UMLS:C0011570 - FACTA Search

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)

The present study examines the effects of resuscitation fluid composition on myocardial function, myocardial high-energy phosphate content, and survival following third-degree anesthetic burn to 35-40% body surface area in the guinea pig. Treatment regimens used were 1) no resuscitation, 2) isotonic saline, 3) Ringer's lactate and 4) Ringer's acetate. Fluids were administered at the rate of 0.334 ml/kg/hr/% burn for 4 hr following injury, at which time myocardial function was assessed. Nonburned animals served as controls. In isolated working hearts, significant depression of myocardial function was observed in nonresuscitated and saline-resuscitated animals as evidenced by decreased cardiac output, dP/dt, -dP/dt, and stroke work. Lactate resuscitation produced some improvement in these parameters but did not restore them to those of nonburned control animals. In contrast, Ringer's acetate resuscitation resulted in normal cardiac output and contractility. Myocardial ATP content of hearts obtained from the various resuscitation groups did not differ from that of nonburned control hearts, except for hearts from Ringer's lactate group, which were significantly lower in myocardial ATP than those of the other groups. No differences were found in creatine phosphate content. Resuscitation with the different fluid regimens for 48 hr produced significant differences in survival. Fluids were given at the rate of 4 ml/kg/% burn for 24 hr. Half of the fluid was given in the first 8 hr and the rest during the remaining 16 hr. Nonresuscitated and saline-resuscitated animals showed significant mortality by 24 hr, whereas lactate- and acetate-treated animals had survival rates of 100% and 87.5%, respectively. However, by 48 hr, only acetate-treated animals survived. These data indicate that important differences exist in the effectiveness of different resuscitation fluids and that Ringer's lactate, the fluid most often utilized clinically, may not provide optimum benefit. In light of these results, serious consideration should be given to the substitution of acetate for lactate during the resuscitation of burn shock patients.
...
PMID:Resuscitation fluid composition and myocardial performance during burn shock. 369 Aug 12

Synaptosomes isolated from rat cerebra were used to study the effects of the inhalational anesthetic, halothane, on cholinergic processes. To identify possible mechanisms responsible for the depression of acetylcholine synthesis, we examined the effects of halothane on precursor metabolite metabolism involved with supplying the cytosol with acetyl-CoA for acetylcholine synthesis. Three percent halothane/air (vol/vol) depressed 14CO2 evolution from labeled pyruvate and glucose. Steady-state 14CO2 evolution from [1-14C]glucose was depressed 84% by halothane, while 14CO2 evolution from [6-14C]glucose and [3,4-14C]glucose was decreased 67 and 52%, respectively, when compared with control conditions. Halothane inhibited the activities of both pyruvate dehydrogenase (14% depression) and ATP-citrate lyase (32% depression). Total synaptosomal acetyl-CoA concentrations were unaffected by halothane. Three percent halothane/air (vol/vol) caused a 77% increase in medium glucose depletion rate from 1.38 nmol (mg protein)-1 min-1 to 2.44 nmol (mg protein)-1 min-1. Production of lactate by the synaptosomes in the presence of halothane increased by 231% from a control rate of 1.44 nmol (mg protein)-1 min-1 to 4.77 nmol (mg protein)-1 min-1. Lactate production rate from pyruvate was also enhanced by 56% in the presence of halothane. These data lend support to the concept that the NAD+/NADH potential may be involved in the halothane-induced depression of acetylcholine synthesis.
...
PMID:Halothane-induced alterations of glucose and pyruvate metabolism in rat cerebra synaptosomes. 392 66

The acute hemodynamic and antiischemic properties of amiodarone were investigated in 16 patients with more than 70% diameter reduction of a left coronary artery. Two successive atrial pacing stress tests (APST I and II) were performed, with an interval of 40 minutes in between, and amiodarone, 5 mg/kg/5 min, was infused 30 minutes after APST I. Hemodynamic changes during amiodarone administration consisted of a 20% decrease in left ventricular (LV) systolic pressure, a 13% decrease in systemic vascular resistance and an 18% decrease in stroke work. Coronary vascular resistance was reduced 19% and coronary sinus flow increased 23%. Despite a secondary 14% increase in heart rate, contractility decreased 21%, accompanied by a 45% increase in LV end-diastolic pressure, which persisted until APST II. Although most hemodynamic changes were observed only during the infusion, contractility and LV systolic pressure were still diminished at the beginning of APST II and remained so during pacing, resulting in a reduction in myocardial oxygen demand compared to APST I. Although overall myocardial oxygen consumption and coronary flow were equal during both pacing tests, amiodarone significantly reduced pacing-induced myocardial ischemia. Lactate metabolism remained normal during APST II (lactate extraction 12 +/- 3% vs -28 +/- 8% (APST I) at maximal pacing rates [p less than 0.05]), while ST-segment depression, LV end-diastolic pressure postpacing and angina were also significantly reduced during APST II. Thus, in humans, intravenous amiodarone reduces vascular resistance and contractility and inhibits pacing-induced myocardial ischemia, presumably by reducing myocardial oxygen demand.
...
PMID:Acute hemodynamic and antiischemic effects of intravenous amiodarone. 397 4

The metabolic and hormonal responses to exhaustive short-term supramaximal exercise were studied in 10 male physical education students. The exercise task was a single bout of running on the treadmill at 22 km X h-1 and 7.5% slope. It was performed with single oral doses of 100 mg Bupranolol (non-selective beta-blockade), 100 mg Metoprolol (beta-1-selective blockade), and placebo. Arterialized capillary and venous blood were sampled until 30 min post exercise. Time to exhaustion was 52.0 +/- 2.6, 47.6 +/- 2.0, and 46.0 +/- 1.9 s in the control, Metroprolol, and Bupranolol experiments. At cessation of exercise, adrenaline and noradrenaline were grossly elevated in all three conditions. Lactate and glucose increased markedly, this being accompanied by increasing insulin in the control and Metoprolol, but not the Bupranolol trials. Glycerol increased moderately, while FFA were depressed. Growth hormone showed a delayed increase at 15 and 30 min post exercise. Cortisol was unaffected by exercise. beta-blockade reduced the increases of lactate, glucose, glycerol, insulin, and growth hormone, exaggerated the depression of FFA and had no effect on cortisol. The results demonstrate that the strong sympatho-adrenal response to exercise of this nature is a major determinant of the increase of glucose at cessation of exercise. The hyperglycemia in concert with beta-2-adrenergic stimulation leads to elevation of insulin. Furthermore, lipolysis is controlled by beta-adrenergic stimulation. The delayed increase of growth hormone seems to be triggered by the declining glucose level during recovery.
...
PMID:Metabolic and hormonal responses to exhaustive supramaximal running with and without beta-adrenergic blockade. 614 64

Prostaglandins (PGA1, PGE1 and PGF2 alpha) were assayed in 15 patients with chronic coronary disease during an anginal attack induced through frequent atrial stimulation. Measurements from eleven patients with intact coronary arteries served as control. Lactate extraction coefficient was used as a biochemical indicator of myocardial ischemia; the latter was associated with increased production of coronary sinus PGF2 alpha and arterial PGA1. No correlation could be established between PG levels in the studied series, the extent of ST depression on electrocardiograms, lactate extraction level and hemodynamic manifestations.
...
PMID:[Prostaglandins A1, E1 and F2 alpha concentrations in the arterial and coronary venous blood of patients with ischemic heart disease during induced myocardial ischemia]. 657 38

The effects of nickel chloride were studied in two human cell lines, HeLa and diploid embryonic fibroblasts, as well as in V79 Chinese hamster cells and in L-A mouse fibroblasts. NiCl2 produces a dose-dependent depression of proliferation and mitotic rate. Effects on viability are accompanied by an increasing release of the intracellular enzyme lactic dehydrogenase. Lactic acid production is stimulated. The plating efficiency is reduced, as are DNA and protein synthesis and, to a lesser degree, RNA synthesis. Comparing these results with those of previous studies of the cytotoxicity of other heavy metals in the same test systems, similar effects are observed though with different intensities and slight differences between the cell lines employed. As regards lethal effects (LC50) the following rank order of cytotoxicity can be established: Ni2+ approximately equal to Pb2+ less than Mn2+ less than Hg2+ less than Cd2+; as regards growth inhibition the same rank order is observed as in the case of the LC50 in HeLa and human fibroblasts, but in L-A cells Ni2+ is more inhibitive than the other metal ions listed above with the exception of Cd2+. With respect to colony formation NiCl2 is less effective than PbCl2, MnCl2, and CdCl2. NiCl2 effects in serum-free medium are much faster and more severe than in medium containing serum or serum albumin indicating that serum constituents, notably albumin, bind the metal effectively and inhibit cellular uptake; this confirms reports of other authors on the serum binding and slow uptake of NiCl2. Synchronized cells are most sensitive in the G1 and early S phases of the cell cycle. Together with the finding that thymidine incorporation is affected to a considerable degree this contributes an explanation of the known genotoxic effects of nickel.
...
PMID:Toxicity of nickel for mammalian cells in culture. 672 Jan 41

Coronary artery disease is considered a contraindication to inducing hypotension during surgery because the combined effects of stenosis and hypotension in reducing distal coronary artery perfusion pressure might produce myocardial ischemia. To study the effect of deliberate hypotension (mean systemic pressure, 50 mmHg) on regional myocardial perfusion, oxygenation, and lactate extraction, we constricted the left-anterior descending coronary artery (LADCA) in dogs. Two degrees of stenosis were studied: "critical" stenosis, which reduced resting coronary blood flow from 34.4 to 31.2 ml/min and abolished reactive hyperemia of the LADCA in response to 10 s of total coronary artery occlusion; and a more "severe" stenosis, which reduced resting coronary blood flow by 40%. LADCA pressure was measured distal to the stenosis, and LADCA perfusion pressure was obtained by subtracting the left ventricular end-diastolic pressure from the coronary artery diastolic pressure measured past the stenosis. Hypotension was induced by administering sodium nitroprusside, halothane at a high concentration, or trimethaphan. Lactate extraction and oxygen consumption were measured across the myocardium distal to the stenosis (from the coronary artery to the great cardiac vein) and across the whole heart (from the coronary artery to the coronary sinus). Regional myocardial blood flow was measured using radioactive microspheres. A transmural electrocardiogram was obtained from electrodes implanted in the subendocardium and the subepicardium in the distribution of the LADCA distal to the stenosis. Although the combination of critical stenosis and hypotension reduced regional myocardial blood flow and lowered LADCA perfusion pressure to 27 +/- 3 (SE) mmHg, myocardial ischemia did not occur, as evidenced by continued lactate extraction and no redistribution of transmural blood flow or change in ST segment. On the other hand, the combination of severe stenosis and hypotension reduced LADCA perfusion pressure to 17 +/- 2 (SE) mmHG and produced evidence of ischemia by regional lactate production, reduction of the subendocardial/subepicardial flow ratio, and depression of the ST segment.
...
PMID:A canine model of acute coronary artery stenosis: effects of deliberate hypotension. 688 88

The effects of manganese chloride were studied in two human cell lines HeLa and human embryonic diploid fibroblasts in V79 Chinese hamster lung cells, and L-A mouse fibroblasts. Manganese produces a dose-dependent depression of proliferation along with a decrease of the mitotic rate. Effects on viability are accompanied by increased release of the intracellular enzyme lactic dehydrogenase. Lactic acid is stimulated indicating enhanced glycolytic activity. The colony forming ability and the rate of DNA synthesis are inhibited in a dose- and time-related fashion. Comparing these results with those of previous studies of the cytotoxicity of lead, mercury, and cadmium in the same test systems, similar effects are observed, though with different intensities and slight differences between the cell lines. As regards depression of viability, the following rank order of toxicity can be established: Pb2+ < Mn2+ < Hg2+ < Cd2+; as regards reduction of proliferation lead is less and cadmium more effective than manganese, while mercury effects vary depending on the cells tested. Concerning colony formation and DNA synthesis the toxicity of manganese is again higher than that of lead and manganese, especially the influence on DNA synthesis, show immediate recovery after cessation of exposure indicates that the genetic material is not directly involved and that the effects on proliferation colony formation, and DNA synthesis are the consequences of several elaborate processes at the cellular level.
...
PMID:[Cytotoxicity of manganese for mammalian cells in vitro--comparisons with lead, mercury and cadmium]. 746 17

This study examines acute changes in circulating levels of atrial natriuretic peptide (ANP) and insulin-like growth factor (IGF-1) during short periods of myocardial ischemia experienced at coronary angioplasty. Ten patients (mean age 55.7 +/- 3.9 years, nine men) undergoing angioplasty to the left anterior descending coronary artery were studied. Angioplasty of the left anterior descending coronary artery was performed with the balloon inflations maintained at 6 to 10 atm for 20 to 90 seconds. Blood was sampled from the coronary sinus for ANP, IGF-1 (both total and free), and lactate levels at (1) after catheterization of the coronary sinus, (2) after the initial left coronary angiography, (3) immediately after balloon deflation, and (4) 5 minutes after deflation. ANP levels (pmol/L +/- SEM) rose significantly at the end of balloon deflation (13.4 +/- 2.8; p < 0.01) compared with baseline levels (8.8 +/- 1.9). This rise was sustained for at least 5 minutes after balloon deflation (13.7 +/- 3.1; p < 0.01). ANP levels were not affected by the injections of angiographic contrast media. Free IGF-1 levels rose after injections of radiographic contrast but not after balloon inflation or deflation. Total IGF-1 levels did not change significantly at any of the sampling times. Lactic acid (mmol/L) levels rose at the end of balloon inflation (2.66 +/- 0.6) compared with baseline (2.13 +/- 0.7; p < 0.05) but returned to normal within 5 minutes of balloon deflation. Neither lactic acid levels nor release of ANP or IGF-1 correlated with the initial left ventricular end-diastolic pressure or the degree of electrocardiographic ST depression during the procedure.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Acute changes in atrial natriuretic peptide, insulin-like growth factor-1, and lactate levels during left anterior descending coronary artery angioplasty. 757 78

The effect of repeated episodes of asphyxia on the fetal cardiovascular system and CNS was examined. The umbilical cord was occluded for 5 min, four times, at 30-min intervals in 11 chronically instrumented fetal sheep (118-126 d). Fetal electrocorticogram (ECoG), cortical impedance, ECG, heart rate, and blood pressure were continuously recorded for 3 d, after which neuronal loss was determined histologically. Each occlusion resulted in fetal hypoxemia and bradycardia accompanied by increased T/QRS ratio. Progressively severe hypotension and lactic acidosis developed during successive occlusions. The ECoG was depressed and cortical impedance increased with each occlusion. During the final occlusion, blood pressure fell to 3.5 +/- 1 kPa and heart rate to 93 +/- 9 bpm, T/QRS ratio increased to 0.44 +/- 0.3, and lactate rose to 7.2 +/- 1.2 mM/L. Three animals died from cardiac fibrillation during recirculation after the third or fourth occlusion. After the asphyxial episodes, blood pressure and heart rate returned to normal, and the T wave was inverted for 310 +/- 155 min. Lactate returned to baseline within 24 h. The ECoG remained depressed for 90 +/- 35 min, and intermittent seizures developed at 3.3 +/- 1.4 h after the last occlusion. Neuronal loss was primarily found in the striatum. The extent of neuronal loss correlated with the degree of hypotension, increase in T/QRS ratio, duration of postasphyxial ECoG depression, and number of seizures. These results indicate that transient asphyxial episodes compromise the ability of the heart to tolerate additional insults and further suggest that neuronal loss is a consequence of cardiovascular compromise secondary to asphyxia.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Repeated episodes of umbilical cord occlusion in fetal sheep lead to preferential damage to the striatum and sensitize the heart to further insults. 765 53

<< Previous 1 2 3 4 5 6 7 Next >>