly inhibit acid secretion. Concomitantly, somatostatin (SOM), neurotensin and vasoactive intestinal peptide are released to the lumen. Duodenal exposure to hyperosmolal polyethylene glycol inhibits acid secretion with a luminal release of SOM only. Thus, luminal acid and hyperosmolal solutions inhibit gastric acid secretion by separate mechanisms. After acid or hyperosmolal challenge, the release of SOM to the circulation indicates gastric acid inhibition in an endocrine manner, while a luminal release of gut peptides indicates a local peptide overflow that might be of importance via paracrine regulatory mechanisms in the intact animal.

Animals↗
PubMed1994

Transforming growth factor-alpha and epidermal growth factor inhibit gastric acid secretion and stimulate release of somatostatin and neurotensin in the conscious rat.

The study compared inhibitory actions of transforming growth factor-alpha (TGF alpha) and epidermal growth factor (EGF) on gastric acid secretion and effects of these peptides on release of gut peptides considered important for acid inhibitory and gastrointestinal protective mechanisms. TGF alpha and EGF did not affect basal acid secretion, but inhibited pentagastrin-stimulated acid secretion in a dose-dependent manner from 0.10 to 1.7 nmol kg-1 h-1 i.v. by maximally 72% for TGF alpha (P < 0.001) and 76% for EGF (P < 0.001). At the highest doses, TGF alpha and EGF caused 194% and 698% increase of somatostatin-like immunoreactivity (SOM-LI) in plasma, respectively (each P < 0.05). Neurotensin-like immunoreactivity (NT-LI) increased 438% by EGF (P < 0.05), but the increase of 700% with TGF alpha did not reach statistical significance. The levels of vasoactive intestinal peptide-like immunoreactivity (VIP-LI) did not change. In gastric juice, SOM-LI increased 80% by TGF alpha i.v. (P < 0.05), but NT- and VIP-LI did not change. EGF i.v. had no effects on levels of SOM-, NT- or VIP-LI in luminal juice. Thus, TGF alpha and EGF inhibit acid secretion, but also promote the release of SOM and NT into the circulation and may be involved in the acid inhibitory effects of these growth factors.

Animals↗
PubMed1990

Fat inhibits pentagastrin-stimulated acid secretion from the duodenum but not from the proximal jejunum in chronic gastric fistula rats.

The effect of fat emulsion in the upper intestine on the maximal gastric acid response to pentagastrin was studied in chronic gastric fistula (GF) rats with a 4-cm blind loop of the duodenum anastomosed to the jejunum (Roux-en-Y). Fat emulsion in the loop inhibited the acid response by 85%. To localize the site of the inhibitory mechanism, GF rats were provided with Thirty-Vella loops of the duodenum (bile and pancreatic ducts transplanted to the proximal jejunum) or with Thirty-Vella loops of the proximal jejunum and a Roux-en-Y loop of the duodenum to prevent gastric juice from entering the duodenum. Perfusion of the duodenal loop with fat emulsion mixed with bile and pancreatic juice reduced the acid response by 49%, but perfusion of the proximal jejunal loop did not alter the response. It is concluded that the intestinal mechanism for inhibition of acid secretion by fat is located in the duodenum in rats.

Anastomosis, Roux-en-Y↗
PubMed1989

Duodenal acidification and jejunal hyperosmolality inhibit pentagastrin-stimulated acid secretion in chronic gastric fistula rats.

In chronic gastric fistula (GF) rats, HCl and a hyperosmolal solution of polyethylene glycol (PEG) in the upper intestine inhibit pentagastrin-stimulated gastric acid secretion by different mechanisms, but their anatomic sites have not yet been established. In the present study GF rats were provided with Thiry-Vella loops of the duodenum and the bile and pancreatic ducts transplanted to the proximal jejunum, or with Thiry-Vella loops of the proximal jejunum. In the latter rats the duodenum was anastomosed as a blind loop to the jejunum to prevent any gastric juice from entering the duodenum. Duodenal loop perfusion with 0.20 M HCl inhibited the acid response to pentagastrin by 62%, but perfusion with 1200 mOsmol x kg-1 of PEG solution did not alter the response. In contrast, acidification of the proximal jejunal loop did not alter but hyperosmolality inhibited the response by 41%. The study shows that the mechanism for inhibition by intestinal acidification is confined to the duodenum and that for inhibition by hyperosmolality is located in the proximal jejunum--but whether only to the proximal part is unknown.

Animals↗
PubMed1988

Acid in proximal and distal duodenum inhibits, but hyperosmolal solution does not inhibit pentagastrin-stimulated acid secretion in chronic gastric fistula rats.

In chronic gastric fistula (GF) rats, hyperosmolal 0.20 M HCl infused into a duodenal loop anastomosed to the jejunum (Roux-en-Y) produced a greater inhibition of the maximal acid response to pentagastrin than HCl or 1200 mosmol kg-1 solution of polyethylene glycol (PEG) alone, suggesting that HCl and hyperosmolal solution inhibit secretion by different mechanisms. In the present study on chronic GF rats with Thirty-Vella loops of the proximal or distal duodenum (bile and pancreatic ducts transplanted to the jejunum), perfusion of the proximal or distal loop with 0.20 M HCl significantly inhibited the maximal acid response to pentagastrin, but perfusion with hyperosmolal PEG solution did not alter the response. The results suggest different anatomical sites for the inhibitory mechanisms, sensitive to acid and hyperosmolal solution.

Animals↗
PubMed1986

Immediate or delayed Küntscher-rodding of femoral shaft fractures.

Early rodding of femoral fractures is preferable from an intensive care point of view. It has, however, been claimed that early rodding leads to impaired healing of the fractures. Healing time and complications in 20 fractures of the femur operated with Küntscher rods within 12 hours after injury were therefore compared with 47 fractures treated with traction for ten days and then Küntscher-rodding. No significant differences in results were found between the two groups concerning complications, but the acutely operated individuals returned to work on an average of two months earlier than the delayed group. If proper shock treatment is given and concomitant injuries with higher priority are treated first, early Küntscher-rodding does not seem to impair the healing of femoral fractures.

Adolescent↗
PubMed1985

Acid and hyperosmolal solutions in the upper intestine of chronic gastric fistula rats inhibit gastric acid secretion by different mechanisms.

In chronic gastric fistula rats 0.20 M HCl and 1200 mOsm X kg-1 solution of polyethylene glycol (PEG) infused into a duodenal loop anastomosed to the jejunum (Roux-en-Y) produced maximal inhibition of pentagastrin-stimulated acid secretion, which amounted to 60% and 50%, respectively. In the present study in Roux-en-Y rats with gastric fistula, perfusion of the loop with hyperosmolal (1200 mOsm X kg-1 of PEG solution) 0.20 M HCl produced a greater reduction of the maximal response to pentagastrin (91% inhibition) than perfusion with 0.20 M HCl (64%), suggesting that HCl and hyperosmolal solution inhibit secretion by different mechanisms. The maximal acid response to histamine was more resistant to inhibition than that to pentagastrin; 0.20 M HCl inhibited secretion by 43%, 1200 mOsm X kg-1 of PEG solution by 42%, and hyperosmolal 0.20 M HCl by 60%. The results suggest that HCl and hyperosmolal solution also inhibit histamine-stimulated secretion by different mechanisms. The anatomical sites of the mechanisms remain to be established.

Animals↗
PubMed1983

Inhibition of pentagastrin-stimulated gastric acid secretion by acid perfusion of the duodenum in chronic gastric fistula rats.

The effect of duodenal acid perfusion on pentagastrin-stimulated gastric acid secretion was studied in Sprague-Dawley rats provided with a chronic gastric fistula, gastroenterostomy, and a 4-cm blind duodenal loop anastomosed to the jejunum. During maximal acid stimulation with intravenous pentagastrin (16 micrograms X kg-1 h-1) the loop was perfused with 0.15 M NaCl or 0.05 M, 0.10 M, or 0.20 M HCl at a rate of 2 ml X h-1. Perfusion with 0.05 M HCl did not significantly alter pentagastrin-stimulated secretion. 0.10 M and 0.20 M HCl reduced the 2-h acid response by 56% and 63%, respectively. Acid secretion returned to control level after cessation of acid perfusion. It is concluded that physiological amounts of HCl in the duodenum inhibits maximal acid secretion stimulated by pentagastrin in rats.

Animals↗
PubMed1982

Inhibition of pentagastrin-stimulated gastric acid secretion by upper intestinal hyperosmolality in chronic gastric fistula rats.

The effects of upper small intestinal perfusion with iso-osmolar or hyperosmolar polyethylene glycol (PEG) solutions on maximal gastric acid secretion stimulated by intravenous pentagastrin was investigated in Sprague-Dawley rats. The animals were provided with a chronic gastric fistula, a gastroenterostomy and a 4-cm duodenal loop anastomosed end-to-side to the jejunum. The oral end of the duodenal loop was closed and intubated for infusion of various solutions. Saline was infused in the control experiments, 2 ml h-1. In the test experiments, saline was replaced with PEG, 300, 900 or 1,200 mosm.kg-1. Duodenal perfusion with iso-osmolar PEG, 300 mosm-kg-1, did not alter maximal acid secretion. Duodenal perfusion with hyperosmolar PEG 900 or 1,200 mosm.kg-1 significantly inhibited the stimulated 2-hour acid output by 47 and 48% respectively (p less than 0.01). Indomethacin, an inhibitor of the prostaglandin synthesis, did not alter the stimulated acid secretion, and the inhibitory influence on acid secretion of duodenal perfusion with PEG 1,200 mosm.kg-1 as not affected by the drug.

Animals↗
PubMedDate not supplied

Expression of lipoprotein lipase in ovaries of the guinea pig.

Guinea pig ovaries were found to have significant lipoprotein lipase (LPL) activity, corresponding to almost one-tenth the activity in paraovarian adipose tissue and in heart per gram of tissue. Northern blot analysis demonstrated the same three species of LPL mRNA in ovaries (1.8, 3.1, and 3.5 kb) as in adipose tissue. In situ hybridization showed LPL mRNA in cells of the follicular wall, and in granulosa and theca lutein cells of the mature corpus luteum. By immunolocalization, LPL was visualized in the vascular endothelium throughout the ovary, but with highest concentration in the endothelium of capillaries and large vessels of the cortical region and capillaries in the stroma of the corpus luteum. These results suggest that in the guinea pig LPL may have a function for the delivery of lipids from lipoproteins to ovarian cells.

Adipose Tissue↗