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

beta-blockers and calcium-channel inhibitors are frequently used for self-poisoning. Propranolol and verapamil, the leading drugs in each pharmacological class, are the most toxic. They interfere with intracellular calcium concentration in muscles. Circulatory insufficiency may be due to vasodilatation, myocardial depression or severe bradycardia. If one respects a specific sequence for administration, the usual antidotes (glucagon, calcium salts, isoprenaline, epinephrine) are usually efficient. One must not underestimate the risk of worsening of an intoxication that is seen at the early stage, that occur in an old person or in a patient with heart disease, or that depress ventilation. Hence, it is important to monitor and treat these intoxications in an intensive care unit.
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PMID:[Acute poisoning by beta-blockers and by calcium inhibitors]. 918 51

1. We measured the ability of glucagon and amrinone, used alone and in combination, to improve the myocardial function in a rat isolated heart model of calcium channel blocker (CCB) cardiotoxicity. 2. Verapamil 10(-4) mol consistently decreased heart rate and cardiac contractile force in our Langendorff rat isolated heart preparations. Glucagon increased the heart rate in a dose-dependent fashion. Amrinone increased the heart rate only at the 1 x 10(-1) mol concentration, and had no significant effect on cardiac contractility. 3. A positive linear correlation was found between the glucagon concentration and the percent recovery of baseline contractile force. 4. Although complete reversal of verapamil-induced myocardial depression occurred at glucagon concentrations of > 3 x 10(-6) mol, amrinone produced only 23.8 +/- 3.6% recovery from baseline at its highest concentration (4 x 10(-3) mol). 5. When glucagon and amrinone were administered together, there was no additional increase over glucagon alone in the increase in contractile force. 6. Glucagon, and not amrinone, is an appropriate agent, capable of reversing verapamil-induced myocardial toxicity in this rat isolated heart model. In vivo studies should be performed to assess whether this may be a reliable therapy in clinical cases.
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PMID:The effects of amrinone and glucagon on verapamil-induced myocardial depression in a rat isolated heart model. 918 18

This study examined the effects of arginine supplement of fluid resuscitation from burn injury on cardiac contractile performance and bacterial translocation after a third-degree burn comprising 43% of the total body surface area in adult rats. Before burn injury, rats were instrumented to measure blood pressure; after burn (or sham injury), paired groups of sham-burned and burned rats were given vehicle (saline), L-arginine, D-arginine, or N-methyl-L-arginine (300 mg/kg in 0.3 ml of saline 30 min, 6 h, and 23 h postburn) plus fluid resuscitation; sham-burned rats received drug only. Twenty-four hours after burn trauma, hemodynamics were measured; the animals were then killed and randomly assigned to Langendorff heart studies or to studies examining translocation of gut bacteria. Burn rats treated with vehicle, D-arginine, or N-methyl-L-arginine had well-defined cardiocirculatory responses that included hypotension, tachycardia, respiratory compensation for metabolic acidosis, hypocalcemia, cardiac contractile depression, and significant bacterial translocation. Compared with values measured in vehicle-treated burn rats, L-arginine given after burn improved blood pressure, prevented tachycardia, reduced serum lactate levels, improved cardiac performance, and significantly reduced bacteria translocation, confirming that L-arginine administration after burn injury provided significant cardiac and gastrointestinal protection. Circulating neutrophil counts fell after burn trauma and serum glucagon levels rose, but these changes were not altered by pharmacological intervention. Our finding of significantly higher coronary perfusate guanosine 3',5'-cyclic monophosphate concentration in L-arginine-treated burn rats suggests that the beneficial effects of L-arginine were mediated by nitric oxide production.
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PMID:Arginine in burn injury improves cardiac performance and prevents bacterial translocation. 947 82

The body's general response to serious thermal injury is characterized by increased vascular permeability immediately after injury and subsequent hypovolemic shock. Skeleto-muscular proteolysis, lipolysis, gluconeogenesis, increased metabolic rate, and a severe systemic inflammatory response induced by local infections or surgical procedures. The increased vascular permeability is mediated by histamine and numerous vasoactive substances, including serotonin, bradykinin, prostaglandins, leukotrienes, and platelet activating factor. Hyper-metabolism is mediated by hormones such as catecholamines, glucagon, and particularly cortisol. In addition, among the putative mediators of the metabolic response to injury, attention has recently been focused on cytokines and lipid mediators which are mainly produced by activated reticuloendothelial cells. Cytokines such as interleukin-1, interleukin-6 and tumor necrosis factor and cortisol responses are interrelated, since cytokines activate the hypothalamo-adrenal axis. The cytokine storm seen in burn patients may be associated with depression of the immune system and with susceptibility to infection. Thermal injury can also lead to activation of the renin-angiotensin-aldosterone system, increased ADH production, and production of atrial natriuretic polypeptide to maintain the circulatory volume. Burn wound infections or surgical procedures can produce and perpetuate a mediator-induced systemic inflammatory response that may lead to multiple organ failure. Serum levels of interleukin-6 are very sensitive to surgical stress, and may be a useful indicator of the general condition of severely burned patients.
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PMID:[Pathophysiologic changes in patients with severe burns: role of hormones and chemical mediators]. 954 40

The influence of distal pancreatectomy on portal and peripheral blood immunoreactive insulin (IRI) and immunoreactive glucagon (IRG) concentrations was evaluated in patients undergoing total gastrectomy. There were 22 patients studied, 12 of whom did not undergo distal pancreatectomy (group 1), and 10 who did (group 2). In group 2, the increase in portal blood IRI concentrations after a glucose infusion of 25 g over 30 min was suppressed, and reelevation of the portal blood IRG concentration after the glucose-induced depression was inhibited compared to group 1. In contrast, the peripheral blood IRI concentration did not reflect these changes in the portal blood IRI concentration. The rise in the arterial ketone body ratio (AKBR) and the fall in the total ketone body concentration after glucose infusion were also attenuated after distal pancreatectomy in group 2. These findings suggest that distal pancreatectomy has an immediate suppressive effect on the pancreatic secretion of insulin and glucagon, and might disturb metabolism in the liver.
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PMID:Acute effects of distal pancreatectomy on portal and peripheral blood insulin concentrations in patients undergoing total gastrectomy. 959 Jun 98

Oligofructose (OFS), a mixture of nondigestible/fermentable fructooligosaccharides, decreases serum triacylglycerol (TAG) when it is included in the standard, fiber-free or high fat diet of rats. This paper summarizes in vivo and in vitro data to establish a biochemical mechanism underlying the hypolipidemic effect of OFS. When OFS is added to the standard (carbohydrate-rich) diet of rats at the dose of 10 g/100 g, a TAG-lowering action occurs as a consequence of a reduction of de novo liver fatty acid synthesis. The depression in the activity of all lipogenic enzymes and fatty acid synthase mRNA suggests that OFS modifies the gene expression of lipogenic enzymes. Through its modulation of de novo lipogenesis, OFS can protect against liver lipid accumulation induced by providing 10% fructose-enriched water for 48 h. OFS also significantly decreases serum insulin and glucose, which are both known to participate in the nutritional regulation of lipogenesis. It also increases the intestinal production of incretins, namely, glucose-dependent insulinotropic peptide and glucagon-like peptide 1. This latter phenomenon results mainly from promotion of intestinal tissue proliferation by oligofructose fermentation end-products. Collectively, a link likely exists between the modulation of hormone and incretin production by OFS, and its antilipogenic effect.
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PMID:Biochemical basis of oligofructose-induced hypolipidemia in animal models. 1039 22

The mechanisms responsible for the glycemic changes associated with endotoxic shock are not fully understood, but are known to involve the ability of the liver to produce glucose. The purpose of the present study was to determine whether endotoxin (LPS) influences the expression and activity of glucose-6-phosphatase (Glu-6-Pase) during the early hyperglycemic phase and the later hypoglycemic phase. Rats were injected with a relatively large dose of LPS (20 mg/kg) or saline (control), and sacrificed at 1 or 5 h post-injection. Both the plasma glucose concentration and glucose production were elevated 1 h post-LPS (2-fold) and both decreased at 5 h postinjection (50%). Compared to time-matched control values, hepatic glucose-6-phosphate and fructose-6-phosphate levels were significantly decreased at both 1 and 5 h. Hepatic Glu-6-Pase activity and mRNA levels were moderately increased, 1 h after injection of LPS. At 5 h, an 88% decrease in mRNA abundance for Glu-6-Pase was associated with a 30% decrease in activity of this enzyme. Plasma insulin concentrations were not different 1 h after LPS and were elevated 2-fold from control values at 5 h. Circulating levels of glucagon and corticosterone were elevated at both time points following LPS. Our data indicate that the LPS-induced hypoglycemia and reduction in hepatic glucose production were accompanied by a depression in Glu-6-Pase activity and gene expression.
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PMID:Endotoxin-induced alterations in hepatic glucose-6-phosphatase activity and gene expression. 1044 5

We report the unusual features of a female patient who had MELAS-specific A3243G mutation in mitochondrial DNA (mtDNA) and diabetes mellitus (DM). The patient showed mitochondrial myopathy, encephalopathy, lactic acidosis, and deafness but lacked the stroke-like episode. Acute hyperglycemia was noted after one attack of status epilepticus. Molecular genetic analysis demonstrated a heteroplasmic A3243G point mutation in the mtDNAs of muscle, blood cells and hair follicles. Glucagon stimulation test exhibited marked depression of pancreatic beta-cell function. However, in a further study neither this mutation, nor MELAS syndrome or DM, was found in all of her maternal relatives. A series of follow-up studies for beta-cell function also showed gradual improvement. The pedigree study led us to believe that this A3243G mutation arose from the germ line cells or occurred later in somatic tissues of the patient. We also suggest that the A3243G mutation of mtDNA may elicit the pathogenesis of a subtype of DM. Nevertheless, environmental stress may be another important factor for provocation of the disease.
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PMID:Absence of maternal A3243G mtDNA mutation and reversible hyperglycemia in a patient with MELAS syndrome. 1066 Jan 56

Poult enteritis and mortality syndrome (PEMS), a disease that affects turkeys between 7 and 28 d of age, causes a severe inflammation of the intestinal tract and is characterized in poults by severe diarrhea, high morbidity, mortality, and stunting. The PEMS-associated mortality and growth depression is related to malabsorption and decreased metabolic activity caused, in part, by a possible insulin deficiency or insensitivity. Insulin receptors are stimulated by the glucose tolerance factor (GTF) that incorporates Cr. Body Cr deficiency can be exacerbated by dietary deficiency and by increased excretion due to stress associated with a diarrheal disease such as PEMS. BioChrome (BC) contains natural, preformed GTF, the bioactive form of Cr. Experiments were conducted in which BC was blended into poult starter feed at 400 ppb during the first 21 d posthatch. Body weights were determined at 1, 7, 14, and 21 d of age, and weekly feed conversions were calculated for each treatment group (control, BC, PEMS, and BC+PEMS). At 6 d post-hatch, each PEMS-designated poult was given a 0.1-mL oral gavage of a 10% suspension of feces from PEMS-infected poults. Blood samples were taken via cardiac puncture from four birds per treatment group at 7, 10, 14, 17, and 21 d of age. Radioimmunoassays were conducted for plasma insulin, glucagon, thyroxine (T4), and triiodothyronine (T3). Plasma insulin levels were depressed in PEMS-infected poults from Days 10 through 17, but plasma glucagon levels in the PEMS-infected poults were significantly elevated at 14 and 17 d, after which they returned to control levels in both of the PEMS-infected groups. The T3 and T4 levels were depressed through Day 21 in PEMS-infected poults, but with BC treatment these blood hormone levels rebounded by Day 21. Body weights of PEMS-infected poults were increased significantly by the BC treatment but not to the level of noninfected controls.
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PMID:Influence of BioChrome on the response of metabolic hormones in PEMS-infected poults. 1082 53

We explored the effect of light therapy upon basal fasting plasma glucagon in 15 patients with winter depression vs. 15 comparison subjects before and after at least 1 week of light treatment. No differences were seen between groups or conditions. There was no correlation between glucagon change and antidepressant response.
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PMID:No effect of light on basal glucagon levels in winter seasonal depressives and comparison subjects. 1088 91


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