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 changes in laryngeal resistance (LR) during respiratory arrest produced by withdrawal of hypoxia stimulation and administration of various respiratory depressants were studied in 14 spontaneously breathing, anesthetized cats (11 cats with alpha-chloralose and three cats with halothane). Withdrawal of hypoxia stimulation caused a transient respiratory arrest with no central inspiratory activity, during which a considerable increase in LR was observed to a level higher than the fixed resistance after muscle paralysis [LR(fix)]. Intravenous injection of thiopentone, ketamine, and lidocaine all caused a transient respiratory arrest. However, the effects on the laryngeal function and the central inspiratory activity were different for each agent. Both thiopentone and ketamine induced an inspiratory apneusis pattern in phrenic nerve discharge, and lidocaine caused a silence of phrenic nerve activity. Thiopentone relaxed the larynx, and LR during thiopentone-induced respiratory arrest was almost equal to LR(fix). Ketamine maintained a dilatation of the larynx, and LR during ketamine-induced respiratory arrest was lower than LR(fix). Lidocaine caused a constriction of the larynx and LR greatly increased, leading frequently to laryngospasm. These results indicate that hypoxia withdrawal, thiopentone, ketamine, and lidocaine all cause different effects on the central inspiratory activity, and that the central respiratory depression produced by these methods is not accompanied by a uniform depression of laryngeal function.
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PMID:Different laryngeal responses during respiratory arrest produced by hypoxia withdrawal, thiopentone, ketamine, and lidocaine in cats. 706 36

The changes in baroreceptor-heart rate reflex properties and in hemodynamics produced by light ketamine anesthesia were studied in one group of rabbits before and after infracollicular decerebration and those produced by althesin anesthesia in another group. Ketamine produced marked depression of baroreceptor reflex-mediated vagal effects on heart rate which was of similar magnitude in intact and pontine decerebrate rabbits; this indicates that its action was largely at or below the pons. Althesin produced much less vagal depression than ketamine in the intact rabbit but in pontine rabbits the depression was greatly enhanced. The smaller vagal depression in the intact rabbit appears to be due to a facilitatory effect through a suprapontine pathway by Althesin which partially masks its depressant effect below the pons. In the intact rabbit ketamine produced a greater rise in blood pressure than Althesin anesthesia for 1 h; the greater pressor response was due to a transient rise in total peripheral resistance (TPR) and a sustained rise in cardiac output. The difference in the blood pressure responses was mainly due to differences in action of the two anesthetics at or below the pons and only the transient rise in TPR during ketamine anesthesia was mediated through a suprapontine pathway.
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PMID:Effects of ketamine and Althesin Anesthesia on baroreceptor--heart rate reflex and hemodynamics of intact and pontine rabbits. 708 66

The circulatory effects of Valsalva-like manoeuvers were studied before and during i.v. infusions of either ketamine, Althesin and thiopentone given in doses that produced similar levels of light anesthesia. The Valsalva-like manoeuvers were of 30 s duration and consisted of applying Valsalva pressures (VP) from 2.5 to 20 mm Hg to the animal's respiratory valve and to a cuff placed around its thorax and abdomen. In the conscious rabbit the major reflex responses to the Valsalva-like manoeuver were VP-related rises in total peripheral resistance (TPR) and in heart rate which were mainly mediated through intrathoracic baroreceptors and were completely abolished by sino-aortic denervation. Ketamine depressed the Valsalva-TPR response by about 30-40% but Althesin and thiopentone were without effect. Ketamine and thiopentone produced marked depression of the Valsalva-heart rate reflex, but Althesin had relatively little effect. We concluded that ketamine produces greater impairment of blood pressure homeostasis mediated through constrictor and heart rate reflexes evoked through arterial and cardiopulmonary baroreceptors than the other two anesthetics.
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PMID:Effect of ketamine, althesin, and thiopentone on the Valsalva-constrictor and heart rate reflexes of the rabbit. 711 59

The effects of ketamine on the peripheral sympathetic nervous system were studied in vitro by observing the amplitude of the nerve-mediated contraction of the vasa deferentia isolated from guinea pigs. Ketamine dissolved in the perfusate of an organ bath was applied to the tissues for 30 minutes and then washed out with a perfusate lacking ketamine for 90 minutes. Ketamine in concentrations of 10(-8) and 10(-7) g/ml had no effect on contraction induced by hypogastric nerve (preganglionic) stimulation. At 10(-6) g/ml, the drug had no significant effect during application but was associated with increased contractions during washout. At 10(-5) and 10(-4) g/ml, the drug showed a dose-related depression during application and an increase in contractions during washout after a 10(-5) g/ml. Ketamine, 10(-5) g/ml, increased contraction following transmural (postganglionic) stimulation and had a depressant effect at a concentration of 10(-4) g/ml. It is concluded (1) that ketamine has dual effects on the nerve-mediated contraction of the vasa defentia and (2) that cardiovascular responses to ketamine include peripheral effects of ketamine on sympathetic ganglia.
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PMID:Ketamine acts on the peripheral sympathetic nervous system of guinea pigs. 718 65

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

Ketamine appears to induce both excitatory and depressant actions in the brain; however, it is not clear which regions are affected. The 2-deoxyglucose functional mapping method of Sokoloff et al. was used to determine regional variations in metabolic activity of rat brain caused by injection of ketamine, 25-75 mg, intramuscularly. To compare the effects of ketamine with those of hippocampal-induced seizures, the 2-deoxyglucose method was used, following injection of penicillin G, 400-800 units, into the hippocampus. The findings from five control, seven ketamine-treated, and three penicillin G-treated rats are given. Ketamine caused a significant increase of metabolic activity in the hippocampal sulci and a decrease of activity in the medial geniculate and the inferior colliculus. Similar changes were found with hippocampal seizures caused by penicillin. The inhibition of the regions associated with sensory systems (medial geniculate and inferior colliculus) may account in part for the anesthetic action of ketamine, while the intense activity of the hippocampus may be related to the excitatory manifestations. The results indicate that ketamine produces seizures in the hippocampus, which in turn inhibit auditory and visually associated nuclei. Thus, the anesthesia may follow from the sensory depression and the cataleptic phenomena may be related to the hippocampal excitation.
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PMID:Ketamine-induced changes in regional glucose utilization in the rat brain. 736 54

Ketamine appears to be the answer to the definite need for a safe and potent intravenously administered anesthetic of short duration for pediatric populations. Ketamine combines analgesic and sleep-producing effects without significant cardiovascular and respiratory depression. Even if the most serious untoward actions occur (eg. hallucinatory emergence phenomena which are unusual in children) can be minimized by exercising "skillful neglect" (ie, permit the patient to awaken in his own time) in reviving the patient, these appear to be small prices to pay for the benefits derived from this anesthetic.
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PMID:Ketamine anesthesia in pediatric ophthalmic surgery. 744 36

In the absence of sympathetically mediated stimulation, ketamine depresses myocardial contractility. This results from a decrease in the availability of intracellular Ca2+ for excitation-contraction coupling. Although sites of action other than the Ca2+ release channel of sarcoplasmic reticulum have been implicated, ketamine-induced alterations in Ca2+ efflux from the sarcoplasmic reticulum remain contentious. The purpose of the present study was to identify interactions of ketamine with the calcium release channel using sarcoplasmic reticulum enriched vesicles from porcine left ventricle. Ketamine did not alter [3H]ryanodine binding at concentrations of 1 mM or less, while binding was almost completely inhibited at 10 mM. Gating and conductance of SR Ca2+ channels studied in planar bilayers was not altered by clinical concentrations of ketamine over the range of physiologic cytoplasmic free Ca2+ concentrations. Channel inactivation was observed at 10 mM ketamine, well in excess of clinical concentrations. These findings indicate that clinical concentrations of ketamine do not alter the function of the Ca2+ release channel. Alterations in intracellular Ca2+ homeostasis that result in depression of myocardial contractility must therefore result from effects at other sites along the excitation-contraction coupling pathway.
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PMID:Ketamine, at clinical concentrations, does not alter the function of cardiac sarcoplasmic reticulum calcium release channels. 757 22

The occurrence of severe head injury, isolated or in connection with polytrauma, is a challenge for all physicians working in emergency care at the scene of an accident or afterwards in hospital care. It is an advantage to have a basic knowledge of neurological assessment. The Glasgow Coma Scale is widely used in this context; we refer to mild, moderate, and severe injuries. It is very important to recognise concomitant injuries, which occur in about 40% of cases. As coexisting hypoxaemia and hypotension have an adverse effect on the time course of head injury by inducing secondary brain damage, it is essential in therapy to quickly restore the vital body functions. Unconscious patients are tracheally intubated and ventilated. Forced hyperventilation over a lengthy period seems to have an unfavourable effect on outcome. Anaesthetic drugs and adjuvant therapies are used that do not increase intracranial vessel diameter and consequently intracranial pressure (ICP). This applies to all i.v. anaesthetics, sedatives, and opioids, as long as no respiratory depression occurs. Ketamine has been useful for many years at the scene of an accident. An existing low blood pressure (BP) is raised while a significantly increased BP is moderately lowered. It is necessary to have adequate cerebral perfusion pressure (CPP), which is defined as mean BP minus ICP. In cases of polytrauma with heavy bleeding, e.g., from the liver or spleen, the blood loss must be stopped before the neurosurgeon begins. Excessive i.v. administration of Ringer's lactate should be avoided. Today, the routine use of osmodiuretics, e.g., mannitol, is not indicated. It has not yet been possible to show that using corticosteroids is definitely beneficial in human brain trauma; there may be a positive effect in connection with spinal trauma. New therapies are being investigated, such as increasing CPP, administering AMPA/NMDA-antagonists, 21-aminosteroids, or hypertonic-hyperoncotic solutions. However, they have not as yet been proven effective for general clinical use or clinical use et al.
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PMID:[Early management of head-brain trauma patients]. 761 87

Spreading depression (SD) in the rat brain is inhibited by N-methyl-D-aspartate (NMDA) receptor antagonists. Because the NMDA receptor glycine recognition site must be occupied for activation of the NMDA ionophore, we hypothesized that antagonism of the glycine receptor would also affect SD. In halothane anesthetized rats, SD was initiated by electrocortical stimulation. Both the initiation threshold and propagation rate of SD were recorded. Rats were then administered the glycine receptor antagonist ACEA-1021 (or vehicle only) or ketamine and the stimulus was repeated. Rats were then killed and terminal depolarization was observed for. Ketamine completely inhibited initiation of SD. In contrast, all rats treated with ACEA-1021 exhibited SD. While ACEA-1021 caused no difference in the stimulation threshold for SD, propagation rate was decreased in a dose-dependent fashion. Terminal depolarization occurred in all rats. Antagonism of glycine at the NMDA receptor recognition site did not inhibit initiation of SD but played a modulatory role in the mechanism of its propagation.
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PMID:Effects of glycine receptor antagonism on spreading depression in the rat. 770 May 95


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