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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 Althesin, diazepam, ketamine, propanidid and thiopentone on the release of acetylcholine was tested at the mouse neuromuscular junction. Althesin, diazepam and thiopentone increased the quantal content of the end-plate potential. Ketamine at low concentration (3.6 micromol litre-1) had a similar effect, but at high concentration (116.7 micromol litre-1) quantal content decreased sharply. Propanidid and cremophor EL did not affect quantal content. The increase in quantal content antagonized the effect of postsynaptic depression on the amplitude of the end-plate potential. The lack of enhancement of acetylcholine release appears to explain the in vitro interaction of propanidid with tubocurarine. The diversity of presynaptic actions of these drugs makes it unlikely that this is an important mechanism in producing anaesthesia.
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PMID:Presynaptic effect of I.V. anaesthetic agents at the neuromuscular junction. 46 58

Anatomic, physiologic and behavioral evidence suggests that the neurons in the nucleus reticularis gigantocellularis of the medial medullary reticular formation may act as a relay station for the transmission of nociceptive information from the spinal cord to higher brain centers. The nucleus reticularis gigantocellularis may also be the site of action of analgesic agents, such as ketamine hydrochloride. Utilizing extracellular microelectrodes in 23 decerebrate cats, the authors measured the effect of ketamine on neurons in the nucleus reticularis gigantocellularis that were excited by electrical stimulation of peripheral nerves. The frequency of spontaneous single-unit firing activity in the nucleus reticularis gigantocellularis was suppressed by 31 +/- 11 (mean +/- 1 SE) and by 62 +/- 7 per cent with ketamine, 1.0 and 2.5 mg/kg, iv, respectively. The frequency of evoked single-unit activity was suppressed by 57 +/- 9 and 79 +/- 5 per cent with ketamine, 1.0 and 2.5 mg/kg, respectively. Ketamine produces significant depression of single-unit activity of the cells in the nucleus reticularis gigantocellularis, suggesting that this may be an important site of its analgesic action.
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PMID:Effects of ketamine on nociceptive cells in the medial medullary reticular formation of the cat. 49 56

The effects of ketamine and barbiturates (pentobarbital, thiopental, methohexital) were studied in an isolated rabbit Langendorff preparation. All agents tested depressed contractility. Ketamine, as well as the lipophilic barbiturates (thiopental, methohexital), caused a relatively greater depression at higher pacing rates such that the force-frequency relation was reversed. Pentobarbital did not reverse Bowditch. The effects of barbiturates on Bowditch correlated directly with lipid solubility, suggesting that their rate-related effects are due to perturbation of the membrane lipid bilayer. Disruption of hydrogen bands between polar membrane components may also be involved. The time course of the effect of thipental at high pacing rates was slower, both in onset and recovery, than at low rates. At a pacing rate of 1 Hz, maximal depression of contraction developed within 5 min. However, at 2.5 Hz, contractility continued to decline for up to 30 min. After 5 min of perfusion with thiopental, Bowditch was still positive, but by 30 min it was reversed. These temporal differences in thipental effects suggest that different mechanisms may dominate in the support of contractility at different ranges of heart rate.
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PMID:Effects of barbiturate anesthetics and ketamine on the force-frequency relation of cardiac muscle. 51 Apr

The neurons located in the mesencephalic ventro-medial tegmentum (VMT) and projecting to the nucleus accumbens, the septum and the frontal cortex were identified by the antidromic activation method. The activity of single VMT cells was extracellularly recorded in Ketamine anaesthetized rats. The effect of the stimulation of the medial frontal cortex on the activity of these identified VMT cells has been studied. The main response observed was an excitation which was followed in some cases by a depression of the spontaneous discharge of the cells.
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PMID:Effects of stimulation of the frontal cortex on identified output VMT cells in the rat. 53 May 20

An hemodynamic study has been performed in eight patients (age 68 +/- 7) suffering from complete atrioventricular block. They had to undergo the definitive implantation of a cardiac pace maker under general anesthesia. The fixed cardiac frequency may help to understand the effect of the anesthetic agent used on the cardiac muscle function. Ketamine is the only agent used directly at an initial intravenous dose of 3 mg.kg-1 followed by a perfusion in a constant rate of 0.20 mg.kg-1. min-1. Hemodynamic data (arterial pressure, pulmonary pressures, thermodilution cardiac output) are performed before induction, then every 5 minutes after induction for a 20 minute period. The absence of respiratory depression (PaCO2: 38 +/- 3 mm Hg) shows that hemodynamic changes are entirely due to ketamine. The peak of these changes takes place after 5 minutes (significant rise (p < 0.05) in systemic and pulmonary resistances, in systemic arterial pressure and in pulmonary arterial pressure). Stroke index decreases moderately. After 20 minutes all the parameters have returned to control values. Use of ketamine is not desirable for two reasons: 1 degree The rise of the afterload may alter the hemodynamic state which can be previously deteriorated in patients suffering from atrio-ventricular block. 2 degree Post-anesthetic agitation can displace the right ventricular electrode.
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PMID:[Ketamine anesthesia for definitive implantation of a cardiac pace maker (author's transl)]. 55 78

The effects of three concentrations of halothane or ketamine were investigated on isolated rabbit hearts, which were perfused with hydralazine, clonidine, propranolol or methyldopa. In hearts not subjected to the influence of an anaesthetic, clonidine was the only drug stimulating myocardial function. In those perfused with halothane or ketamine alone, both anaesthetics exerted a negative chronotropic and inotropic action in a dose-related manner. Ketamine markedly increased the coronary flow. Clonidine distinctly reduced the myocardial depression caused by halothane or ketamine. Hydralazine had no marked effects with either of these anaesthetics, except that it sensitized the hearts to the arrhythmic action of a high concentration of halothane. Propranolol, when combined with halothane, aggravated myocardial depression and decreased coronary flow. With ketamine, propranolol caused no other harmful interactions, apart from inhibiting the increase in coronary flow caused by this anaesthetic. Methyldopa intensified the myocardial depression induced by halothane, but tended to diminish that caused by ketamine. The results suggest that clonidine has a stimulatory cardiac action when combined with either of these anaesthetics. Disadvantageous interactions may exist between methyldopa or propranolol and halothane.
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PMID:The combined effects of antihypertensive drugs and anaesthetics (halothane and ketamine) on the isolated heart. 72 70

The phencyclidine derivative, ketamine hydrochloride, combines cardiovascular stimulating effects with antiarrhythmic properties and, therefore, the drug has been shown to be a highly suitable anesthetic for coronary artery surgery. This intravenously and intramuscularly administered "dissociative" anesthetic selectively depresses pathways and regions of the central nervous system associated with pain conduction and perception, thereby avoiding undesirable total nervous system depression. 129 patients suffering from marked coronary artery insufficiency underwent aortocoronary by-pass surgery, ketamine being the main anesthetic agent. Ketamine-induced anesthesia proved to be a simple and safe method of pain control during coronary artery reconstructive surgery and, compared with halothane anesthesia, showed a marked reduction of postoperative mortality (5%).
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PMID:[Use of ketamine in cardiac surgery. A preliminary report]. 80 35

Ketamine, currently being evaluated as an obstetric anaesthetic agent, is said to provide analgesia without depression of the protective airway reflexes or depression of the respiratory or cardiovascular systems. We have studied the effects of ketamine on the uterine blood flow, the foetus and the newborn in five monkeys (Macaca nemistrina). Uterine blood flow, (UBF) was measured by the steady-state infusion technique using tritiated water as the indicator. All of the variables were measured during a control period and again at 10 and 90 min after the administration of ketamine in doses of 2 mg/kg in three monkeys or 1 mg/kg in two. Maternal respiration was maintained at normal physiological levels without significant variation. The maternal mean arterial pressure (MAP), cardiac output (CO), and stroke volume (SV) did not change significantly, but heart rate (HR) did increase significantly following the injection of ketamine and remained increased for the duration of the study. UBF, a-v oxygen difference, and the oxygen consumption of the uterus and its contents remained stable throughout. During the intrauterine period the foetus did not seem to be affected by the two doses of ketamine. However, the three newborn monkeys delivered of the mothers who had reveived ketamine 2 mg/kg had profound respiratory depression. This was not seen in the two infants delivered from mothers receiving 1 mg/kg. Others have shown that neonatal depression is dose- and time-related. We conclude that ketamine should be administered to obstetric patients in small single doses or by continuous infusion in very low concentrations.
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PMID:Respiratory depression in newborn monkeys at Caesarean section following ketamine administration. 81 Dec 35

1 A pithed rabbit preparation is described that allows selective stimulation of the vertebral outflows. 2 The responses to stimulation of sympathetic vasopressor fibres were blocked by hexamethonium and phentolamine but potentiated by cocaine, whereas the responses to stimulation of cardioaccelerator fibres were blocked by propranolol. 3 Ketamine, althesin and pentobarbitone enhanced the effects of noradrenaline and attenuated the effects of sympathetic nerve stimulation. Thiopentone enhanced the effects of both noradrenaline and sympathetic nerve stimulation. 4 In pithed rabbits a transient, dose-related cardiovascular depression was produced by each agent irrespective of whether vasomotor tone was present whereas in decerebrate rabbits the corresponding cardiovascular depression was longer lasting. 5 It is concluded that the cardiovascular depression produced by intravenous anaesthetics in intact rabbits is due to a combination of central and peripheral effects.
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PMID:The effects of intravenous anaesthetics on the cardiovascular system of the rabbit. 92 49

The responses of rabbit aortic strips superfused with noradrenaline, adrenaline and 5-HT were studied alone and in combination with ketamine (50 mug/ml). Ketamine caused a slight depression of the isolated aorta but potentiated responses to adrenaline but not to noradrenaline or 5-hydroxytryptamine. Ketamine did not potentiate aortic strips contracted to a stable level by pyrogallol and adrenaline. Experiments carried out with COMT from homogenates of rat liver showed that, in contrast to pyrogallol (10(-5) M), ketamine (10(-3) M) did not inhibit the enzyme. Other experiments with rabbits given 6-hydroxydopamine showed that aortas of these rabbits responded in a similar manner to controls when treated with ketamine and catecholamines. Results obtained with aortas contracted by adrenaline and noradrenaline with ketamine present, followed by oil immersion, showed that ketamine prolonged greatly the relaxation induced by adrenaline and to a lesser extent the relaxation induced by noradrenaline. The results of these studies indicate that ketamine prevented catecholamines from reaching the intracellular site of COMT. In this respect, ketamine can be termed an inhibitor of uptake site 2. If this hypothesis is valid then the action of ketamine on vascular tissue might explain the cardiovascular effects of the drug in man and experimental animals.
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PMID:The actions of ketamine on vascular smooth muscle. 95 82


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