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)

Proteolytic enzymes, lipase, kinins, and other active peptides liberated from the inflamed pancreas convert inflammation of the pancreas, a single-organ disease of the retroperitoneum, to a multisystem disease. Adult respiratory distress syndrome, in addition to being secondary to microvascular thrombosis, may be the result of active phospholipase A (lecithinase), which digests lecithin, a major component of surfactant. Myocardial depression and shock are suspected to be secondary to vasoactive peptides and a myocardial depressant factor. Coagulation abnormalities may range from scattered intravascular thrombosis to severe disseminated intravascular coagulation. Acute renal failure has been explained on the basis of hypovolemia and hypotension. The renin-angiotensin alterations in acute pancreatitis (AP) as mediators of renal failure need to be studied. Metabolic complications include hypocalcemia, hyperlipemia, hyperglycemia, hypoglycemia, and diabetic ketoacidosis, of which hypocalcemia has been long recognized as an indicator of poor prognosis. The pathogenesis of hypocalcemia is multifactorial and includes calcium-soap formation, hormonal imbalances (e.g., parathyroid hormone, calcitonin, glucagon), binding of calcium by free fatty acid-albumin complexes, and intracellular translocation of calcium. Subcutaneous fat necrosis, arthritis, and Purtscher's retinopathy are rare. The various prognostic criteria of AP and other associated laboratory abnormalities are manifestations of systemic effects. Early recognition and appropriated management of these complications have resulted in improved prognosis of severe AP.
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PMID:Acute pancreatitis: a multisystem disease. 804 85

A group of pulmonologists from different sites of Argentina convened to establish consensus guidelines for treatment of acute and chronic bronchial asthma. General acceptance that in fatal asthma diagnosis and hospital admission are usually too late and treatment insufficient prompted the need for this meeting. The purpose of treatment was devised to keep the patient symptomless, decrease frequency of exacerbations and the risk of severe attacks. Peak expiratory flow rate (PEFR) measurement in all patients was decided. inhalation of anti-inflammatory drugs (corticosteroids, CE, and/or disodium cromoglycate, DSG, in those younger than 20 years) was established as first line of treatment. Inhaled CE (even in high doses such as 2 mg/day) do not provoke significant adverse systemic effects (immune depression, Cushing syndrome, hyperglycemia in diabetics or osteopenia). Secondary local adverse effects are however frequent: oral and pharyngeal candidiasis and dysphonia. It is advisable considering present evidence, that bronchodilators (Bd) be used preferentially on demand. On account of small bronchodilator effect and frequent secondary adverse effects, use of theophylline should be limited to patients not adequately responsive to anti-inflammatory drugs in high dosage. Immunotherapy is not useful in asthma. Four clinical levels were defined in chronic asthma considering severity of dyspnea, frequency of nocturnal bronchial obstruction, levels of PEFR and amount of required Bd. Guidelines of treatment were established for each clinical level considering increasing dosage of CGS, inhaled CE (up to 2 mg/day) and regular administration of Bd. Indications for systemic CE administration were also established. Three levels of acute asthma (sudden worsening of symptoms) were accepted based on clinical evidence and PEFR values. Treatment was quantitatively adjusted to severity. Criteria for hospital admission either in emergency or intensive care areas and treatment procedures were established.
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PMID:[Standards established by consensus for the treatment of bronchial asthma and its exacerbations]. 811 34

The three-compartment model of brain acid-base regulation postulates that under circumstances of changing function or disease, hydrogen ion concentrations may differ considerably in the interstitial space (ISS), the neurons and the glial cells. During hyperglycemia plus profound ischemia, for example, direct measurements by microelectrodes followed by intracellular HRP staining show that intraglial pH can fall transiently as low as 3.9, although more often the nadir drops to the 4.5-5.5 range. Concurrently, ISS-pH and, by calculation, neuronal pH fails to and remains constant (but not necessarily the same) at pH 6.2. By contrast, during spreading depression, ISS and intraglial pH at first move rapidly and transiently in opposite directions, ISS [H+] rising, intraglial falling. These two then gradually stabilize, whereas neuronal pH remains substantially more steady and near normal, shifting only minimally from resting baseline levels over several minutes' time. Similar but less pronounced effects follow direct electrical stimulation. The net change represents complex biophysical transmembrane and buffering mechanisms that appear to guard neuronal homeostasis. Studies carried out on embryonic rat forebrain neurons and glia show that these cells have considerably different vulnerabilities to extracellular acidity depending on the anionic nature of the acid in the bathing medium. In cultures to which HCI was added to the medium, neurons and neuronal processes almost all survived ten minute exposures to pH 3.8, whereas glial cells succumbed after ten minute exposures at pH not lower than 4.2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vivo and in vitro control of acid-base regulation of brain cells during ischemic and selective acidic exposure. 842 56

Cerebral blood flow (CBF) decreases during acute hyperglycemia but the mechanism of this change is unknown. The role that plasma osmolality plays in this effect was reexamined in pentobarbital-anesthetized rats using a continuous measure of CBF, laser-Doppler flowmetry. CBF decreased 25% during acute elevation of plasma osmolality induced by intraperitoneal injection of concentrated solutions of glucose or mannitol. In addition there were brief transient increases of CBF with peak magnitude 2-4-times the baseline level that were not accompanied by transient depression of electroencephalographic activity. These transient CBF increases may explain why discontinuous methods of CBF measurement fail to detect flow decreases after mannitol injection. Decreased CBF measured during acute hyperglycemia may be the result of increased plasma osmolality.
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PMID:Decreased cerebral blood flow during acute hyperglycemia. 871 26

The placental transfer of local anaesthetics (LA) depends on maternal, placental and fetal factors. The assessment of effects of LA and epidural anaesthesia (EA) on the fetus is based on the monitoring of fetal heart rate (FHR) and the measurement of the fetal pH. Apgar score and neurobehavioral tests allow an evaluation of the neonatal effects of the drugs used. Direct effects of LA: a diminution of variability of FHR was observed shortly after the beginning of an EA using lidocaine but there was no modification of FHR after EA using bupivacaine or lidocaine with epinephrine. Fetal neurological toxicity is rare and there are very few alterations of neurobehavioral scores after EA. Indirect effects on uteroplacental blood flow (UBF): in high concentration, LA can induce vasoconstriction of uterine arteries but maternal arterial hypotension that impedes directly uteroplacental blood flow is the main effect. Prevention of aortocaval compression is essential because it allows better Apgar scores and arterial pH at birth. Use of colloids has not a better preventive efficacy than an equal volume of cristalloids while dextrans are formally contra-indicated because of serious fetal accidents. Large iv infusion of dextrose solutions are responsible for maternal and fetal hyperglycemia and hyperinsulinemia leading to neonatal hypoglycemia. The utilization of IM prophylactic ephedrine is not useful while the therapeutic administration of ephedrine to treat maternal arterial hypotension is efficient. Phenylephrine used in case of maternal arterial hypotension seems as efficient as is ephedrine. Epidural narcotics: the use of morphine by epidural route can induce neonatal respiratory depression and low neurobehavioral scores. The epidural administration of fentanyl does not alter the variability of the FHR and does not modify neither Apgar or neurobehavioral scores, nor respiratory adaptation of the newborn. Use of epidural alfentanil or sufentanil does not lead to low neurobehavioral scores unless very high doses are used. For elective caesarean section, newborns present a lower Apgar score at 1 min and necessitate respiratory assistance more frequently after general anaesthesia (GA) than after EA. Neurobehavioral scores are better after EA than after GA. For emergency caesarean section, the percentage of newborns with an Apgar score < 4 or necessitating a respiratory assistance is more important after GA than after EA. However, the perinatal mortality is not more important after GA than after EA.
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PMID:[Conduction anesthesia and the newborn infant]. 874 46

Hyperglycemia is known to reduce dehydroepiandrosterone (DHEA) circulating levels; however, the mechanism by which hyperglycemia decreases DHEA is not elucidated. In this study, serum DHEA and DHEA sulfate (DHEA-S) levels were compared in 50 men with non-insulin-dependent diabetes mellitus (NIDDM) and 50 age-matched men with impaired glucose tolerance (IGT) receiving only diet therapy. Serum concentrations of DHEA and DHEA-S in the NIDDM group were significantly lower than in the IGT group (7.8 and 9.7 nmol/l vs 3.4 and 4.9 mumol/l, respectively; p < 0.01) but there was no significant difference in immunoreactive insulin between the two groups. When the results from both groups were combined, HbA1C was significantly inversely related to DHEA (r = -0.243, p < 0.01) and DHEA-S (r = -0.305, p < 0.01). Immunoreactive insulin showed no correlation with DHEA and DHEA-S. Multiple regression analysis showed that HbA1C was independently negatively related to both DHEA and DHEA-S. We conclude that hyperglycemia may decrease serum DHEA and DHEA-S in Japanese men with NIDDM, but the depression of DHEA(-S) is independent of serum insulin level.
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PMID:Depression of dehydroepiandrosterone in Japanese diabetic men--comparison between non-insulin-dependent diabetes mellitus and impaired glucose tolerance. 876 81

Six Welsh gelding ponies (weight 246 +/- 6 kg) were premedicated with 0.03 mg/kg of acepromazine intravenously (i.v.) followed by 0.02 mg/kg of detomidine i.v. Anaesthesia was induced with 2 mg/kg of ketamine i.v. Ponies were intubated and lay in left lateral recumbency. On one occasion anaesthesia was maintained for 2 h using 1.2% halothane in oxygen. The same group of ponies were anaesthetized 1 month later using the same induction regime and anaesthesia was maintained with a combination of detomidine, ketamine and guaiphenesin, while the ponies breathed oxygen-enriched air. Electrocardiogram, heart rate, mean arterial blood pressure, cardiac output, respiratory rate, blood gases, temperature, haematocrit, glucose, lactate and cortisol were measured and cardiac index and systemic vascular resistance were calculated in both groups. Beta-endorphin, met-enkephalin, dynorphin, arginine vasopressin (AVP), adrenocorticotrophic hormone (ACTH) and catecholamines were measured in the halothane anaesthesia group only and 11-deoxycortisol during total intravenous anaesthesia (TIVA) only. Cardiorespiratory depression was more marked during halothane anaesthesia. Hyperglycaemia developed in both groups. Lactate and AVP increased during halothane anaesthesia. Cortisol increased during halothane and decreased during TIVA. There were no changes in the other hormones during anaesthesia. Recovery was smooth in both groups. TIVA produced better cardiorespiratory performance and suppressed the endocrine stress response observed during halothane anaesthesia.
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PMID:Cardiorespiratory, endocrine and metabolic changes in ponies undergoing intravenous or inhalation anaesthesia. 886 52

Recent studies indicate that experimentally induced hyperinsulinemia may reduce serum dehydroepiandrosterone (DHEA) and dehydroepiandrosterone-sulfate (DHEA-S). Serum DHEA and DHEA-S decrease in diabetic patients, but the mechanism by which hyperglycemia decreases DHEA and DHEA-S is unknown. In this study, we investigated the effect of hyperglycemia on DHEA and DHEA-S in impaired glucose tolerance (IGT) by means of the 75g-oral glucose tolerance test (OGTT). We selected 30 male IGT patients receiving diet therapy only, whose insulinogenic Index was under 0.3. Oral glucose challenge significantly reduced DHEA (P = 0.0001) and DHEA-S (P < 0.05) at 60 and 120 min after OGTT. Setting the value of DHEA and DHEA-S at time zero as 100%, we calculated the DHEA and DHEA-S values at 60 and 120 min after OGTT as %DHEA(-S) 60 min and %DHEA(-S) 120 min, respectively. DHEA and DHEA-S at time zero showed no correlation with BMI, HbA1c, the sum of insulin values (sigma IRI) or the area under the curve of plasma glucose (AUC). We found decreases in %DHEA 60 min (r = -0.411, P < 0.05), %DHEA-S 60 min (r = -0.508, P < 0.01) and %DHEA-S 120 min (r = -0.393, P < 0.05) as AUC increased, but sigma IRI showed no correlation with %DHEA(-S) 60 min or %DHEA(-S)120 min. We conclude that the depression of DHEA and DHEA-S after OGTT is attributable to hyperglycemia in male Japanese IGT with low insulin response.
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PMID:Hyperglycemia decreases dehydroepiandrosterone in Japanese male with impaired glucose tolerance and low insulin response. 888 22

The present study was undertaken to study the effects of chronic treatment with lisinopril on the cardiovascular complications in streptozotocin (STZ) diabetic and deoxycorticosteroneacetate (DOCA) hypertensive rats. Injection of STZ produced severe glycosuria (> 2%), hyperglycemia, hypoinsulnaemia, polydypsia, polyphagia and loss of body weight. It also produced hypothyroidism, hypercholesterolaemia, hypertriglyceridaemia, hypertension, bradycardia and decreased left ventricular developed pressure (LVDP). Elevation in serum creatinine level and increased activity of liver enzymes were also found in STZ treated animals. DOCA by itself did not produce any change in blood glucose but reduced serum insulin levels in non-diabetic animals. However, in the diabetic group, DOCA reduced blood sugar levels. Treatment of STZ-diabetic rats with DOCA did not aggravate cardiac depression or hyperglycaemia. Treatment of rats with lisinopril (1 mg kg-1, p.o. daily for six weeks), in diabetic and diabetic hypertensive animals prevented STZ induced loss of body weight and hypertension, bradycardia and hypothyroidism. It also prevented STZ induced hyperglycemia and hypoinsulinaemia in both diabetic and diabetic hypertensive animals. There was a reduction in cholesterol, triglyceride, and LDL levels; the ratio between total cholesterol to HDL and LDL to HDL and an improvement in LVDP at higher filling pressure in diabetic as well as diabetic hypertensive animals. Treatment with lisinopril also prevented hypertrophy and elevated levels of serum creatinine, SGOT and SGPT in diabetic animals. In conclusion, the present data suggests that STZ-DOCA model may not be considered as the ideal model for the study of cardiovascular complications of combined treatment hypertension and diabetes. However, the present investigation presents a number of beneficial effects of lisinopril treatment in diabetic with or without hypertensive rats and it may be considered as one of the drugs of choice in treatment of hypertension when it is associated with diabetes mellitus.
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PMID:Effects of chronic treatment with lisinopril on cardiovascular complications in streptozotocin diabetic and DOCA hypertensive rats. 907 44

We investigated the effect of hyperglycemia on the initiation and propagation of spreading depression-like peri-infarct ischemic depolarization (SD) induced by focal cerebral ischemia in rats. Peri-infarct SD were monitored during the initial 15 minutes after remotely induced middle cerebral artery occlusion (MCAO) using serial diffusion weighted magnetic resonance imaging. Maps of the apparent diffusion coefficient (ADC) were calculated and ADC decreases were monitored over time. Hyperglycemic rats (n = 6) had a significant prolongation of the time from induction of MCAO to the start of the ADC decrease as compared with normoglycemic control rats. The time to the maximal ADC decrease was significantly delayed and recovery of transient ADC declines in the area adjacent to the ischemic core was significantly faster in hyperglycemic rats. We conclude that hyperglycemia delays the terminal depolarization in the ischemic core and supports a faster repolarization in severely mal-perfused penumbral tissue after SD, which reflects the increased availability of energy substrates in the state of hyperglycemia.
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PMID:Hyperglycemia delays terminal depolarization and enhances repolarization after peri-infarct spreading depression as measured by serial diffusion MR mapping. 918 99


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