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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of the fentanyl fluanisone combination (Hypnorm) and pentobarbitone sodium (Pentobarbital) anaesthesia on blood glucose, insulin and glucagon were tested in rats in the fed and fasted state. Blood glucose was measured before and at 10, 20 and 30 min after injection of the anaesthetic agents. At 30 min the rats were sacrificed, and blood was drawn for measurement of glucagon and insulin. Pre-anaesthetic values for insulin and glucagon were established in separate groups of fasted and fed rats. In fasting rats given Hypnorm, blood glucose and plasma insulin were unchanged while there was a non-significant increase in plasma glucagon. The fasted rats given Pentobarbital had unchanged blood glucose and plasma insulin and a non-significant depression of glucagon. The fed rats given Hypnorm had a significant increase in blood glucose at 10 min and nearly a doubling of glucose values at 20 and 30 min (P < 0.001). Glucagon increased far less than in the fasted group, whereas insulin was doubled from preanaesthetic values (P < 0.05). The fed rats given Pentobarbital, had unchanged blood glucose, a slight non-significant depression of glucagon and a significant increase in insulin (P < 0.01). Thus Hypnorm induced hyperglycaemia in fed but not in fasted rats, probably because more glucose was available in the fed state. Fed animals are a modification of the standard fasted animal model, and may be preferable when exploring hyperglycaemic or other reactions to anaesthetic agents.
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PMID:Increased plasma glucose levels after Hypnorm anaesthesia, but not after Pentobarbital anaesthesia in rats. 796 63

There are two phases to the behavioral response to injection of formalin. After an initial vigorous response, a period of reduced pain occurs 10 to 15 min after formalin, followed by reemergence of pain-related behaviors. These phases are believed to represent acute chemical stimulation of afferent neurons followed by injury-related inflammatory pain. Pentobarbital (10, 15, or 25 mg/kg), diazepam (0.5, 1.5, or 5.0 mg/kg), or ethanol (0.5, 1.0, or 1.5 g/kg) attenuated the diminution of pain between the two phases, so that pain was continuous throughout 60 min of testing, but had no effect on pain scores during the peaks of either phase. The effects of pentobarbital and diazepam were blocked by picrotoxin (2.5 mg/kg), which itself had no effect. Ro 15-1788 also blocked the effect of diazepam. Picrotoxin did not effectively antagonize the effect of ethanol. A high dose of picrotoxin (5.0 mg/kg) caused seizures in some rats and also eliminated the interphase depression of pain. The results suggest that the biphasic time course of formalin pain is produced by a central antinociceptive mechanism that is inhibited by GABAA receptors.
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PMID:Pentobarbital, diazepam, and ethanol abolish the interphase diminution of pain in the formalin test: evidence for pain modulation by GABAA receptors. 827 43

Chloral hydrate, pentobarbitone and urethane were evaluated and compared for onset, duration and depth of anaesthesia, cardiovascular and respiratory effects, nociception and mortality in adult male rats. Chloral hydrate (300 and 400 mg/kg) severely depressed the cardiovascular and respiratory systems. Duration of anaesthesia was linearly related to dose, and anaesthetic depth and analgesia were excellent. Pentobarbital (40 mg/kg) produced a short period of light surgical anaesthesia. Moderate to severe respiratory and cardiovascular depression occurred. Duration of anaesthesia was not related to dose. Urethane (1.2 and 1.5 g/kg) caused moderate cardiovascular depression. In addition, mortality was high at the 1.5 g/kg dose. Duration of anaesthesia was greater than 24 h for most animals. Anaesthesia depth and analgesia were excellent.
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PMID:Anaesthetic effects of chloral hydrate, pentobarbitone and urethane in adult male rats. 836 72

1. The action of pentobarbitone on the N-methyl-D-aspartate (NMDA) receptors of neurones freshly dissociated from the olfactory bulb and olfactory tubercle has been studied using patch-clamp techniques. 2. Pentobarbitone produced a concentration-dependent depression of the currents evoked by NMDA with an IC50 value of c. 250 microM. 3. Analysis of the NMDA-evoked noise produced power spectra that could be fitted by the sum of two Lorentzians with corner frequencies of 17 and 82 Hz. Pentobarbitone increased the corner frequency of the high frequency component but did not alter the apparent single channel conductance estimated from the noise. 4. Single channel recordings in either the cell-attached or outside-out patch configurations revealed that NMDA (20 or 50 microM) opened channels with a main conductance level around 55 pS and a principal subconductance around 44 pS. The uncorrected mean open time of the channels was 3.4 ms and mean burst length was 6.0 ms. Mean cluster length was about 12 ms. 5. Pentobarbitone produced a concentration-dependent reduction in both mean open time and burst length. Mean cluster length was much less affected. Pentobarbitone did not decrease unitary current amplitude or bias the open-state current amplitude distribution in favour of a particular substate. 6. From these data it appears that pentobarbitone depresses the inward current evoked by NMDA by reducing the probability of channel opening and this results from a shortening of the lifetime of the channel open state and by decreasing burst length.
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PMID:Pentobarbitone modulation of NMDA receptors in neurones isolated from the rat olfactory brain. 868 Jul 36

Forty-six near-adult pigs (mean age 10 months, mean weight 156 kg) were anaesthetised for laparoscopy. After intramuscular azaperone (1.0 mg/kg) and ketamine (2.5 mg/kg), 14 of the pigs received intravenous etomidate (200 micrograms/kg) and midazolam (100 micrograms/kg) and 17 were given ketamine (2 mg/kg) and midazolam (100 micrograms/kg). The other 15 pigs were anaesthetised with pentobarbitone (15 to 20 mg/kg) without pre-anaesthetic medication. The duration and adequacy of anaesthesia, recovery rate, and seven physiological variables (ECG, heart rate, indirect arterial blood pressure, respiratory rate, minute volume, mean end-tidal carbon dioxide concentration and percentage oxygen saturation of haemoglobin) were compared. Repeated injections were needed in 29 of the 46 cases. Pentobarbitone was the least satisfactory drug because although the haemodynamic variables were greater, it caused more respiratory depression and a higher overall complication rate than the other methods. Apnoea occurred in two pigs, and was fatal in one, and positive pressure ventilation with oxygen was needed in three others. Intubation conditions were poorer and the times to standing, walking and rooting were longer in the pigs anaesthetised with pentobarbitone.
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PMID:Comparison of three injectable anaesthetic techniques in pigs. 928 42

Six men and 3 women on each of 4 days received 10 mg of methylphenidate or placebo (2 times a day) at 0800 and 1200 after 8 hr or 0 hr of sleep. Sleep latency was measured by the Multiple Sleep Latency Test (MSLT) at 0930, 1130, 1330, 1530, and 1730. Participants also completed divided-attention and auditory vigilance tasks at 1000 and 1400 and the Profile of Mood States (POMS) and the Addiction Research Center Inventory (ARCI) after the 0930 and 1330 latency tests. The drug increased mean latency on the MSLT in both sleep conditions. Performance only showed drug effects after prior sleep deprivation. On the POMS, the drug increased Vigor and reduced Fatigue and Depression scale scores, primarily after sleep deprivation. The drug increased the ARCI Amphetamine and Morphine-Benzedrine scores only in the basal state. The ARCI Pentobarbital score was increased by sleep deprivation and decreased by the drug.
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PMID:Alerting effects of methylphenidate under basal and sleep-deprived conditions. 938 61

We investigated the contribution of adenosine neuromodulation to mechanisms of pentobarbital-induced depression of excitatory synaptic transmission in vitro. Transverse hippocampal slices were prepared from brains removed from isoflurane-anesthetized male Wistar rats. Field excitatory postsynaptic potentials (fEPSPs), elicited by orthodromic electrical stimulation of Schaffer collateral at 0.05 Hz, were recorded from the CA1 region in oxygenated artificial cerebrospinal fluid. Amplitude of fEPSP was analyzed for assessing drug effects. Pentobarbital (100 microM) transiently depressed fEPSPs (P<0.01); i.e., fEPSP was initially depressed to approximately 60% of control and then recovered to approximately 80% of control. The fEPSP depression was partially suppressed by pretreatment with 50 microM aminophylline, a nonselective adenosine receptor antagonist, and 0.2 microM 3, 7-Dimethyl-1-propagylxanthine, an adenosine A(1) receptor antagonist (P<0.01 each). However, the fEPSP depression was not affected by pretreatment with 10 microM 8-cyclopentyl-1, 3-dipropylxanthine, an A(2) receptor antagonist, or 10 microM bicuculline, a gamma-aminobutyric acid (GABA) A receptor antagonist. The results indicate that adenosine neuromodulation through A(1) receptors and other undefined mechanisms, which are independent from GABAergic mechanisms, are involved in pentobarbital-induced depression of excitatory synaptic transmission.
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PMID:The involvement of adenosine neuromodulation in pentobarbital-induced field excitatory postsynaptic potentials depression in rat hippocampal slices. 1109 14

The effects of anesthetics on the generation of cortical spreading depression (CSD) were investigated. Volatile anesthetics halothane, isoflurane, sevoflurane (0.5, 1.0, and 2.0 MAC), and the intravenous anesthetic pentobarbital were studied. Cortical spreading depression was induced by 3M-KCl applied to a surface of brain cortex for 30 minutes. Direct current (DC) potential was recorded, and the number, amplitude, and duration of CSDs were observed. With increasing concentrations of each volatile anesthetic, there was a dose-related reduction in CSD frequency but not in CSD amplitude. At 2.0 MAC of sevoflurane the suppression of CSD was less than with the other volatile anesthetics. In addition, the influence of anesthetics on expression of c-fos mRNA was investigated. Additional animals anesthetized by isoflurane or sevoflurane were studied. Five CSDs were elicited by electric stimulation (0.5 mV, 1 second) in each animal. In situ hybridization with 35S-labeled oligonucleotides was used to evaluate the level of c-fos mRNA. The expression of c-fos was observed in the hemisphere in which CSD was elicited, but there was no difference in expression of c-fos among the groups. We conclude that volatile anesthetics can induce suppression of CSD elicitation in a dose dependent manner, but that at high concentrations sevoflurane is significantly less effective than other volatile agents. Pentobarbital has the least effect on KCl-induced CSD. These data suggest that the choice of anesthetics can impact the results of studies examining membrane depolarization and the ionic changes initiated by CSD.
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PMID:The effects of anesthetics on cortical spreading depression elicitation and c-fos expression in rats. 1114 74

Many people living with HIV use marijuana to manage agitation, spasms, chronic pain, depression, nausea arising from chemotherapy, and loss of appetite. Concerns over the use of marijuana or dronabinol (a pharmaceutical version of tetrahydrocannabinol or THC) include potential contamination from pesticides or other chemicals used in the growing process, and the potential of increasing the likelihood of lung infections. Use of THC is associated with reduced levels of testosterone and may have similar effects on other hormones in women. THC can also interact with other mood-altering medications such as Valium, librium, Xanax, seconal, Nembutal, or phenobarbital, by exaggerating their effect.
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PMID:Medical marijuana and dronabinol. 1136 69

Pentobarbital, a general anesthetic, has received extensive study for its ability to potentiate inhibition at GABA(A) subtype of receptors for GABA. Using whole cell current-clamp techniques and bath applications, we determined the effects of pentobarbital and GABA receptor antagonists on the membrane properties and tonic or burst firing of medial geniculate neurons in thalamic slices. Pentobarbital (0.01-200 microM) induced depressant effects in 50 of 66 neurons (76%). Pentobarbital hyperpolarized neurons by a mean of 3 mV and decreased the number of action potentials in tonic firing, evoked by current pulse injection from near the resting potential. Pentobarbital also decreased burst firing or low threshold Ca(2+)-spikes, evoked by current pulse injection into neurons at potentials hyperpolarized from rest. The blockade of tonic and burst firing, as well as low threshold Ca(2+)-spikes, was surmountable by increasing the amplitude of input current. The GABA(A) receptor antagonists, bicuculline (100 microM) and picrotoxinin (50-100 microM), did not block the depressant effects of pentobarbital (10 microM). The GABA(B) receptor antagonist, saclofen (200 microM), and GABA(C) receptor antagonist, (1,2,3,6-tetrahydropyridine-4-yl)methylphosphinate (10-50 microM), did not significantly alter the depressant effects. Pentobarbital produced excitatory effects (0.1-50 microM) on 11 neurons (17%) but had no effects on 5 neurons (7%). The excitation consisted of approximately 3 mV depolarization, increased tonic and burst firing and the rate of rise and amplitude of low threshold Ca(2+) spikes. These effects were associated with a increase in input resistance. In contrast, the depressant effects of pentobarbital correlated to a decreased input resistance measured with hyperpolarizing current pulse injection (IC(50) = 7.8 microM). Pentobarbital reduced Na(+)-dependent rectification on depolarization and lowered the slope resistance over a wide voltage range. Tetrodotoxin eliminated both Na(+)-dependent rectification and the pentobarbital-induced decrease in membrane resistance at depolarized voltages in two-thirds of the neurons. The pentobarbital-induced decrease in membrane resistance at voltages hyperpolarized from rest was not evident during co-application with Cs(+), known to block the hyperpolarization-activated rectifiers. In summary, the pentobarbital acted at low concentrations to depress thalamocortical neurons. The depression resulted from decreased rectification on depolarization, which no longer boosted potentials over threshold, and an increased conductance that shunted spike generation. The depressant effects of pentobarbital did not involve known types of GABA receptor interactions.
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PMID:Pentobarbital depressant effects are independent of GABA receptors in auditory thalamic neurons. 1246 30


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