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)

A new thin-film, multisensor probe was used to determine tissue oxygen tension, tissue temperature, and electrical activity at two depths below the brain surface in chloral hydrate- or nitrous oxide/halothane-anesthetized rats. Brain tissue temperature at both depths was found to be lower than core temperature by 1-2 degrees C. Electrical activation, spreading depression, and pentylenetetrazol seizures all resulted in transient increases of brain tissue temperature of a few tenths degree centigrade. Vasodilation, induced by hypercapnia or hypoxia, caused a warming of brain tissue. Near-maximum oxygen metabolism, reached upon reoxygenation after severe hypoxia, was accompanied by tissue temperature rises of greater than 1 degree C. It was concluded that brain tissue temperature in the anesthetized rat is lower than core temperature due to extensive radiative and conductive heat loss to the environment through the head. Transient increases in tissue temperature during activation are caused by vasodilation and increased metabolism.
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PMID:Stimulus-activated changes in brain tissue temperature in the anesthetized rat. 260 41

Hypoxia in fetal sheep depresses respiratory activity. To determine if this effect is counterbalanced by hypercarbia we studied the effects of two levels of asphyxia produced by occlusions of the maternal uterine artery. Moderate asphyxia (PaO2 16.8 +/- 1.6 (SEM) PaCO2 48.9 +/- 1.0 torr) produced no changes in the percent time fetal breathing movements occupied each hour which ranged from 25.6 +/- 7.0 to 32.4 +/- 6.2%. However, a more marked asphyxia (PaO2 12.0 +/- 0.3, PaO2 57.0 +/- 1.6) resulted in a decrease in fetal respiratory activity to 8.7 +/- 3.7% during the first hour. This depression was sustained over the next 2 h but by the 5th hour breathing had returned to 26.2 +/- 7.3%. We concluded that hypercarbia can offset the respiratory inhibition of acute moderate hypoxia, but not that of a more marked lowering of PaO2 in fetal sheep. Severe asphyxia causes an initial inhibition of respiration which is followed by a return to normal respiratory activity.
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PMID:Effect of asphyxia on respiratory activity in fetal sheep. 262 16

Many of the drugs used in anesthesia and intensive care may cause blockade of the central cholinergic neurotransmission. Acetylcholine is of significance in modulation of the interaction among most other central transmitters. The clinical picture of the central cholinergic blockade, known as the central anticholinergic syndrome (CAS), is identical with the central symptoms of atropine intoxication. This behaviour consists of agitation including seizures, restlessness, hallucinations, disorientation or signs of depression such as stupor, coma and respiratory depression. Such disturbances may be induced by opiates, benzodiazepines, phenothiazines, butyrophenones, ketamine, etomidate, propofol, nitrous oxide, and halogenated inhalation anesthetics as well as by H2-blocking agents such as cimetidine. There is an individual predisposition for CAS--but unpredictable from laboratory findings or other signs. Reports of postanesthetic occurrence of the CAS requiring treatment are not unanimous, varying between 1 and 40%. Differential diagnosis of the CAS includes disorders of glucose and electrolyte metabolism, severe hormonal imbalance, respiratory disorders (hypoxia, hypercarbia), hypothermia, hyperthermia and neuropsychiatric diseases (cerebral hypoxia, stroke, catatony, acute psychosis). The CAS may considerably impair the postanesthetic period especially when agitation is prevalent, which may endanger the patient or the surgical results. The diagnosis is confirmed ex iuvantibus by the sudden increase in the acetylcholine level in the brain. This is achieved with physostigmine, a cholinesterase inhibitor able to easily cross the blood-brain barrier. Its peripheral muscarinic effects are minimal. Postanesthetic CAS can be prevented by administration of physostigmine during the anesthesia procedure. During intensive care (IC), agitated forms of CAS may occur in patients undergoing mechanical ventilation, particularly during prolonged high-dose sedation. Artificial ventilation of such patients becomes very difficult and muscle relaxation may be necessary. In these cases of IC-CAS, physostigmine is of value and has proven beneficial during weaning from mechanical ventilation. Dealing with the CAS for more than a decade has improved knowledge of the central cholinergic transmission. For example, it can be said that CAS occurs alongside general anesthesia, being no more than a frequent side-effect. Furthermore, acetylcholine is involved in nociception through the endorphinergic and the serotoninergic systems. There is a close relation between the central cholinergic transmission and actions of nitrous oxide. Moreover, cholinergic transmission is involved in withdrawal from (among others) alcohol, opiates, hallucinogens and nitrous oxide. In some intoxications with psychoactive agents, physostigmine is useful for reversal of the central nervous symptoms of the acute intoxication itself. In addition it can be used for prevention of some withdrawal states. In
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PMID:Central anticholinergic syndrome (CAS) in anesthesia and intensive care. 268 49

The syndrome of obstructive sleep apnoea is associated with an increased morbidity (the consequence of diurnal hypersomnolence and cardiovascular complications). The contraction of the dilator muscles of the upper airways (nose and pharynx) allows their patency at the time of inspiration. The obstruction of the airways resulted in a disequilibrium between the forces which tend to their collapse (negative inspiratory transpharyngeal pressure gradient) and those which contribute to their opening (muscle contraction). The mechanisms which underlie the triggering of obstructive apnoea are multiple including a reduction in the calibre of the superior airways, an increase in their compliance, and a reduction in the activity of the muscle dilators. This latter is intimately linked to the respiratory muscles and these muscles respond in a similar manner to a stimulation or a depression of the respiratory centre. The ventilatory fluctuations observed during sleep (alternately hyper and hypo ventilation of periodic respiration) thus favours an instability of the superior airways and the occurrence of oropharyngeal obstruction. The depth of post-apnoeic desaturation depends on the value of the arterial oxygen saturation at the beginning of apnoea, the duration of the period of apnoea and the pulmonary volume as the period of apnoea passes off. The cardiovascular consequences of apnoea include disorders of rhythm (bradycardia, auriculoventricular block, ventricular extrasystoles) and haemodynamic (pulmonary and systemic hypertension). This results in a stimulatory metabolic and mechanical effect on the autonomic nervous system. The electroencephalographic awakening which precedes the easing of obstruction of the upper airways is responsible for the fragmentation of sleep. The factors implicated in the cessation of the apnoea include hypoxia and hypercapnia but one also invokes a role for the negative pressure generated during the course of the apnoea.
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PMID:[Physiopathology of obstructive sleep apneas]. 269 Feb 8

Patients with IPD often develop oxygen desaturation during sleep. We investigated whether or not the degree of falls in SaO2 during sleep were correlated with the daytime data of pulmonary function tests, arterial blood gas tensions, or ventilatory responses to chemical stimuli. Fourteen patients with IPD who had restrictive ventilatory impairment were studied to evaluate these relationships. The magnitude of SaO2 depression from awake to REM sleep was inversely correlated with the level of baseline SaO2. Hypercapnic ventilatory response was inversely related to the amount of maximal desaturation in both REM and NREM sleep. These results indicate that patients with IPD who have insufficient ventilatory response to hypercapnia reveal larger falls in SaO2 during sleep, particularly if they have lower baseline SaO2.
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PMID:Arterial oxygen desaturation during sleep in interstitial pulmonary disease. Correlation with chemical control of breathing during wakefulness. 270 87

We examined mitochondrial oxidative function 5 minutes and 2 hours after a gradual asphyxial insult in newborn lambs. We subjected 16 ventilated newborn lambs to 75-90 minutes of hypoxia and hypercarbia that resulted in bradycardia and systemic hypotension over the final 15 minutes of the insult. At the end of asphyxia, the lambs were resuscitated and returned to control ventilator settings. Samples of brain were removed 5 minutes (n = 8) and 2 hours (n = 8) after asphyxia. Each group of eight lambs was subdivided into those less than 3 or greater than 3 days old to evaluate the effect of age on postasphyxia mitochondrial function. After classification into nonsynaptic and synaptic mitochondria, mitochondrial respiration (oxygen consumption) was measured using five different substrates. Data from asphyxiated lambs were compared with that from a control group of ventilated nonasphyxiated lambs (n = 8). In the lambs less than 3 days old, there was significant depression of mean +/- SEM nonsynaptic mitochondrial state 3 (adenosine diphosphate-dependent) respiration to 29.5 +/- 5.2% of control with four of the five substrates and of state 4 respiration to 33.7 +/- 0.9% of control with three of the five substrates 5 minutes after asphyxia. By 2 hours after asphyxia, mean +/- SEM nonsynaptic mitochondria state 3 respiration increased to 70.4 +/- 6.4% of control while state 4 respiration increased to 58.2 +/- 4.5% of control. In contrast, lambs greater than 3 days old exhibited no inhibition of nonsynaptic mitochondrial function after asphyxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mitochondrial function after asphyxia in newborn lambs. 271 9

The mechanisms underlying the apnea associated with both hypoxia and high-voltage electrocortical activity (HV ECOG) in the fetal lamb are not clearly understood. We have previously shown that lesions in the rostral lateral pons change the depressive response to hypoxia to one of stimulation. We now present evidence that lesions in this area also affect the fetal response to H+/CO2. Lactic acidemia and 5-6% hypercapnia both caused almost continuous breathing throughout both HV and low-voltage (LV) ECOG in seven of eight fetuses with lesions that reversed the depressive response to hypoxia. In five intact control fetuses and seven fetuses with lesions that did not affect the response to hypoxia, neither CO2 nor lactic acidemia induced continuous breathing. We conclude that the lateral pontine area, which is involved in the hypoxic depression of breathing in the fetus, is also involved in the inhibitory mechanisms operating during HV ECOG. Furthermore the inhibition of breathing during HV ECOG appears to be related to a raised threshold for fetal breathing, which is sensitive to H+/CO2.
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PMID:Lateral pontine lesions affect central chemosensitivity in unanesthetized fetal lambs. 279 3

The effects of selective opioid receptor agonists and antagonists on neural discharge recorded from carotid body arterial chemoreceptors in vivo were studied in anaesthetized cats. Mean ID50 values were determined for each agonist and used to assess chemodepressant potency on intracarotid (i.c.) injection in animals artificially ventilated with air. [Met]enkephalin, [Leu]enkephalin, [D-Ala2, D-Leu5]enkephalin and [D-Pen2, D-Pen5]enkephalin were more potent chemodepressants than [D-Ala2, Me-Phe4, Gly-ol5]enkephalin, dynorphin (1-8) or ethylketocyclazocine; morphiceptin (mu-agonist) was inactive. The rank order of potency was compatible with the involvement of delta-opioid receptors in opioid-induced depression of chemosensory discharge. ICI 154129, a delta-opioid receptor antagonist, was used in fairly high doses and caused reversible dose-related antagonism of chemodepression induced by [Met]enkephalin. It also antagonized depression caused by single doses of [Leu]enkephalin, [D-Ala2, D-Leu5]enkephalin, [D-Ala2, Me-Phe4, Gly-ol5]enkephalin or dynorphin (1-8). ICI 174864, a more potent and selective delta-opioid receptor antagonist, also antagonized chemodepression induced by [Met]enkephalin or by the selective delta-receptor agonist [D-Pen2, D-Pen5]enkephalin. Comparison of background or 'spontaneous' chemosensory discharge during the 30 min periods immediately before and after injecting ICI 174864 (0.1-0.2 mg kg-1 i.c.) showed a significant increase in discharge in one experiment, but in four others discharge was either unaffected or decreased after the antagonist, which argues against a toxic depression of chemosensors by endogenous opioids under resting conditions in our preparation. Sensitivity of the carotid chemoreceptors to hypoxia (ventilating with 10% O2) was increased significantly after ICI 174864, which could be taken as evidence that endogenous opioids depress chemosensitivity during hypoxia. In contrast, responsiveness to hypercapnia was reduced after the antagonist, implying that endogenous opioids may potentiate chemoreceptor sensitivity during hypercapnia. The results obtained using 'selective' agonists and antagonists provide evidence that depression of chemosensory discharge caused by injected opioids involves a delta type of opioid receptor within the cat carotid body. Endogenous opioids may modulate arterial chemoreceptor sensitivity to physiological stimuli such as hypoxia and hypercapnia.
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PMID:Characterization of opioid receptors in the cat carotid body involved in chemosensory depression in vivo. 287 62

Local anaesthetic systemic toxicity is a rare but often dramatic complication of regional anaesthesia. Convulsions often follow warning signs, easily recognized when looked for; but they may occur from the first. They are rapidly followed by hypoxia and hypercapnia which greatly enhance the risk of severe cardiac depression, mainly with bupivacaine or etidocaine. Thiopentone is able to stop convulsions quickly, but may further depress the cardiovascular system. Diazepam has been shown to be effective in the treatment of local anaesthetic-induced convulsions. It gives less myocardial depression, but is much slower in effect. Midazolam, a new short-acting benzodiazepine, should be the best choice. Should tracheal intubation become necessary, suxamethonium can be used. Indeed, the principal use of these drugs is to make ventilation easier, so as to restore rapidly correct oxygenation. Severe cardiac depression, often leading to cardiac arrest, may occur from the first or after the appearance of convulsions. It generally follows a regional block carried out with bupivacaine. A few antiarrhythmic drugs have been used to treat ventricular arrhythmias, either in experimental studies (lidocaine, bretylium) or after clinical accidents (lidocaine). Their efficacy and innocuity have to be proved before they can be proposed to treat these accidents. Bradycardia only needs treatment with atropine when it causes severe haemodynamic disturbances. When cardiac arrest occurs, cardiopulmonary resuscitation must be carried out; its mainstays are: oxygen, sodium bicarbonate, adrenaline, calcium and perhaps glucagon. This must be continued for a long time, as late successes have been published.
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PMID:[How should a toxic accident be treated?]. 290 Jun 15

In pentobarbitalized rats, hypoxia induced by inhalation of O2 8%-N2 92%, produces a transient hyperventilation which is followed by a respiratory depression and an apnea. A cardiovascular collapse is then observed. Correction of the hypocapnia depending on the initial hyperventilation, by inhalation of a gas mixture containing 4% CO2 maintains the hyperventilation and suppresses the cardiovascular collapse. Carbon dioxide activity is both a direct one by stimulation of respiratory centers and an indirect one by increasing the sensitivity of the peripheral arterial chemoreceptors to hypoxia. Four percent carbon dioxide just compensating hypocapnia are sufficient to prevent apnea and vascular collapse. The increase of this concentration up to hypercapnia complicates the interpretation of the results by addition of hypoxic and hypercapnic effects.
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PMID:[Effects of the addition of carbon dioxide on manifestations of acute hypoxia in rats]. 297 Feb 83


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