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)

The properties of Althesin (anticonvulsant activity, depression of oxygen consumption, lowering of ICP, rapid excretion) led us to use this steroid combination to treat 11 patients in status epilepticus resistant to the standard drugs (benzodiazepines and barbiturates). The administration of Althesin by slow intravenous injection was ineffective in 2 of the 3 patients thus treated. The doses used (2--10 ml) were probably too small. One only administration of a 10% solution of Althesin in 10% fructose by intravenous drip (the rate was calculated so as to obtain the burst suppression stage at the EEG) stopped status epilepticus in 7 of the 9 patients thus treated. In this group the doses used varied from 25 to 50 ml. The 2 patients in whom it was necessary to repeat Althesin administration and combine it with other drugs had both been operated on for severe brain injuries involving marked cerebral edema. In spite of the very small number of cases, the definitive arrest of status epilepticus obtained in 8 out of 11 patients first treated with other drugs is encouraging: Althesin probably may be regarded as an adjunct in the treatment of status epilepticus.
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PMID:The use of althesin in drug-resistent status epilepticus. 47 37

In anesthetised cats, breathing pattern, blood gases, and ventilatory response to CO2 were recorded before and during intermittent 10-minute episodes of hydrostatically raised intracranial pressure. The first effect on breathing was a stimulation which was followed at higher pressures by irregularity, depression, and periods of apnea; hyperventilation at high intracranial pressure (ICP was rare. Raised ICP did not consistently depress the ventilatory response to CO2 until ventilation during airbreathing was already depressed; therefore, we cannot experimentally justify applying this test clinically to detect incipient ventilatory depression. When hypoxemia developed during raised ICP, it was compatible with the degree of hypoventilation due to central depression of breathing; thus, there was no evidence of a neurally mediated effect on the lungs, causing defective gas exchange.
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PMID:Effect of intermittently raised intracranial pressure on breathing pattern, ventilatory response to CO2, and blood gases in anesthetized cats. 124 58

It is well known that vasodilating antihypertensive drugs induce intracranial hypertension. A considerable number of papers have reported nitroglycerin-induced ICP elevation during anesthetized operations. However, except for Gagnon's report, most papers dealt with normal patients. Our study, using an extradural pressure transducer clinically, deals with the nitroglycerin drip infusion and its effect on high ICP state. Mean ICP value before infusion was 42 mmHg+ 14.8 (N = 10). Three cases out of ten showed ICP elevation corresponding with blood pressure depression. Six cases out of ten revealed ICP depression corresponding with blood pressure depression. One case did not show any difference in ICP. There was a statistically significant difference between the ICP elevated group and the depressed group. These results suggest that very high ICP state, like vasomotor paralysis, does not have a potential to open the vascular bed in the cranium and blood pressure depression induced by nitroglycerin infusion causes ICP depression. We would like to conclude that nitroglycerin can be used for postoperative blood pressure control even in the neurosurgical field.
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PMID:[Post-operative blood pressure management by nitroglycerin in the field of neurosurgery]. 251 60

The effects of spontaneous respiration and mechanical ventilation on ICP were examined by investigating the interaction between elevated pressure and alcohol intoxication. 200 ml ethanol 48% were infused in 11 young pigs with elevated cerebral pressure during mechanical ventilation (Group 1), 7 young pigs with elevated intracranial pressure during spontaneous respiration (Group 2), and 4 young pigs without elevated intracranial pressure during spontaneous respiration (Group 3). While the behaviour of intracranial pressure during mechanical ventilation in the animals from Group 1 was inhomogeneous with a tendency to rise (29 mmHg to 34 mmHg), intracranial pressure (28 mmHg to 55 mmHg) increased dramatically in Group 2. This increase was associated with a sharp rise of paCO2 (37.6 mmHg to 73.3 mmHg) and a decline of paO2 (74 mmHg to 13 mmHg). None of the animals in Group 2 survived. paCO2 also rose in alcoholized animals without elevated ICP (Group 3) (41.9 mmHg to 63.9 mmHg); intracranial pressure, however, remained within the normal range. All animals in Group 3 survived. Our findings indicate that elevated intracranial pressure and alcohol intoxication have a cumulative or potentiating effect on depression of the respiratory centre. Respiratory depression can be prevented by mechanical ventilation and, therefore, a further rise of intracranial pressure can be generally avoided.
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PMID:[Effect of various types of artificial respiration on raised intracranial pressure, associated with acute alcoholic intoxication]. 310 36

This discussion has illustrated the enormous variety found within the category of familial intrahepatic cholestasis. It has also demonstrated how much more there is to learn about these fascinating disorders, which may be examples of experiments in nature on bile formation. This analysis should be recognized to be the author's own, and there is much debate about this classification. For example, some workers in this field contend that North American Indian cholestasis is in reality Byler's syndrome. Such an identity seems unlikely, given the differences between the two syndromes (Table 2). This is a field that is changing rapidly. Recently, a new cholestatic syndrome, bearing some similarities to benign recurrent intrahepatic cholestasis, but dissimilar in several ways, has been reported. There is evidence that cholestasis of pregnancy may be inherited as an autosomal dominant, sex-limited trait. If further studies confirm a genetic etiology, this syndrome would be the most common form of familial intrahepatic cholestasis. The assessment of any individual case remains difficult, particularly early in the course. Table 2 can serve as a guide to the differential diagnosis of these conditions. When faced with a neonate with jaundice, all of the usual causes must be ruled out first. The pattern of bile acids in serum is useful for ruling out Zellweger's syndrome. A good family history and physical examination, particularly of the heart, are important. An ophthalmologic examination by a specialist, often under anesthesia, and a spine radiograph can be useful in confirming a diagnosis of Alagille's syndrome. A liver biopsy, carefully interpreted with input from the clinician, is useful in pointing toward one direction or another. Often a firm conclusion cannot be reached, or is reached prematurely, so the clinician would be advised to inform the parents of all diagnostic possibilities in order to avoid false hopes or unwarranted depression. The diagnostic pitfalls to be avoided in this evaluation are many. No histologic findings are clearly pathognomonic for one syndrome or another. Giant cell transformation and paucity of intrahepatic bile ducts may be found in several syndromes. Biliary atresia, or at least failure to demonstrate a patent biliary tree from the liver to the cystic duct, may be present in patients with Alagille's syndrome. In that syndrome, the eye findings, particularly the posterior embryotoxon, may not be appreciated except on extensive ophthalmologic testing, including gonioscopy. Butterfly vertebrae may not be visible at birth and may be no longer evident in adulthood.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Familial intrahepatic cholestatic syndromes. 330 44

Hemodynamic changes and left ventricular performance were investigated by simplified mechanocardiography using finger plethysmography instead of carotid artery pulse tracing in patients who received 4 volatile anesthetics with or without nitrous oxide. Systolic blood pressure (Ps), diastolic blood pressure (Pd), heart rate (HR), pre-ejection period (PEP), left ventricular ejection time (LVET), isovolemic contraction time (ICP), PEP/LVET, Pd/ICT, and 1/PEP2 were selected as indices which represent hemodynamics and systolic time intervals. Enflurane 0.6 and 1.2MAC prolonged PEP, and shortened 1/PEP2 and Pd/ICT significantly. Addition of nitrous oxide caused more depression. Halothane 0.6MAC prolonged PEP, and shortened 1/PEP2 and Pd/ICT. Sevoflurane 1.2MAC shortened only 1/PEP2. Addition of nitrous oxide prolonged PEP and PEP/LVET, and shortened Pd/ICT. Isoflurane 1.2MAC lowered Ps and increased HR. The results indicate that cardiac performance was depressed by volatile anesthetics in the order of enflurane, halothane, sevoflurane and isoflurane.
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PMID:[Volatile anesthetics suppress cardiac function in man; an investigation based on systolic time intervals]. 843 99

The number of parameters (i.e., EEG or ICP-intracranial pressure) routinely monitored under clinical situations is limited. The brain function analyzer described in this paper enables simultaneous, continuous on-line monitoring of cerebral blood flow (CBF) and volume (CBV), intramitochondrial NADH redox state, extracellular K+ concentrations, DC potential, electrocorticography and ICP from the cerebral cortex. Brain function of 14 patients with severe head injury (GCS < or = 8), who were hospitalized in the neurosurgical or general intensive care unit was monitored using this analyzer. Leao cortical spreading depression (SD) has been reported in many experimental animals but not in the human cerebral cortex. In one of the patients monitored, spreading depression was observed. This is the first time that spontaneous repetitive cortical SD cycles have been recorded from the cerebral cortex of a patient suffering from severe head injury. Typical SD cycles appeared 4-5 h after the beginning of monitoring this patient. During the first 3-4 cycles the responses of this patient were very similar to the responses to SD recorded in normoxic experimental animals. Electrocorticography was depressed whereas extracellular K+ levels increased. The metabolic response to spreading depression was characterized by oxidation of intramitochondrial NADH concomitant to a large increase in CBF. During brain death, an ischemic depolarization, characterized by decrease in CBF and an irreversible increase in extracellular K+, was recorded.
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PMID:Cortical spreading depression recorded from the human brain using a multiparametric monitoring system. 897 24

In order to evaluate the relationship between brain oxygen supply and demand (O2 balance) in real time, it is necessary to use a multiparametric monitoring approach. Cerebral blood flow (CBF) is a representative parameter of O2 supply. The extracellular level of K+ is a reliable indicator of O2 demand since more than 60% of the energy consumed by the brain is utilized by active transport processes. Mitochondrial NADH redox state can represent the balance between O2 supply and demand. In order to monitor the brain of experimental animals or patients, we constructed the multiparametric assembly (MPA) and the following parameters were monitored simultaneously and in real time: CBF, CBV, NADH redox state, extracellular K+, DC potential, EEG, tissue temperature and ICP. Animals were exposed to hypoxia, ischemia, hypercapnia, hyperoxia and spreading depression (SD) and the relative changes in CBF and NADH were calculated and found to be significant indicators of brain energy state. Monitoring these two parameters increases the possibility of differentiating between various pathophysiological states. Each added parameter increases the power of diagnosis and determination of the functional state of the brain. Preliminary results obtained in patients monitored in the ICU or in the OR show that the responses to hypercapnia, spreading depression or ischemia are similar to those measured in experimental animals.
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PMID:Multiparametric monitoring of brain oxygen balance under experimental and clinical conditions. 958 30

Carrots were grown in seven experimental plots (A-G) containing mixtures of arsenic-contaminated and uncontaminated soil at concentrations ranging from 6.5 to 917 microgram g(-1) (dry mass). The carrots harvested from plots A-D (6.5-338 microgram g(-1) arsenic in the soil mixtures) showed a gradually increasing depression of growth with increasing level of contamination. At the experimental plots E-G with soil arsenic concentrations above 400 microgram g(-1) no carrots developed. Whether this effect was caused by arsenic or the concomitant copper content which ranged from 11 to 810 microgram g(-1) in the soil mixtures is unknown. The arsenic species extracted from the soils and carrots were separated and detected using anion-exchange HPLC coupled with ICP-MS. In the less contaminated soils from plots A and B arsenite (AsIII) was more abundant than arsenate (Asv) in the soil using 1 mmole 1-1 calcium nitrate as extractant. In the soils from plots C and D however, Asv dominated over AsIII whereas in the corresponding carrots Asv and AsIII were found at similar concentrations. Methylated arsenic species were sought after but not detected in any of the samples. The soil-to-carrot uptake rate (bioavailability) of arsenic was 0.47 +/- 0.06% (average +/- one standard deviation) of the arsenic content in the soils from plots A-D. In contrast to arsenic, the increasing copper content in the soils from plot A through D was not available to the carrots as the concentration of this element did not increase with increasing soil copper content. The ingestion of the potentially toxic inorganic arsenic via consumption of carrots grown in soil contaminated at 30 microgram g(-1) in arsenic (plot B) was conservatively estimated at 37 microgram week (-1). This was equivalent to only 4% of the provisional tolerable weekly intake (PTWI) for inorganic arsenic as suggested by the WHO and was therefore toxicologically safe. Consumption of carrots grown in more intensely arsenic-contaminated soils, however, would lead to a higher intake of inorganic arsenic and is therefore not recommended.
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PMID:Bioavailability and speciation of arsenic in carrots grown in contaminated soil. 970 75

To accommodate a spaceflight experiment with moss (SPM), experiment-unique equipment (EUE) was developed by engineers at Kennedy Space Center. The hardware allows sterile culture for an extended period of time in commercial petri dishes, lateral illumination of each culture with light of a specific wavelength (660 nm; other wavelengths are possible) and a range of intensities (0.05-5 micromoles photons m-2 s-1), incubation in complete darkness, and chemical fixation to terminate the experiment under conditions of microgravity. The use of a fixative required triple containment to protect the astronaut crew. An external panel on the experiment container allowed the timing of illumination and fixation to be controlled by the crew. Light quality is provided by light emitting diodes (LEDs) that are located in the lid of the outer container, the BRIC (Biological Research In Canisters)-LED. Each canister accommodates 6 Petri Dish Fixation Units (PDFUs), and each PDFU holds one 6 cm petri dish. All components are autoclavable. LED illumination is piped through a transparent glass rod. Each PDFU contains fixative in a reservoir that is released by the depression of an actuator. This hardware performed well during its first flight, the 16-day STS-87 mission in Nov./Dec., 1997 as part of the Collaborative USA and Ukrainian Experiment (CUE). It supported vigorous and sterile moss growth, cells were maintained in position and were well-fixed, and there was a vigorous and consistent response to light. Although here used for moss, in future flight experiments this unique new hardware can be used for many types of organisms normally grown in petri dishes, with or without a requirement for illumination.
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PMID:Spaceflight hardware allowing unilateral irradiation and chemical fixation in petri dishes. 1154 22


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