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)

Toxicosis was induced in pregnant heifers by feeding 25,000 mg/head/day of FireMaster BP-6, a commercial blend of polybrominated biphenyls (PBB). The PBB feeding decreased dry matter intake approximately 50% by 4 days exposure. Emaciated animals became anorexic a few days prior to death at 33 to 66 days. Weight losses of heifers average 80 kg. Other clinical signs observed were dehydration, diarrhea, excessive salivation and lacrimation, fetal death, abortion, and general depression as evidenced by depressed heart and respiratory rates. Clinical signs were apparent after 10 days exposure and progressively intensified along with loss of condition until death. Clinicopathologic changes included significantly increased serum glutamic-oxaloacetic transaminase and decreased serum calcium by 30 days exposure. Lactate dehydrogenase, urea nitrogen, and bilirubin were elevated, and serum albumin decreased by 36 to 40 days. Principal urine changes were decreased specific gravity and moderate proteinuria. Pregnant heifers fed 0.25 or 250 mg/head/day for 60 days and nonpregnant heifers fed 250 mg/head/day for 180 days displayed neither clinical signs nor clinicopathologic changes indicating adverse effects from PBB exposure. Post-exposure, all heifers exposed to PBB for 60 days calved normally with zero calf mortality and were successfully rebred. Milk production was not different from control animals. Birth weights of calves from dams exposed to 250 mg PBB/head/day were significantly greater than calves of dams exposed to 0 mg or 0.25 mg/head/day. PBB exposure of dams produced no detrimental effects on calves as indicated by clinical signs, clinicopathologic changes, or performance.
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PMID:Effects of PBBs on cattle. I. Clinical evaluations and clinical chemistry. 21 5

Human red cells were incubated at pH 8.2 and 30 mM phosphate concentration with glucose, glucose plus methylene blue, or inosine. In 16 normal subjects, the lactate production rate (LPR) from glucose alone was 92.2 +/- 7.5 mumoles per minute per liter red blood cell. With methylene blue added, the mean LPR was 118.5 +/- 7.4 per cent of control glucose values. With inosine as substrate the mean LPR was 68.5 +/- 6.0 per cent of that from glucose. Lactate/glucose ratios averaged 1.36, presumably because of accumulation of intermediates under conditions of high pH and Pi. Patients with various kinds of anemias had LPR's from glucose that were usually markedly higher than normal, but the LPR's from inosine were generally about 2/3 of those from glucose. The LPR's of the anemic patients correlated with their degree of reticulocytosis and several patients with pyruvate kinase (PK) deficiency showed normal LPR if the red cell population age was ignored, byt marked depression when compared to expected LPR for degree of reticulocytosis. The LPR from glucose of red cells of G6PD-deficient subjects was decreased (not increased) by methylene blue. Methylene blue, while stimulating the pentose phosphate pathway, also mediated some oxidation of NADH, thus complicating the stoichiometry of the overall system. In addition, the results suggested that the dye may have attacked -SH groups on some enzymes. In normal red cells, the lower LPR from inosine than from glucose was explained as due to consumption of ATP for hexose utilization (thus generating more ADP for the triose reactions). In confirmation, when red cells were incubated without substrate to deplete their ATP-, and enhance their ADP-, levels, the LPR from inosine exceeded that from glucose. Fluoride and iodoacetate affected LPR from glucose more than from inosine, suggesting the necessity of adequate ATP levels in hexose utilization. Overall glycolysis in the red cell is seen as the resultant of a network of metabolic reactions in which ADP and ATP levels are important control parameters.
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PMID:Incubation studies on human red cells utilizing glucose or inosine under various conditions. 24 Aug 98

In an effort to compare the effects of anesthetics on cardiac functions and metabolism, mongrel dogs were anesthetized with morphine (3 mg/kg, N2O 50% in oxygen) or halothane (0.7%, N2O 50% in oxygen). Hb, Ht, pO2, pCO2, pH, O2 content, lactate, and pyruvate in the arterial and coronary sinus blood were measured and ECG, LVP, CVP, AP, and CO were recorded. Aorta was cross-clamped for 30 min under cardiopulmonary bypass (CPB). Hemodynamic and metabolic survey were continued until 120 min of recovery period. Results were as follows: Hemodynamics, such as LVP, AP, and CO, were depressed after CPB, then gradually returned to control level. Subendocardial ischemia observed through ST depression and QRS widening on ECG, as well as DPTI/TTI ratio under 1.0, disappeared in the recovery period. Lactate was produced by the heart after anoxic arrest and was extracted at 120 min after CPB. Halothane and morphine did not show any significant differences of effects on cardiac function and metabolism in this study.
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PMID:Effects of morphine and halothane on canine cardiac function before and after cardiopulmonary bypass. 103 47

To study the efficacy of isosorbide dinitrate in prevention of myocardial ischemia, 20 patients with angiographically proved coronary artery disease underwent atrial pacing (mean rate 138/min) before (P1), 10 minutes after (P2) and 65 minutes after (P3) sublingual administration of 5 mg of isosorbide dinitrate. The symptomatic, hemodynamic and metabolic responses were evaluated at rest and during each pacing period. Angina occurred in all subjects during P1. Angina did not recur or was less severe in 17 of 19 patients during P2 and in 19 of 20 patients during P3. Resting left ventricular end-diastolic pressure for the group was normal at 11 plus or minus 4 mm Hg (mean plus or minus standard deviation). On interruption of pacing at 4.5 minutes during P1, average end-diastolic pressure during sinus rhythm was abnormal (18 plus or minus 6 mm Hg). After administration of isosorbide dinitrate mean left ventricular end-diastolic pressure was significantly decreased at rest and remained normal when pacing was interrupted during P2 and P3. Brachial arterial pressure, cardiac index, tension-time index, left ventricular stroke work index and maximal rate of rise of left ventricular pressure were all diminished at rest before and during P2 and P3. S-T segment depression was less during P2 and P3 than during P1. Before isosorbide dinitrate was given, resting myocardial lactate extraction was 15 plus or minus 11 percent during P1 lactate extraction decreased to minus2 plus or minus 25 percent. Lactate extraction was significantly greater during P2 and P3 than during P1. This study demonstrates that sublingual administration of 5 mg of isosorbide dinitrate has a significant protective effect against pacing-induced myocardial ischemia at 10 and 65 minutes after administration.
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PMID:Effects of isosorbide dinitrate on the response to atrial pacing in coronary heart disease. 115 42

Hemodynamic and metabolic responses to pacing from either the coronary sinus or right atrium were evaluated in 41 patients with chest pain and normal coronary arteriograms. A group of patients (group II) with angina, lactate production, or significant ST segment depression had a significantly higher mean pulmonary capillary pressure on peak pacing or angina than did a group of patients considered to have a normal pacing response (group I). In 6 of 9 group II patients, the left ventricular end-diastolic pressure either rose abnormally with pacing or was greater than 14 mm Hg immediately after pacing and resembled that of a group of patients with coronary artery disease; Patients with a prolapsing mitral valve (group III) also had a significantly higher pulmonary capillary pressure on peak pacing as compared to those of group I, although abnormal left ventricular pressure responses occurred in only 2 of 9 of these patients. The stroke index was significantly lower in group III on peak pacing while group II was no different from group I. Lactate production occurred in 6 of 9 group II patients. However, only 1 of 6 patients with a prolapsing mitral valve who were studied for lactate production was found to produce lactate, suggesting a different mechanism for their pain.
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PMID:Hemodynamic and metabolic responses to pacing in patients with chest pain and normal coronary arteriograms. 120 72

The effects of glucose-insulin-potassium infusion (GIK) on atrial pacing-induced angina, ST depression, abnormal left ventricular end-diastolic pressure during pacing interruption (LVEDPi) and lactate metabolism (L), were studied in 18 patients: ten had angina during pacing = Ischemic group, and eight (5 normals and 3 with coronary artery disease) remained asymptomatic = Nonischemic group. The study consisted of 8-10 minute periods of control, pacing and recovery, before and after GIK. No untoward effects were observed. Comparison of the pacing responses (GIK vs pre-GIK states) showed that during GIK, angina occurred in only 4 patients, while significantly less severe changes were observed in ST depression (1.4 +/-0.5 vs 2.4 +/- 0.4 mm) and LVEDPi (16 +/- 3 vs 23 +/- 3 mm Hg). Lactate extraction was also higher (8.1 +/- 10.9 vs -5.2 +/- 11.1%), but not significantly so, although L became normal in 4 subjects and improved in another. These results indicate that GIK infusion was well tolerated and had a beneficial effect on pacing-induced myocardial ischemia.
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PMID:The protective effect of glucose-insulin-potassium on the response to atrial pacing. 127 28

It is now well documented that both cocaine (Coc) and methamphetamine (Meth) are independently capable of inducing injurious effects on the adult and developing myocardium. In addition, when these drugs are used concomitantly such as in polydrug abuse, it has been suggested that they may cause synergistic adverse effects on the myocardium. In this investigation, primary myocardial cell cultures were established from 3-5-day-old Sprague-Dawley rats to describe the adverse effects of Coc and Meth on the myocardium. After the cells were in culture for 4 days, they were exposed to 1 x 10(-5) and 1 x 10(-3) M Coc alone; 1 x 10(-5) and 1 x 10(-3) M Meth alone; and combinations of 1 x 10(-3) M Coc with 1 x 10(-5) M Meth and 1 x 10(-5) M Coc with 1 x 10(-5) M Meth. Lactate dehydrogenase (LDH) release, morphology, and beating activity were evaluated after exposure to the drugs for 1, 4 and 24 h. With all treatment groups for the first 4 h, LDH release was not significantly different from untreated controls. Significant LDH release (P less than 0.001) was exhibited at 24 h with 1 x 10(-3) M Coc alone, 1 x 10(-3) M Meth alone, and 1 x 10(-3) M Coc with 1 x 10(-5) M Meth. For 24 h of treatment, cellular injury (pseudopodia, vacuolization, granulation) induced by 1 x 10(-3) M and 1 x 10(-5) M Coc alone was extensive and minimal, respectively. When 1 x 10(-5) M Meth was added with 1 x 10(-5) M Coc, pseudopodia formation was extensive. No measurable beating activity was observed at 1, 4 and 24 h exposure to 1 x 10(-3) M Coc alone and 1 x 10(-3) M Coc with 1 x 10(-5) M Meth. At 1 h, beating activity after treatment with 1 x 10(-5) M Coc alone and 1 x 10(-5) M Meth alone was not significantly different from untreated controls; however, the percentage of areas exhibiting contractile activity was depressed. Addition of Meth (1 x 10(-5) M) potentiated Coc-induced (1 x 10(-5) M) depression of contractile activity at all 3 time-points. These data suggest that Coc and Meth may interact synergistically at the cellular level to directly potentiate injury to postnatal myocardial cell cultures.
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PMID:A primary culture system of postnatal rat heart cells for the study of cocaine and methamphetamine toxicity. 157 Jun 32

We have investigated the effect of an exogenous lactate load given during machine haemofiltration treatment in 22 patients with acute renal failure and 12 patients with chronic renal failure, without any overt evidence of liver disease. Hyperlactataemia occurred in all patients, but the expected changes in acid base status, an increase in bicarbonate and a reduction in arterial hydrogen ions were observed in less than 40% of the treatments in the acute renal failure group. Ultrafiltrate losses of lactate and bicarbonate could not alone explain the changes in acid-base status. There was a positive correlation between the increase in arterial lactate and hydrogen ion concentrations, r = 0.52, p less than 0.01. Lactate accumulation in patients at, or close to, their threshold for lactate utilisation may result in further depression of cardiac function and peripheral lactate utilisation. Hyperlactataemia due to use of lactate-based dialysis/haemofiltration solutions in critically ill patients may result in a worsening of the acid-base status, and arterial pH should be monitored so that bicarbonate solutions can be substituted if the changes are progressive.
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PMID:Hyperlactataemia and metabolic acidosis during haemofiltration using lactate-buffered fluids. 175 38

Coronary hemodynamics, myocardial metabolism and left ventricular function at rest and after incremental atrial pacing were evaluated in 12 patients with stress-induced angina and ST segment depression, angiographically normal coronary arteries and no evidence of spasm, generally labeled as syndrome X, and in 10 normal subjects. At baseline study, great cardiac vein flow was comparable in patients and control subjects. During pacing, an equivalent rate-pressure product was reached in the two groups, but the slope of the relation between rate-pressure product and great cardiac vein flow was significantly less steep in patients than in normal subjects (0.0027 vs. 0.0054 ml/mm Hg.beat, p less than 0.001). Nevertheless, the left ventricular ejection fraction was comparable in both groups at rest (66 +/- 6% vs. 71 +/- 7%, p = NS) and during pacing (71 +/- 7% vs. 66 +/- 5%, p = NS). At baseline study, myocardial glucose extraction was more efficient in patients with syndrome X (p less than 0.05), but net myocardial exchange of pyruvate and alanine was, respectively, smaller and greater than in control subjects. Lactate was extracted to a similar extent in the two groups and in no instance was net lactate release observed during pacing or recovery. During pacing and recovery, patients with syndrome X showed net pyruvate release, unlike the control subjects in whom net pyruvate exchange was positive. In addition, patients with syndrome X continued to show net myocardial extraction of alanine during spacing and recovery, whereas normal subjects produced alanine throughout the study. Myocardial carbohydrate oxidation increased significantly during maximal pacing in normal subjects but not in patients, in whom it always remained below (p less than 0.01) the concurrent rate of myocardial uptake of carbohydrate equivalents (glucose, lactate, pyruvate, alanine). Myocardial energy expenditure was significantly lower in patients than in control subjects at maximal rate-pressure product levels (p less than 0.01). The metabolic pattern in patients with syndrome X therefore is not consistent with classic ischemia, although differences in the net exchange of circulating substrates (glucose, pyruvate, alanine) can be demonstrated. Thus, in patients with syndrome X, the symptoms, electrocardiographic signs and impairment in the increase in great cardiac vein flow during pacing coexist with preserved global and regional left ventricular function and myocardial energy efficiency.
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PMID:Coronary hemodynamics and myocardial metabolism in patients with syndrome X: response to pacing stress. 203 78

Anterior segment necrosis is an acute or chronic process occasioned by embarrassment of the blood supply of the anterior segment of the eye. In the acute form this vascular obstruction leads to severe corneal oedema, necrosis of anterior uvea, hypotony and cataract formation. Depression of aqueous humour formation accounts for severe reduction of glucose levels in corneal stroma and aqueous humour lasting for two days after cautery of the long posterior ciliary arteries (LPCA) in rabbits. Lactate levels are initially significantly elevated but return to normal after one week. Stromal hydration was elevated for one week but then returned to normal. Corneal epithelial glycogen was diminished at one and two days after surgery but then returned to normal. Although unproven, oxygen deprivation probably plays a major role in endothelial ischaemia and therefore corneal oedema. It is concluded that the abnormalities seen in anterior segment necrosis stem from changes in aqueous metabolic components resulting from severely reduced aqueous turnover. Hyperbaric oxygen and intracameral metabolite substitution are unproven treatments but merit further experimental study.
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PMID:The intraocular changes of anterior segment necrosis. 207 Aug 80


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