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)

Cardiopulmonary arrest in childhood is usually due to respiratory failure leading to hypoxemia, acidosis, cardiac dysfunction, and terminal asystole. Respiratory failure is the end result of either impaired oxygenation, impaired ventilation, or both. We report a case of severe fecal impaction in an eight year old that resulted in a significant depression of ventilation by severely restricting respiratory mechanics and that ultimately progressed to respiratory failure and circulatory compromise. Physicians should be aware of this rare but possible etiology for life-threatening events in children.
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PMID:Fecal impaction: a rare cause of respiratory arrest in childhood. 789 19

Organophosphate insecticides may cause serious poisoning either accidentally or by deliberate ingestion. Toxic symptoms are produced by acetylcholine accumulation at cholinergic receptors. Diagnosis is based on history of exposure or ingestion, symptoms and signs of cholinergic overactivity and a decrease in serum pseudocholinesterase levels. Following diagnosis, grading of disease severity may identify patients with serious poisoning who should receive treatment in intensive care using adequate doses of anticholinergic drugs. Complications, particularly ventricular arrhythmias, central nervous system depression or seizures, and respiratory failure, should be anticipated and treated. Relapse may occur after seemingly successful treatment. Public education with regard to symptoms of toxicity must be encouraged, and physicians must provide skilled treatment for a potentially lethal condition.
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PMID:Organophosphate and carbamate poisoning. 801 98

Thirty-eight patients with chronic respiratory failure, including 28 patients receiving HOT, were studied from the psychosomatic viewpoint. Assessment of psychological state was based on the following 5 psychometrical tests; Cornell Medical Index (CMI), Self Rating Questionnaire for Depression (SRQ-D), State Trait Anxiety Inventory (STAI), Minnesota Multiphasic Personality Inventory Alexithymia Scale (MMPI-Alexithmia scale) and egogram Check List (ECL). Tweleve HOT patients were also interviewed individually over a three-year period. The ECL showed overadaptation of non-HOT female patients, as compared with their HOT counterparts. There was an inverse correlation between PaO2 (room air) and the SRQ-D score. A significant correlation was also found between age and the SRQ-D score in both HOT and non-HOT patients. HOT patients were observed for 3 years (1-4 years after HOT introduction). Depressive state was observed in 16.6-36.4% of the patients throughout this observation period. Alexithymia was noted in 25.0% only 1 year after the initiation of HOT. However, the average scores for SRQ-D, STA-I and the MMPI-Alexithymia scale remained unchanged for 3 years. PaCO2 (room air, O2, inhalation) was significantly related to the STAI-1 score up to 2 years after starting HOT. Furthermore, a significant correlation was seen between HOT duration and MMPI-Alexithymia scales in HOT patients. Blood gas analysis parameters (delta PaO2, PaCO2 and pH) correlated significantly with respiratory scores on CMI somatic profiles. These results suggest that blood gas status (PaO2, PaCO2) may have an effect on the psychological states of patients early in the course of HOT. However, social factors, such as familial or economical problems, seem to have a greater influence in later stages. Thus, more attention must be given to psychosomatic treatment in the care of HOT patients.
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PMID:[Psychosomatic aspects of chronic respiratory failure managed with home oxygen therapy (HOT)]. 804 Oct 35

The current study was undertaken to evaluate the effects of cholinomimetic drugs on cocaine-induced central cardiorespiratory depression. Cats anesthetized by urethane (2.0 g/kg) were subjected to topical application at the caudal ventrolateral medullary surface (cVMS) of cocaine and two cholinomimetic pretreatment drugs. The following drug regimens were tested: 37 mM cocaine 1) given alone; 2) given 5 min after 2.7 mM carbachol pretreatment; and 3) given 5 min after 3.6 mM physostigmine pretreatment. In 7 of 11 cats, pretreatment with physostigmine decreased the incidence of cocaine-induced apneusis and hypoventilation significantly (p < 0.05); these animals showed no significant change in the mean arterial blood pressure during the 5-min pretreatment before administration of cocaine. In 4 of 11 cats, the physostigmine pretreatment produced a significant decrease in mean arterial blood pressure followed by lethal cardiorespiratory arrest when cocaine was administered. Pretreatment with carbachol resulted in cardiorespiratory responses which were not significantly different from those produced by cocaine alone. In anesthetized cats not exhibiting hypotensive responses to physostigmine, pretreatment may ameliorate cocaine-induced respiratory failure by ventral brainstem control mechanisms.
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PMID:Effects of cholinomimetics on cocaine-induced hypotension and apneusis at a ventral brainstem cardiorespiratory control site. 819 26

The mechanism of death following exposure to anticholinesterases, such as the highly toxic nerve agents soman and VX, and other organophosphate anticholinesterases such as the insecticide parathion, remains unclear, although evidence from nerve agent research suggests that death occurs by an atropine blockable respiratory failure mediated through mechanisms involving the central nervous system. It is proposed that REM sleep pathways, which can be triggered by acetylcholine accumulation in the pontomedullar reticular field, mediate respiratory failure through the inhibition of respiratory muscles. Cholinergic activation of REM sleep activities may also account for other physiological and behavioural effects that follow exposure to nerve agents. These include forebrain activation, which is associated with EEG desynchronization and seizures, locomotor depression with concomitant loss of righting reflex, and limb jerks and extensions. Pharmacologic evidence for atropine and clonidine protection against soman intoxication effects is entirely consistent with a scenario of cholinergic receptor activation in the pontomedullar reticular field.
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PMID:REM sleep pathways and anticholinesterase intoxication: a mechanism for nerve agent-induced, central respiratory failure. 823 94

Effects of saxitoxin (STX; 10 micrograms/kg; i.p.) on cardio-respiratory activities were evaluated in urethane-anesthetized guinea-pigs. Concurrent recordings were made of electrocorticogram (ECoG), bulbar respiratory-related unit activities, diaphragmatic electromyogram (DEMG), electrocardiogram (Lead II ECG), blood pressure, heart rate, end-tidal CO2, arterial O2/CO2 tensions, and arterial pH. The average time to STX-induced respiratory failure was about 10 min. The most striking effect prior to apnea was a state of progressive bradypnea which emerged 5-7 min after the toxin administration. Other noteworthy responses included (i) a time-dependent decrease in ECoG amplitudes which typically began before the development of a bradypneic profile; (ii) an increasing degree of diaphragm neuromuscular blockade; (iii) a state of combined hypercapnia and uncompensated acidemia; (iv) a declining blood pressure; (v) an incrementally dysfunctional myocardial performance; and (vi) an increasingly degenerative central respiratory activity profile which ultimately culminated in a complete loss of central respiratory drive. The therapeutic effect of intratracheally administered oxygen was equivocal in that the cardio-respiratory activities, be they of central of peripheral nature, remained conspicuously dysfunctional and precarious despite 100% oxygen ventilation. What can be inferred from this study is two-fold. First, STX-induced ventilatory insufficiency can be attributed to a loss of functional integrity of both central and peripheral respiratory system components. That is, although diaphragm blockade contributes significantly to STX-induced respiratory failure, analyses of single respiratory unit activity data revealed that the central respiratory rhythmogenic mechanism also appeared to play a pivotal role in the development of a bradypneic profile which promotes, and directly causes, a complete loss of respiratory drive. Second, a state of unabating depression of central respiratory activities, which seemed to be refractory to the effect of O2, suggests STX has a direct and persistent action on medullary rhythmogenic mechanisms. In conclusion, these findings indicate that both central and peripheral cardio-respiratory components are critically involved in STX-induced apnea, dysfunctional cardiovascular performance, and lethality.
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PMID:Central and peripheral cardio-respiratory effects of saxitoxin (STX) in urethane-anesthetized guinea-pigs. 833 95

Psychiatric disorders occur frequently in patients with COPD, but therapy with psychotropic drugs is often limited by concomitant depression of ventilatory drive. We present a patient with COPD and major depression who developed hypercapnic respiratory failure while receiving nortriptyline and oxazepam. Because of known respiratory depressant effects of the latter drug, nortriptyline alone was resumed upon recovery. Depression of CO2 sensitivity and ventilatory load compensation with a concomitant increase in exercise tolerance with decreased dyspnea was observed while she was receiving nortriptyline. These results demonstrate a previously unreported depressant effect of nortriptyline on ventilatory control, and they suggest the need for further investigation of the ventilatory effects of this drug in patients with pulmonary disease.
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PMID:Nortriptyline-induced depression of ventilatory control in a patient with chronic obstructive pulmonary disease. 848 48

Meconium aspiration syndrome (MAS) is found in 0.2-6 per 1000 lifeborn neonates. Aspiration of meconium particles may occur before, during or after delivery, associated with deep inspiratory movements due to fetal depression. Aspiration of meconium may cause mechanical obstruction of the airways, chemical pneumonitis, and surfactant inactivation. The disease is commonly associated with the development of pulmonary hypertension and severe respiratory insufficiency. MAS may be prevented, at least in some infants, by appropriate suctioning at birth. Great progress has been made in the treatment: early administration of surfactant improves gas exchange in many neonates. High frequency oscillatory ventilation, NO-inhalation and extracorporal membrane oxygenation have a role in severe respiratory failure.
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PMID:[Meconium aspiration syndrome]. 899 48

A case of Hodgkin's disease (HD), lymphocyte depression (LD) type in an immunosuppressive patient is described. The patient was a 48-year-old male and his parents were born in the Kyushu area, which is an endemic area for adult T cell lymphoma/leukemia (ATL). He was seropositive for ATL virus (ATLV, also referred to as HTLV-I) and showed a marked immunosuppressive condition. He developed LD-HD and Pneumocystis carinii pneumonia, and died due to respiratory failure. The immunohistochemical and in situ hybridization analyses revealed that the Reed-Sternberg-like cells in the lymph node biopsy sample were positive for Ber-H2 (CD30), Leu-M1 (CD15), L-26 (CD20), Bcl-2, p53 and EBER, the viral genome of Epstein-Barr virus (EBV).
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PMID:Epstein-Barr virus-related Hodgkin's disease showing B cell lineage in an immunosuppressive patient seropositive for HTLV-I. 941 42

Transgenic/knockout mice with pre-defined mutations have become increasingly popular in biomedical research as models of human diseases. In some instances, the resulting mutation may cause cardiorespiratory distress in the neonatal or adult animals and may necessitate resuscitation. Here we describe the design and testing of a miniature and versatile ventilator that can deliver varying ventilatory support modes, including conventional mechanical ventilation and high-frequency ventilation, to animals as small as the newborn mouse. With a double-piston body chamber design, the device circumvents the problem of air leakage and obviates the need for invasive procedures such as endotracheal intubation, which are particularly important in ventilating small animals. Preliminary tests on newborn mice as early as postnatal day O demonstrated satisfactory restoration of pulmonary ventilation and the prevention of respiratory failure in mutant mice that are prone to respiratory depression. This device may prove useful in the postnatal management of transgenic/knockout mice with genetically inflicted respiratory disorders.
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PMID:A miniature mechanical ventilator for newborn mice. 947 87


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