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

The effect on arterial pressure, EEG, preganglionic sympathetic nervous activity and pulse rate of repeated intravenous administrations of lidocaine (3 mg/kg) was investigated in cats anaesthetized with nitrous oxide. A continuous high voltage, burst-suppression EEG indicating constant seizure activity was found, whereas arterial pressure and sympathetic nervous activity did not change significantly. Although the onset of EEG seizure activity did not change the mean sympathetic activity level, the pattern of firing changed dramatically as every EEG seizure triggered a burst of sympathetic impulses. Barostatic reflexes were active after lidocaine administration unless seizure activity occurred. Thiopental 5 mg/kg given intravenously to cats during continuous lidocaine-induced EEG seizures always abolished the seizure activity without excessive depression of arterial pressure.
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PMID:Sympathetic nervous system response to lidocaine induced seizures in cats. 69 18

The purpose of the study was to compare the actions of propofol and thiopental on myocardial contractility and cellular electrophysiologic behavior. Isometric tension of isolated guinea pig right ventricular papillary muscle was studied in normal and 26 mM potassium Tyrode's solutions at various stimulation rates (after rest up to 3 Hz). Normal and slow action potentials were also recorded by conventional microelectrodes. Propofol (30, 100, and 300 microM) applied in the commercial 10% Intralipid emulsion caused dose-dependent depression of contractions at all stimulation rates, whereas Intralipid alone had no effect. Thiopental (10, 30, and 100 microM) caused depression similar to the threefold greater concentrations of propofol. Although neither drug altered the normal action potential (AP) amplitude or dV/dt max, thiopental (30 microM) increased AP duration. In the partially depolarized (26 mM potassium) beta-adrenergically stimulated myocardium, propofol and thiopental caused dose-dependent contractile depression similar to that in normal Tyrode's solution. Whereas propofol did not alter slow AP characteristics, 30-100 microM thiopental increased slow AP duration (consistent with decreased potassium conductance), and 100 microM thiopental depressed dV/dt max (consistent with decreased calcium channel ionic influx). Comparing the clinical plasma concentration ranges required for an equivalent anesthetic effect, propofol depresses myocardial contractility less than thiopental.
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PMID:Propofol and thiopental depression of myocardial contractility. A comparative study of mechanical and electrophysiologic effects in isolated guinea pig ventricular muscle. 153 21

The effects of antihypertensive drugs, such as nifedipine, chlorpromazine, reserpine and thiopental on mean arterial blood pressure (ABP), mean intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were studied in 43 patients with systemic hypertension and intracranial hypertension due to hemorrhagic cerebrovascular diseases and other causes. These drugs are commonly used in neurosurgical practice for the treatment of systemic hypertension. Nifedipine, chlorpromazine and reserpine reduced the mean ABP, raised the mean ICP and decreased the CPP. The effects of these drugs on mean ICP and CPP were more pronounced in patients with severely increased ICP (more than 40 mmHg) than in patients with moderately increased ICP (20-40 mmHg). Thiopental reduced both mean ABP and ICP, whereas the CPP was unchanged from the preadministration level. During thiopental administration, however, respiratory depression was observed, and hence, intubation and ventilation were required. We suggest that, in the treatment of systemic hypertension in patients with increased ICP, barbiturates are more desirable than agents with calcium channel or alpha-adrenergic blocking actions, despite the problem of respiratory control.
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PMID:Effects of antihypertensive drugs on intracranial hypertension. 195 Feb 24

We have developed a chronically instrumented rat model that uses changes in electroencephalographic wave forms to estimate continuously the degree of central nervous system (CNS) depression induced by thiopental. Such changes were subject to aperiodic signal analysis, a technique that breaks down the complex EEG into a series of discreet neurologic "events" which are then quantitated as waves/sec. We thus obtained a continuous measure of CNS drug effect. In addition we continuously recorded central arterial blood pressure and heart rate and monitored ventilatory status using arterial blood gas determinations. We also determined, with frequent arterial blood sampling, the distribution and elimination of thiopental in individual animals. The time lag occurring in the curve representing arterial concentration of thiopental vs. EEG effect suggests that arterial plasma is not kinetically equivalent to the EEG effect site. Application of semiparametric pharmacodynamic modeling techniques enabled us to estimate equilibration rate constant (Keo) for concentrations of thiopental between arterial plasma and the effect site. The half-life for equilibration of thiopental with the EEG (CNS) effect was less than 80 sec. Knowledge of the rate of equilibration permitted characterization of the relationship between the steady state plasma concentrations and CNS effect of thiopental, as measured by activation and slowing of the EEG. At concentrations of thiopental below 5 micrograms/ml, EEG activity was 180% higher than during the baseline awake state. Thiopental produced an activated EEG over more than 20% of the concentration-effect relationship. Further increases in the concentration of thiopental at the site of effect depressed EEG activity progressively until complete suppression of the EEG signal occurred (at which time, the concentration was approximately 80 micrograms/ml). This report describes our model and its application to the assessment of the pharmacodynamics of thiopental as manifested by changes on the EEG.
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PMID:Pharmacodynamic characterization of the electroencephalographic effects of thiopental in rats. 201 36

The effects of halothane and thiopental on the respiratory efferent activities in the phrenic, recurrent laryngeal and hypoglossal nerves were studied in decerebrate, paralyzed and artificially ventilated cats. Inhalation of halothane (2%, 90 s) and intravenous injection of thiopental (2-3 mg/kg) produced a similar change in the breathing pattern, characterized by an increase in respiratory frequency and a decrease in the respiratory burst discharge in the three nerves studied. Depression of the respiratory activity was greatest in the hypoglossal nerve, intermediate in the recurrent laryngeal nerve, and least in the phrenic nerve. Both drugs diminished the whole power spectral densities of the three nerves. Thiopental selectively attenuated the high frequency peaks of these spectra and shifted the peak frequencies to lower values. Bilateral section of the vagus and carotid sinus nerves had no effect on the action of thiopental on the respiratory neural activities, whereas it decreased, but did not eliminate, the action of halothane. The present results demonstrate that both halothane and thiopental produce a selective depression of the upper airway motor activities, with stronger effects on the hypoglossal nerve. Effects on the peripheral receptors and the central respiratory drives differ between the two drugs.
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PMID:The influence of halothane and thiopental on respiratory-related nerve activities in decerebrate cats. 251 28

The depressing effect of GABA on excitation of nerve cells as well as the action of bicuculline, penicillin and thiopental on this process were examined on CA1 pyramidal neurons using rat hippocampal slices. It was found that GABA effectively and reversibly reduced the amplitude of antidromic population spike both in the region of somata and dendrites. The sensitivity of apical dendrites to GABA was greater by one order than that of somata, increasing along dendrites from their proximal to distal parts. The somata of pyramidal neurons showed strong desensitization to GABA. In distal parts of dendrites desensitization to GABA was absent. Bicuculline and penicillin antagonized the action of GABA at all investigated levels of CA1 pyramidal cells. Bicuculline blocked the effect of GABA on the somata and dendrites approximately equally. The antagonistic action of penicillin was 10 times larger in the pyramidal layer than in the region of dendrites. Thiopental intensified the depression produced by GABA. Potentiating effect of thiopental was stronger in dendrites. It is concluded that the membrane of CA1 pyramidal neurons has two types of bicuculline-sensitive GABA-receptors differing in their location (mainly on the soma or dendrites), in pharmacology and in ability to be desensitized by GABA.
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PMID:[Sensitivity to GABA of the soma and dendrites of pyramidal cells in isolated sections of hippocampus in the rat]. 300 93

A 5 years old girl with status epilepticus refractory to treatment with Diphenylhydantoin at a dose of 30 mg/kg/day and Thiopental in continuous IV perfusion at a dose of 4 mg/kg/h is presented. Control of status was achieved by continuous IV perfusion of Chlormethiazole at a dose of 10 mg/kg/h which also caused respiratory depression. Seizure activity reappeared after IV perfusion of Chlormethiazole was retired, and could be controlled only with Sodium Valproate. Mechanisms of action of Chlormethiazole and its effectiveness in treatment of refractory status epilepticus are revised.
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PMID:[Treatment of refractory status convulsivus with chlormethiazole]. 314 89

The effect of three modes of anesthesia was evaluated with regard to regional damage to central cyclic nucleotide systems in the gerbil brain as a consequence of bilateral ischemia (clamping the common carotids) followed by various periods of recirculation. The injection of thiopental as much as 90 min before stroke prevented damage to chemical activation [catecholamines, guanosine triphosphate (GTP), or forskolin] of adenylate cyclase. However, the basal enzyme activity was lower in all brain regions whether thiopental was administered to stroke or sham-operated animals. Injection of ketamine drastically shortened the survival times of gerbils undergoing stroke followed by recirculation. About 90% of the animals could tolerate a maximum of only 15 min stroke with 15 min recirculation. At this time frame the patterns of activation of adenylate cyclase in only the olfactory tubercle and hippocampus were altered. When procaine was used as a local anesthetic agent during surgery, damage to catecholamine-, GTP-, or forskolin-activated adenylate cyclase was evident to varying degrees in the frontal cortex, hippocampus or olfactory tubercle, but not in the nucleus accumbens and olfactory bulb of gerbils subjected to 60-min stroke followed by 15 or 150 min of recirculation. The degree of enzyme damage was neither correlated with the fed vs. fasted state of the animal nor with the whole blood concentration of glucose. A depression in the amplitude of visually evoked potentials correlated to neurological signs and to enzyme damage. During anesthesia, ketamine increased steady-state concentrations of cyclic AMP in the frontal cortex and hippocampus from gerbil brains that had been rapidly inactivated by microwave irradiation. Thiopental increased steady-state cyclic AMP in only the olfactory tubercle. Cyclic GMP concentrations were unchanged by any anesthetic agent. In animals completely recovering from anesthesia and occluded for a brief period followed by 10 min of reflow, steady-state concentrations of only cyclic AMP were augmented.
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PMID:Regional cyclic AMP systems during secondary ischemia in gerbils: influence of anesthetic agents. 632 54

In rats pretreated with phenobarbital breathing 10% oxygen, subanesthetic doses of halothane, isoflurane, enflurane, thiopental, and fentanyl caused hepatic injury. Because hypoxia per se can produce such injury, we hypothesized that the anesthetic-induced injury resulted from increased hypoxemia secondary to respiratory depression. Male Sprague-Dawley rats were pretreated with phenobarbital; half of the rats were fed and the other half were deprived of food for the 24 h before study. Isoflurane anesthesia was given for the placement of a catheter into the femoral artery. After 1 h of recovery, the rats were exposed to 10% oxygen. Control samples were obtained and halothane, isoflurane, enflurane, thiopental, or fentanyl was administered. Rats given food had higher PaCO2 and lower pH values than starved rats. Also, arterial oxygen saturation (SaO2) tended to be lower in rats given food. At concentrations of 0.15-0.2 MAC or higher, halothane, isoflurane, and enflurane slightly increased PaCO2 values relative to values for a control group exposed only to hypoxia. However, SaO2 and PaO2 did not show significant drug-induced changes. Fentanyl transiently decreased PaO2 and SaO2. Thiopental caused no changes. Thus, we conclude that subanesthetic doses of anesthetics may depress the ventilatory response to hypoxia but that this depression is inconsistent and appears to be too small to cause hepatic damage.
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PMID:Effects of halothane, isoflurane, enflurane, thiopental, and fentanyl on blood gas values in rats exposed to hypoxia. 640 54

The cardiopulmonary effects and tendencies to produce ventricular arrhythmias were evaluated in 13 dogs given a surgical plane of anesthesia by thiopental (IV) or a combination of thiopental and lidocaine (IV). Thiopental (22 mg/kg of body weight) was compared with a combination of thiopental (11 mg/kg) and lidocaine (8.8 mg/kg). Preanesthetic agents were not given. Both methods for IV anesthesia provided a smooth induction suitable for easy intubation. The thiopental/lidocaine combination had a shorter duration, produced no arrhythmias, and resulted in less cardiopulmonary depression than did thiopental alone. Bigeminy developed after intubation during 19 of 20 thiopental inductions as compared with that in 0 of 22 thiopental/lidocaine inductions. The bigeminies were preceded by systemic hypertension and tachycardia which developed as the trachea was being intubated. The increase in aortic pressure and heart rate was minimal after intubation during the thiopental/lidocaine inductions. Five minutes after administration of thiopental alone, increases in heart rate, aortic pressure, total peripheral vascular resistance, and left ventricular systolic and end-diastolic pressures were observed. When these increases in rate, preload, and afterload were considered in relation to a stabile maximum positive first derivative of left ventricular pressure, left ventricular contractility was considered to be decreased. Mild respiratory acidosis and hypoxemia were present at 5 and 10 minutes after thiopental induction. Because the combination of thiopental/lidocaine had less cardiopulmonary depressive effects and protected against arrhythmias, it would appear to be a good method for anesthetic induction of the patient with cardiopulmonary disease. In the patient with normal cardiopulmonary function, thiopental produces only a moderate and reversible depression.
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PMID:Cardiopulmonary effects of thiopental/lidocaine combination during anesthetic induction in the dog. 682 18


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