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 effect of pentobarbitone on Ca2+ current (ICa), separated from other ionic currents was studied under voltage clamp using a suction pipette technique in Helix neurones. Pentobarbitone depressed the maximal peak amplitude (MPA) of ICa in a concentration-dependent manner without shifting the current-voltage (I-V) relationships along the voltage axis. Increases in external Ca2+-concentration [( Ca2+]o) overcame the inhibitory action of the agent on MPA. Pentobarbitone markedly accelerated the decay phase of ICa which took a distinctly different time course from that of the control. The accelerating action of the agent on the decay phase of ICa was not overcome by increases in [Ca2+]o. In the presence of internal EGTA (20 mM), pentobarbitone also accelerated the decay of ICa. Changes in pH of the external perfusing solution altered the potency of pentobarbitone in depressing MPA; in the presence of pentobarbitone (3 X 10(-4) M) at pH of 7.0, 8.0 and 9.0, fractional inhibition was approx. 46%, 21% and 4%, respectively. Internal application of pentobarbitone (10(-4)-10(-3) M) inhibited MPA, but exerted no effect on the decay phase of ICa. Pentobarbitone (10(-4) M) markedly accelerated the decrease of MPA of ICa induced by repetitive stimuli applied at an interval of 150 ms, indicating a use-dependent depression of MPA. Results provide evidence that pentobarbitone has a dual action on ICa, inhibiting MPA and accelerating the decay phase of ICa.
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PMID:Accelerating effects of pentobarbitone on the inactivation process of the calcium current in Helix neurones. 631 18

The effects of naloxone, pentobarbitone, or their combination, on arterial blood gases were studied in urethane-anaesthetised rats. Naloxone itself did not significantly alter the blood gases. Pentobarbitone significantly decreased PO2 and elevated PCO2, and these effects were prevented by pretreatment with naloxone. Arterial blood pH was unaffected by any of the drugs. The findings suggest that naloxone lacks a specific analeptic effect, but can antagonise respiratory depression induced by pentobarbitone.
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PMID:Antagonism of pentobarbitone-induced respiratory depression by naloxone in rats. 641 81

The following three regimens of anesthesia in mice were compared: (1) Ketamine 100 mg--xylazine 5 mg/kg b.wt. i.m., (2) pentobarbitone 50 mg/kg b.wt. i.p., and (3) carfentanyl 0.003 mg--etomidate 15 mg/kg b.wt. i.m. For these dosage rates the respiratory variables, i.e., respiratory rate, paO2, paCO2, pHa, BEa, HCO-3a, and the circulatory parameters, i.e., heart rate, mean arterial pressure and hematocrit, were determined during the conscious state, during surgical anesthesia, and at waking time. With ketamine and xylazine, the respiration was moderately decreased whereas the cardiovascular system was strongly depressed. Pentobarbitone induced a high respiratory depression but a lesser degree of circulatory depression. Analgesia was inadequate. Although there was a moderate respiratory and circulatory depression during anesthesia with carfentanyl and etomidate the drug-induced excitation and muscle spasms do not recommend this anesthetic combination for mice. Of these three methods, the combination of ketamine and xylazine is considered the most reliable for anesthesia of mice.
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PMID:A comparative study with various anesthetics in mice (pentobarbitone, ketamine-xylazine, carfentanyl-etomidate). 647 5

We have used a model for measuring renal clearances in the undisturbed rat to assess the role of the renal nerves in the depression of renal function during sodium pentobarbital anesthesia. One group of rats was studied with renal nerves intact and a second group was studied 7-9 days after bilateral renal denervation. Rats were prepared by placement of cannulae an average of 5 days prior to the clearance experiments. Renal function was measured before and after the injection of saline as the control vehicle and 2-3 days later, before, and after the injection of sodium pentobarbital (50 mg/kg) in the same rat. Sodium pentobarbital produced comparable decreases in glomerular filtration rate, para-aminohippuric acid clearance, urine flow rate, and sodium excretion in rats with denervated or innervated kidneys. Injection of saline resulted in no differences in measured variables between the rats with intact or sectioned renal nerves. Sodium pentobarbital caused a drop in arterial pressure in the denervated group but not in the innervated group. In a second series of experiments rats with denervated kidneys were implanted with an inflatable occluder around the aorta. This occluder was inflated to limit the drop in arterial pressure during anesthesia. When the blood pressure to the kidneys was maintained, renal function did not decrease during sodium pentobarbital anesthesia. These experiments suggest that the renal nerves are involved in the decrease in renal function during sodium pentobarbital anesthesia.
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PMID:Renal function in rats with innervated and denervated kidneys before and during sodium pentobarbital anesthesia. 674 12

The blockade in the rat of the estrous FSH surge was investigated by the injection of anti-LHRH serum in order to clarify whether LHRH controls this postovulatory surge as well as the preovulatory LH-FSH surge. A single iv injection of anti-LHRH serum at 1300 h on proestrus not only inhibited ovulation but also eliminated both the preovulatory LH-FSH surge and the second FSH surge in estrus. A single iv injection of anti-LHRH serum at 2200 h on proestrus after the LH-FSH surge did not inhibit either the estrous FSH surge or ovulation, although plasma LH was lowered, and the number of ova ovulated was reduced. Depression of plasma FSH and LH levels was also observed after a single iv injection of pentobarbital sodium (Nembutal; 35 mg/kg BW) at 1300 h on proestrus, but no such effect was observed when pentobarbital was injected at 2200 h on proestrus. A single injection of 10 IU hCG at 1800 h on diestrous II induced precocious ovulation and a concomitant increase in FSH secretion. It was not possible to inhibit the induced secretion of FSH and ovulation by a simultaneous injection of anti-LHRH serum, but plasma LH was completely suppressed. These results demonstrate that the second FSH surge is not controlled by LHRH.
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PMID:Regulation of the second surge of follicle-stimulating hormone; effects of antiluteinizing hormone-releasing hormone serum and pentobarbital. 678 59

Pentobarbitone, phenobarbitone, methohexitone, chloralose and alphaxalone produced 10-fold increases in the duration of an inhibitory post-synaptic conductance (i.p.s.c.) as recorded intracellularly from neurones of the guinea-pig olfactory cortex in vitro. Higher concentrations slightly depolarised these neurones and reduced their input resistance (Ri), presumably a spontaneous activation of the inhibitory conductance. The excitatory potentials were also depressed. Ketamine, halothane and urethane doubled the i.p.s.c. duration. Higher concentrations depressed synaptic activity and the action potential, as did lignocaine. Ketamine also increased Ri. These results confirm the idea that these compounds produce anaesthesia by prolonging inhibition (accompanied by a depression of the e.p.s.p. with some anaesthetics).
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PMID:Potentiation of inhibition by general anaesthetics in neurones of the olfactory cortex in vitro. 719 Jun 80

(I.) Toxicity of ionic coronary arteriography contrast media has been shown to depend on their cationic and anionic composition and their osmolality. Using a right coronary injection technique in the dog, the authors have shown a relationship between toxicity as manifested by occurrence of ventricular fibrillation and the presence of calcium binders in the contrast media. Sodium citrate and EDTA have been identified as the specific agents in certain contrast media that significantly increase the incidence of fibrillation in laboratory experiments. (II.) A deleterious synergism between water-soluble angiographic and urographic media and digitalis compounds has now been demonstrated, based on mortality studies (LD50) using bolus intravenous injections in white mice. The testing of a number of other classes of drugs for a similar effect has shown thus far that only the digitalis class exhibits this synergism. Surprisingly, the nonionic contrast medium, metrizamide, has been shown to have a greater synergistic effect with digitalis drugs than diatrizoate ionic media. (III.) In dog experiments under Nembutal anesthesia in which aortic flow, pulmonary artery and vein pressures, systemic arterial pressure, and EKG were monitored, left atrial pressure increases as soon as or before pulmonary artery pressure rises, even at low doses of ionic contrast media administered intravenously. This may indicate 1) flow to the left heart increases dramatically, or 2) there is a very early myocardial depression. The significance of the above findings and application to clinical practice will be discussed.
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PMID:Cardiovascular radiology. Possible factors in intravascular contrast media toxicity. 720 28

When virgin Syrian hamsters aged 6 to 8 wk were mated during estrus and anesthetized with sodium pentobarbital (Nembutal) 4 to 5 hr before estimated ovulation, pregnancy wastage in the newly conceived litter was observed. This was manifested by polyspermy of moribund eggs and death of fertilized eggs, deficits of expected zygotes, and triploidy and tetraploidy in 3-day-old surviving embryos. Multiple factors determined the nature of this wastage, including dosage of Nembutal [sodium 5-ethyl-5-(1-methyl butal) barbiturate], route of its administration, degree of resulting respiratory depression, and ultimately a pH imbalance (below 7) in the mother. Polyspermy appeared to result from the penetration of degenerating ova by 10-20 sperm, triploidy to polar body retention, and tetraploidy to endoreduplication of chromosomes before cell cleavage; identification of 2N/4N mosaics supports this inference.
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PMID:Sodium pentobarbital-induced mutations in the hamster. 731 70

The mechanism of decreased lymphocyte responsiveness after major surgery is unclear. Because sodium pentobarbital, and intermediately long-acting barbiturate, will reproducibly induce anesthesia in experimental animals, we utilized a canine model to investigate its effect on lymphocyte proliferation induced by the mitogenic lectins erythroagglutinating phytohemagglutinin (E-PHA) and leukoagglutinating phytohemagglutinin (L-PHA). Although no effect was observed at 10 minutes or 1 hour after an anesthetic dose of sodium pentobarbital, after 1 and 3 hours of anesthesia, canine lymphocytes were significantly suppressed, as demonstrated by decreased responsiveness to E-PHA and L-PHA mitogen stimulation. After 3-hours the majority of animals had mitogenesis values of less than 50% of the preanesthetic control values. Recovery, as measured by a return to at least 70% of the preanesthetic mitogenesis value, was noted in the majority of animals at 24, 48, and 72 hours. In order to investigate the machanisms of the in vivo capability of sodium pentobarbital to induce immunosuppression of lymphocyte transformation, in vitro studies were carried out. Sodium pentobarbital was found to significantly inhibit mitogen-induced canine mononuclear cell blastogenesis at anesthetic (1.5 to 3.0 mg%) drug concentrations in vitro. Lymphocytes pretreated with barbiturate and washed prior to plating did not show this inhibiting effect. Our findings suggest that depression of the immune response reported in patients after operation could result from short-acting barbiturates administered during the induction phase of clinical anesthesia. Furthermore, the suppression may involve in vivo metabolism of pentobarbital, hormones or other in vivo factors, since washed lymphocytes from the in vivo but not the in vitro experiments demonstrated suppression. These results indicate that anesthesia may be an important factor in the immunosuppression reported after major surgery.
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PMID:Alteration of lymphocyte function due to anesthesia: in vivo and in vitro suppression of mitogen-induced blastogenesis by sodium pentobarbital. 736 8

Decerebrate animals are often used in investigations of the control of breathing because anesthesia-induced depression of respiratory reflexes is absent. We therefore investigated the level of tone and responsiveness of airway smooth muscle in seven decerebrate, paralyzed, and ventilated cats. Specifically, we measured the changes in pulmonary resistance (RL) and dynamic pulmonary compliance (CLdyn) in response to hypoxia and hypercapnia. All cats responded to hypoxia (approximately 10% O2 in N2) with significant increases (mean 49%, range 5-156%) in RL from a mean control value of 0.0197 +/- 0.0081 (SD) cmH2O.ml-1.s. During inhalation of 5% CO2 in O2, RL increased significantly (mean 59%, range 16-135%) from a mean control value of 0.0190 +/- 0.0056 cmH2O.ml-1.s. Decreases in CLdyn during hypoxia and hypercapnia were much smaller, averaging -9 and -11%, respectively. After atropine was administered, average control RL fell 50%, from 0.0269 to 0.0134 cmH2O.ml-1.s (P < 0.05; n = 4). Hypoxic and hypercapnic gas mixtures did not affect pulmonary mechanics after atropine was administered. In three cats, oscillations of RL were synchronized to phrenic activity but only at low respiratory frequencies (approximately 12 cycles/min), indicating that airway smooth muscle responded slowly to vagal input. Pentobarbital sodium, like atropine, reduced control RL in three cats. These cats lost their bronchoconstrictor response to hypercapnia but had augmented responses to hypoxia compared with preanesthetic responses. We conclude that decerebrate cats possess resting bronchomotor tone and retain their responsiveness to hypoxia and hypercapnia. Thus the decerebrate cat is a useful model for studying the control of tracheobronchial smooth muscle.
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PMID:Bronchomotor responses to hypoxia and hypercapnia in decerebrate cats. 771


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