Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study we examined the role of oxygen-derived free radicals in the pathogenesis of acute gastric mucosal lesion induced by obstructive jaundice in rats. Rats were divided into 4 groups as follows: control (sham operation), jaundiced (ligation and dissection of bile duct), vagotomized (truncal vagotomy), and vagotomized with jaundice group. The water immersion restraint procedure was performed. The water immersion restraint procedure was performed. The results obtained are as follows: jaundiced group showed significant increase of ulcer index (UI) and significant decrease of gastric mucosal blood flow (GMBF) and gastric mucosal potential difference (PD). However, intragastric pH (pH) was unchanged compared to the control group. Oxygen radical generating system (gastric mucosal XOD activity and thiobarbiturate acid) and oxygen radical scavenging system (gastric mucosal SOD activity and GSH-px activity) were higher than those of control group. Vagotomized group showed significant increase of pH compared to the control group. Oxygen generating system and scavenging system were unchanged compared to the control group. Vagotomized with jaundice group showed depression of UI and improvement of oxygen radical generating system and scavenging system. However GMBF, PD nad pH were unchanged compared to the jaundiced group. These results suggest that oxygen radical play some role in the development of acute gastric mucosal lesion induced by obstructive jaundice.
 ...
PMID:[Role of oxygen radicals in the pathogenesis of acute gastric mucosal lesion under obstructive jaundice]. 831 98

Insulin and glucagon metabolism in the pancreas with obstructive jaundice caused by complete ligation of the common bile duct and in the cholestatic liver caused by hepatic duct ligation was evaluated experimentally using dogs. The isolated perfused pancreas in obstructive jaundiced dogs, which showed a low insulin response in the peripheral blood after intravenous glucose administration, revealed depression of insulin production and no change of glucagon production in response to cholecystokinin octapeptide. The extraction of insulin in the cholestatic lobe of the liver was decreased compared with that in the noncholestatic lobe. The extraction of glucagon, on the other hand, in the cholestatic lobe and in the noncholestatic lobe showed no significant difference. So the imbalance of glucose metabolism in obstructive jaundice does not depend on the enhanced extraction of insulin in the liver, but on the depression of insulin production in the pancreas.
 ...
PMID:Metabolism of insulin and glucagon in liver and pancreas in dogs with obstructive jaundice. 846 Jan 1

High morbidity and mortality in surgical management for patients with obstructive jaundice was greatly attributed to the metabolic derangements in jaundiced liver mitochondria. Isolated liver mitochondria from jaundiced rat, produced by common bile duct ligation, were used to study the relationship among NADH level, oxygen consumption, and extramitochondrial calcium concentration. Alterations in NADH percentage and oxygen consumption were accomplished by incubating mitochondria with different substrates and monitoring oxygen consumption and NAD(P)H fluorescence simultaneously. In jaundiced liver mitochondria with glutamate + malate as substrate, respiration increased after the addition of exogenous Ca2+ at concentrations of 1 x 10(-7), 5 x 10(-7), and 1 x 10(-6) M. The maximal effect occurred at 5 x 10(-7) M. With different NADH-related substrates, the NAD(P)H fluorescence measurements (X axis) correlated linearly with state 3 respiration (Y axis), the slopes of the correlation curves being 2.27 and 0.79 in control and jaundiced mitochondria, respectively. After the addition of 5 x 10(-7) M Ca2+, the respirations of both control and jaundiced mitochondria increased and the slope for jaundiced mitochondria rose to 1.67. The matrix free Ca2+ concentration in jaundiced mitochondria, measured by fluo-3 loading, was higher than that in controls (162.1 +/- 16.7 nM, vs 129.7 +/- 12.6 nM, P < 0.01), while the matrix free/total Ca2+ ratio decreased from 34.9 +/- 6.0 (x10(-6)) to 27.2 +/- 4.4 (x10(-6), 9- < 0.05. The amplitude of the change in NAD(P)H fluorescence was reduced in jaundiced rat liver mitochondria and this correlated with the depression of respiration. A decrease in free/total Ca2+ ratio may be closely related to mitochondrial respiratory impairment in jaundice.
 ...
PMID:Restricted redox oscillation in oxidative phosphorylation in jaundiced rat liver mitochondria and its relation to calcium ion. 902 18

Cholestatic jaundice is the major complication of total parenteral nutrition (TPN) in infancy. We have previously shown that the TPN solution is directly toxic to the liver, and that this toxicity appears to be mediated by one or more amino acids. Elevated serum methionine levels, without corresponding increases in its metabolites, suggest that accumulation of this toxic amino acid may cause TPN cholestasis. Nine-week-old rabbits (n = 28) were divided into three groups. The FED group was fed standard rabbit chow ad libitum. The TPN group was not fed and received only i.v. TPN (including methionine 121 mg.kg-1.d-1), and lipids. The EXP group was fed chow ad libitum and received i.v. methionine (121 mg.kg-1.d-1). After 14 d, we evaluated bile flow, bromosulfophthalein excretion, serum liver enzymes, liver histology, and serum amino acid levels. Bile flow was significantly depressed in the TPN and EXP groups compared with FED controls (32.9 +/- 9.4 and 45.7 +/- 14.4 versus 82.9 +/- 13.8). Excretion of the bilirubin analog bromosulfophthalein tended to be delayed by methionine infusion (p = 0.15). Serum liver enzymes (aspartate transaminase, alanine aminotransferase, gamma-glutamyltransferase, and alkaline phosphatase) were normal in all groups. Histologic liver injury in the EXP group was similar to that caused by TPN. Balloon degeneration, and portal inflammation were seen in both groups. Homocysteine, an early metabolite of methionine, was elevated in the TPN and EXP groups compared with FED controls. Intravenous methionine is hepatotoxic. Despite full oral feeding, it produces a depression of bile flow and histologic liver injury similar to that seen with TPN. Elevated homocysteine levels suggests an enzymatic block early in the pathway of methionine metabolism. We believe that methionine may be an important factor in the pathogenesis of TPN cholestasis.
 ...
PMID:Methionine infusion reproduces liver injury of parenteral nutrition cholestasis. 1023 61

The aim of this study was to investigate the relationship between the obstructive jaundice-induced cellular immune suppression and endotoxin challenge with respect to the levels of tumor necrosis factor (TNF), interleukin-10 (IL-10), and interleukin-2 (IL-2). Rats underwent either bile duct ligation or sham operation. At 21 days, all rats were challenged either with lipopolysaccharide (LPS) or saline. In the sham-operated group LPS injection significantly increased TNF levels at 90 min. The common bile duct ligated group showed a significant increase in TNF levels compared with all other groups, including the sham-operated, LPS-injected group, at 90 min. At 180 min following LPS challenge, TNF levels decreased, and there was no difference between any of the LPS-challenged groups at 180 min and any of the saline groups at either 90 or 180 min. In the sham-operated group, LPS injection significantly increased IL-10 levels at both 90 and 180 min. In the bile duct ligated group, LPS injection significantly increased IL-10 levels compared with saline injection at both 90 and 180 min. On the other hand, bile duct ligated animals had significantly less increase in IL-10 levels following LPS challenge at 90 min but not at 180 min. In common bile duct ligated rats, LPS challenge induced a significantly greater increase in IL-2 levels compared with all other groups. In conclusion, in the presence of obstructive jaundice, endotoxemia primes a more vigorous inflammatory response despite cellular immune depression.
 ...
PMID:Endotoxin challenge causes a proinflammatory state in obstructive jaundice. 1520 55

Anisodamine is a naturally occurring atropine derivative that has been isolated, synthesized and characterized by scientists in the People's Republic of China. Like atropine and scopolamine, anisodamine is a non-specific cholinergic antagonist exhibiting the usual spectrum of pharmacological effects of this drug class. It appears to be less potent and less toxic than atropine and displays less CNS toxicity than scopolamine. Anisodamine has been shown to interact with and disrupt liposome structure which may reflect its effects on cellular membranes. Experimental evidence implicates anisodamine as an anti-oxidant that may protect against free radical-induced cellular damage. Its cardiovascular properties include depression of cardiac conduction and the ability to protect against arrhythmia induced by various agents. Anisodamine is a relatively weak alpha(1) adrenergic antagonist which may explain its vasodilating activity. Its anti-thrombotic activity may be a result of inhibition of thromboxane synthesis. The T(1/2) of anisodamine in humans is about 2-3 h. Numerous therapeutic uses of anisodamine have been proposed including treatment of septic shock, various circulatory disorders, organophosphorus (OP) poisoning, migraine, gastric ulcers, gastrointestinal colic, acute glomerular nephritis, eclampsia, respiratory diseases, rheumatoid arthritis, obstructive jaundice, opiate addiction, snake bite and radiation damage protection. The primary therapeutic use of anisodamine has been for the treatment of septic shock. Several mechanisms have been proposed to explain its beneficial effect though most mechanisms are based upon the assumption that anisodamine ultimately acts by an improvement of blood flow in the microcirculation. Preliminary studies suggest another important therapeutic use of anisodamine is for the treatment of OP poisoning. Additional research is needed to delineate further the clinical usefulness of anisodamine relative to other anti-muscarinic drugs such as atropine and scopolamine.
 ...
PMID:The pharmacological properties of anisodamine. 1718 68


<< Previous 1 2