摘要:

Interferons are known to prevent liver collagen by an antifibrogenic mechanism that involves mRNA procollagen regulation. The aim of the present work was to determine whether interferon could also decrease collagen by increasing its degradation. Fibrosis was induced in male Wistar rats by double ligation and section of the common bile duct. Interferon-α2b (100,000 IU/rat s.c.) was administered to bile duct ligated rats daily after surgery for 4 weeks. Interferon increased the capacity of the liver to degrade type I and III collagens and matrigel. In addition, the plasminogen activator activity also increased. Since plasminogens are thought to be key participants in the balance of proteolytic activities that regulate extracellular matrix degradation, their elevation may also provide another antifibrotic (proteolytic) mechanism of action of interferon

ISSN:0031-7012    

DOI:10.1159/000139345

出版商:S. Karger AG    

年代:1995

数据来源: Karger

摘要:

Indometacin pretreatment potentiates the natriuretic action of the mixed α2-adrenoceptor/imidazoline receptor agonist clonidine. In the present study we determined the effects of indometacin pretreatment on natriuretic actions of the selective I1 imidazoline receptor agonist. In anaesthetized rats, an intrarenal infusion of moxonidine (0, 0.3, 1, and 3 nmol/ kg/min) increased urine flow rate and sodium excretion without altering blood pressure or creatinine clearance. Indometacin pretreatment abolished the subsequent natriuretic response to an intrarenal infusion of moxonidine (1 nmol/kg/ min) without altering blood pressure or creatinine clearance. Administration of prostaglandin E2, at an infusion rate (1 µg/ kg/min) which alone failed to alter urine flow rate, sodium excretion, blood pressure, or creatinine clearance, partially, but not completely, restored the natriuretic response to moxonidine. The ability of indometacin pretreatment to potentiate natriuretic actions of an α2-adrenoceptor agonist and to attenuate those of an imidazoline agonist indicates that these two receptors in the kidney are unique and may serve distinct functions in the regulation of sodium and water excreti

ISSN:0031-7012    

DOI:10.1159/000139346

出版商:S. Karger AG    

年代:1995

数据来源: Karger

摘要:

Crude ethanolic extract of Lawsonia inermis L. (0.25-2.0 g/ kg) produced significant and dose-dependent anti-inflammatory, analgesic, and antipyretic effects in rats. The extract also produced significant increases in pentobarbitone-induced sleeping time. Using a liquid-liquid extraction procedure, the extract was fractionated into chloroform, butanol, and water fractions, and these were tested for the above activities. The butanol and chloroform fractions showed more potent anti-inflammatory, analgesic, and antipyretic effects than the crude extracts, while the aqueous extract showed significantly less effect. As compared with the other extracts, the butanolic extract (500 mg/kg) was the most effective in the analgesic test. From the chloroform extract, a pure compound was isolated and identified, using chromatographic and spectroscopic techniques, as 2-hydroxy-1,4-naphthaquinone (lawsone). The isolated compound was found to possess significant anti-inflammatory, analgesic, and antipyretic activity. It potentiated significantly the pentobarbitone-induced sleeping time. The anti-inflammatory effect of lawsone (500 mg/kg) was not significantly different from that of the reference drug phenylbutazone (100 mg/kg).

ISSN:0031-7012    

DOI:10.1159/000139347

出版商:S. Karger AG    

年代:1995

数据来源: Karger

摘要:

Previous studies in our laboratory have indicated that ethanol alters β-endorphin (β-EN) levels in specific rat brain regions. The present investigation was conducted to evaluate the effects of an adenosine agonist and an adenosine antagonist on these alterations. Male Sprague-Dawley rats weighing 150–200 g were used in this study. The animals were injected intra-peritoneally at 11.00 h with ethanol (3 g/kg as a 22.5% w/v solution in saline), N6-cyclohexyladenosine (CHA; 0.1 mg/kg), theophylline (30 mg/kg), a combination of ethanol and CHA, or a combination of ethanol and theophylline. The control rats received saline. The animals were sacrificed 1 h after injection. Frontal cortex (CTX), hypothalamus (HY), hippocampus (HI), and midbrain (MB) were dissected, and their β-EN levels were determined by radioimmunoassay. Ethanol administration significantly increased the β-EN levels in HY (39% increase), HI (28% increase), and MB (19% increase), but had no effect in CTX. The adenosine agonist (CHA) produced similar significant increases in β-EN levels in HY and MB, but did not alter these levels in CTX or HI. In contrast, the adenosine antagonist theophylline did not alter β-EN levels in any brain region studied. However, theophylline pre-treatment significantly reduced ethanol-induced changes in β-EN levels in HY, completely blocked ethanol effects in HI, and reversed ethanol alterations in MB. On the other hand, CHA, concurrently administered with ethanol, potentiated ethanol-induced increases of β-EN levels in HY and HI. These findings suggest that the ethanol-induced increases in β-EN levels in specific rat brain regions may be modulated by adenosinergic compounds and that adenosine receptors may play a role in ethanol effects on rat brain leve

ISSN:0031-7012    

DOI:10.1159/000139348

出版商:S. Karger AG    

年代:1995

数据来源: Karger

摘要:

Dorsal medullary brain slices containing primarily the nucleus tractus solitarius (NTS) were obtained from normal or 40- to 50-day streptozotocin-diabetic rats and employed for superfusion studies of evoked transmitter release. Electrically stimulated (25 mA, 2-ms pulses, 3 Hz, 1 min) release of [3H]norepinephrine ([3H]NE) or [3H]5-hydroxytryptamine ([3H]5-HT) from 400-µm NTS slices stimulated at 75 min (S1) and 130 min (S2) resulted in S2/S1 release ratios that were not different between normal controls or diabetic control groups. Perfusion of normal [3H]NE-loaded slices with 0.1 µmol/l clonidine reduced the S2/S1 ratio by 23% (p < 0.05) which was uniform in the caudal, subpostremal, and intermediate segment levels of the NTS. In diabetic NTS slices, the S2/S1 ratio was significantly less reduced by clonidine in both the subpostremal (–3%) and intermediate (–11%) slice regions. Blockade of α2-adrenoceptors with yohimbine (0.1 µmol/l) enhanced (p < 0.05) [3H]NE release (S2/S1 ratios) in slices from both normal and diabetic rats. Perfusion of [3H]NE-loaded slices with 5 mU/ml insulin did not affect S2 release. Evoked S2/S1 release ratios from NTS slices loaded with [3H]5-HT did not differ between normal control and diabetic control groups. Clonidine (0.1 µmol/l) reduced S2-evoked release in both normal (–30%) and diabetic (–44%) slices, but the groups were not different from each other. Superfusion with 5 mU/ml insulin did not alter S2/S1 ratios in normal [3H]5-HT loaded slices, but did increase the diabetic NTS slice S2/S1 ratio to 1.40 ± 0.06 (p < 0.01). In summary, it appears that α2-adrenoceptor-mediated inhibition of [3H]NE release in the NTS was selectively attenuated in a regionally specific manner in diabetic animals. Release inhibition may be associated with receptor downregulation in NTS regions associated with cardiovascular reflex transmission. Insulin superfusion augmented [3H]5-HT release in the diabetic NTS slices, possibly through increased transmitter synthesis or improved sy

ISSN:0031-7012    

DOI:10.1159/000139349

出版商:S. Karger AG    

年代:1995

数据来源: Karger

摘要:

There were no differences between mesenteric arteries from sham or 14-day portal hypertensive (PH) rats in the potency of or maximum endothelium-dependent relaxations (EDR) to acetylcholine. There were no differences between sham-operated and PH rats in the effects of the combination of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (100 µmol/l) and methylene blue (10 µmol/l) in causing a significant reduction in the EDR to acetylcholine. The degree of portal-systemic shunting, as measured by 57Co-labeled microspheres, was unaffected by acute administration of NG-monomethyl-L-arginine (50 mg/kg) or methylene blue (5 mg/ kg). In conclusion, nitric oxide is the main mediator of EDR in rat mesenteric artery, and no evidence was found for an increased role for endothelial-derived nitric oxide in PH rat

ISSN:0031-7012    

DOI:10.1159/000139350

出版商:S. Karger AG    

年代:1995

数据来源: Karger

摘要:

Calcium channel blockers like verapamil have been shown to potentiate ethanol-induced gastric mucosal damage. However, the exact mechanism for this adverse drug interaction is still unknown. We used felodipine to study the ulcerogenic mechanisms of calcium channel blockers and the pathogenesis of ethanol-induced ulceration. The experiment was conducted in an ex vivo gastric chamber prepared in anesthetized animals. Felodipine (0.25, 0.5, 1.0, or 2.0 mg/kg s.c.) dose-dependently reduced the systemic blood pressure which was accompanied by a decrease in gastric mucosal blood flow (GMBF), with an insignificant change in heart rate. Ethanol lowered the GMBF and produced gastric mucosal lesions, and these actions were potentiated by felodipine. Preincubation with calcium gluconate but not the sodium salt attenuated the adverse effects of ethanol on GMBF and lesion formation; it also significantly prevented the gastric effects of felodipine but not the decrease of the systemic blood pressure. It is concluded that felodipine aggravates ethanol ulceration through a depressive action on the GMBF. These actions were attenuated by the supplementation with calcium ions in the gastric mucosa. Therefore, maintenance of calcium homeostasis in the gastric wall could play a significant role in the prevention of ethanol ulceration in rats.

ISSN:0031-7012    

DOI:10.1159/000139351

出版商:S. Karger AG    

年代:1995

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000139352

出版商:S. Karger AG    

年代:1995

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000139353

出版商:S. Karger AG    

年代:1995

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000139344

出版商:S. Karger AG    

年代:1995

数据来源: Karger