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)

Depression is a well-known reaction to separation in all species of macaques studied except the bonnet (M. radiata), in whom this reaction has never before been observed. We have produced the depressive response of postural collapse and social withdrawal in a bonnet infant by altering the social structure of the group in which it lived in a way calculated to interfere whith the species-typical system of social support.
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PMID:Depression can be induced in a bonnet macaque infant. 41 90

The philtrum point VG 26 (Jen Chung) was needled in 69 cases of respiratory depression or apnoea in dogs and cats during induction or maintenance of general anaesthesia. Respiration was restored to normal or near normal rates within 10 to 30 seconds of insertion of the needle in all the cases. In seven cases of anaesthetic apnoea with concurrent cardiac arrest and absence of vital signs, the revival rate was 43 per cent. Those which recovered required four to 10 minutes of acupuncture stimulation. In eight cases of collapse due to other causes, the revival rate was 25 per cent. The cases included five sheep in shock following liver biopsy, two cases of haemorrhagic shock (dog, cat) and one terminal collapse in chronic congestive heart failure (dog).
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PMID:Respiratory and cardiac arrest under general anaesthesia: treatment by acupuncture of the nasal philtrum. 51 10

Blood loss of sufficient magnitude to over-ride compensatory mechanisms and result in a lowering of arterial pressure will ultimately lead to irreversible circulatory collapse. Identification of the organ or tissues which may trigger a terminal cascade remains controversial. The weight of evidence supports the view that cardiac performance deteriorates with prolonged oligemic hypotension, although this may not be the initiating or sole reason for irreversible failure of the circulation. Controversy regarding the heart as an important target organ is no doubt in part due to the multiplicity of preparations and protocols, and variety of methods used to characterize cardiac function. We have used ventricular function curves to calibrate LV performance in terms of pump function, while arterial pressure remains at a pre-determined level. With this approach, a progressive decline in stroke volume for a given LV end diastolic pressure is consistently observed in hemorrhagic shock (AP, 30 mmHg). If arterial pressure is briefly re-elevated at 30 minute intervals, permanent deterioration is prevented. However, if the hypotension is sustained for 2 hours, LV performance remains depressed following pressure re-elevation. Among the mechanisms responsible for deterioration of performance, coronary perfusion pressure (CPP) exerts a pivotal role. Thus, no LV depression occurs after 2 hours of shock provided CPP is maintained at normotensive levels. But if myocardial O2 availability falls below 10 ml/min/100 gm of heart, both O2 uptake and extraction decline and this is uniformly accompanied by cardiac failure. This likely reflects mitochondrial damage and impaired aerobic metabolism. These changes are potentiated by the appearance of metabolic acidosis and failure of sympathetic neurohumoral activity. Both factors directly reduce myocardial contractility, but assume much greater importance during shock. While E. coli endotoxin has been shown to reduce cardiac performance, the relative importance of bacterial products which may enter the circulation during hemorrhagic shock in uncertain. Reduced O2 availability, metabolic acidosis and adrenergic failure appear the major determinants of diminished cardiac performance and thereby may contribute to irreversible collapse of circulatory function.
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PMID:Cardiac performance in hemorrhagic shock. 55 6

Clinical and roentgenographic findings were compared in patients 40 years of age and over and in those under 40 who were treated for acute unilateral pneumothorax. Dyspnea and anxiety were pominent in the older individuals, although pneumothoraces were usually small. Because physical findings were often unreliable, roentgenograms were required. In the presence of pulmonary emphysema, loss of retractility prevented total collapse of the underlying lung. Increased intrapleural pressure caused over-expansion of the chest wall and the depression of the diaphragm without much mediastinal shifting. Partial collapse of emphysematous lobes demonstrated bullae that were not previously obvious. Respiratory failure developed in five patients over 40 years of age, but four of them recovered after relief of the pneumothorax. Mortality for the group was low and related to associated pulmonary diseases.
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PMID:Pneumothorax complicating pulmonary emphysema. 117 69

We investigated whether or not the adaptation of peripheral chemoreceptor (PCR) activity can contribute to hypoxic ventilatory depression (HVD) during sustained hypoxia for 20 min in both healthy subjects and patients with sleep apnea. Effects of HVD on diaphragm (DIA) and genioglossal muscle (GG) were also assessed. Withdrawal test, which is well established to solely represent the function of PCR, was repeatedly conducted at 5 and 20 min during sustained hypoxic condition. The results suggested that PCR did not play an important role in the development of HVD. When HVD ensued during sustained hypoxia, minute ventilation and EMGDIA were suppressed to the same extent in both groups. On the other hand, EMGGG was strongly and consistently attenuated in OSAS, whereas it was not always the case in healthy subjects. We speculate that treatment for hypoxic conditions can induce improvement of impaired regulation of breathing via central mechanisms, and it can be an important factor reducing the incidence and the severity of upper airway occlusion or collapse.
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PMID:[Hypoxic ventilatory response and hypoxic depression]. 130 12

A 13-week oral repeated dose toxicity study of suplatast tosilate (IPD-1151T), a new anti-allergic agent, as well as a 5-week recovery study were carried out at dose levels of 0 (control), 50, 150, 450 and 1350 mg/kg/day using male and female beagle dogs. The results were as follows: 1. In general conditions, soft feces and diarrhea with specific smell were dose-dependently observed in males and females given 450 mg/kg/day or more. Both sexes given 1350 mg/kg/day, revealed reeling with dropped head, abnormal gait, dysstasia, lying at lateral or prone position, sedation, and tremor, and one male and one female in this group died after showing respiratory depression, collapse and cyanosis. 2. There were no significant or remarkable changes in body weight, food consumption, water consumption, ophthalmology, electrocardiogram, urinalysis, hematology, biochemistry, fecal occult blood test, and absolute and relative organ weights. 3. Pathological examination in dead animals revealed hemorrhagic change in the heart and slight vacuolar changes in hepatocytes. In survived animals, there were no pathological changes attributable to the IPD-1151T. 4. In electron microscopic examination, there were no abnormalities in the liver and kidney attributable to the IPD-1151T. 5. After 5-week recovery period, above-mentioned changes disappeared. 6. From the above results, the non-effective dose level and the toxic dose level were estimated to be 150 mg/kg/day and 1350 mg/kg/day, respectively, and no sex differences were found.
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PMID:[A thirteen-week oral repeated dose toxicity study of suplatast tosilate (IPD-1151T) in dogs]. 132 Dec 64

Local anaesthetics are responsible for 5 to 10% of all reported adverse reactions to anaesthetic drugs. Adverse effects may be classified as: (a) those associated directly with blocking ion channels in cell membranes, such as cardiovascular and CNS toxicity; (b) those due to other effects of drug or vehicle (mainly peripheral nerve complications); (c) allergic reactions (often a mistaken diagnosis); and (d) mechanical or other effects of technique, such as needle trauma or introduction of infection. Signs and symptoms of CNS toxicity include convulsions, followed by coma and respiratory depression. Convulsions are due to disinhibition of nervous conduction, probably by an action at the gamma-aminobutyric acid (GABA) receptor complex, while depressant effects, which predominate at higher doses, are due to blockade of sodium channels. CNS toxicity is potentiated by hypoxia and hypercapnia, so acute management must minimise these. Cardiovascular toxicity also involves sodium channel blockade, reducing contractility and interfering with conduction. Bupivacaine differs from lidocaine (lignocaine) in the sudden occurrence of dangerous ventricular arrhythmias including fibrillation at subconvulsant doses. Ropivacaine is a newer amide local anaesthetic with toxicity intermediate between these but potency similar to bupivacaine. Neurotoxic complications leading to prolonged deficit after intraspinal administration are uncommon. Causes are multifactorial, and include pH of and additives to preparations. Allergic reactions account for only 1% of untoward reactions, but anaphylactoid collapse can be lifeth-reatening and requires rapid and effective management.
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PMID:Adverse effects of local anaesthetics. 150 66

Dried, milled Cestrum laevigatum plant material was drenched to 6 ewes at doses ranging from 2,5 to 10 g/kg/day for 1 to 47 days. The most noticeable clinical signs were depression, anorexia and ruminal stasis. These signs were accompanied by clinical pathological changes indicative of liver involvement such as increases in the serum activities of aspartate transaminase, lactate dehydrogenase and gamma-glutamyltransferase. Hepatosis characterized by accentuated lobulation, and centrilobular to midzonal coagulative necrosis, haemorrhage and congestion occurred in 2 of the 3 ewes given high doses of plant material. Liver lesions in the other animals included disappearance of hepatocytes and collapse of the reticulin stroma in the centrilobular areas. Spongy changes in the cerebral white matter were evident in the ewes of the high-dose group. Ultrastructural changes in the liver comprised degeneration and necrosis of hepatocytes and occasionally endothelial cells, and disruption of sinusoidal walls.
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PMID:Experimentally-induced Cestrum laevigatum (Schlechtd.) poisoning in sheep. 151 94

SK&F 101926 is a synthetic octapeptide which was designed to promote free water excretion by antagonizing the action of antidiuretic hormone. The clinical and pathologic changes in rats resulting from lethal doses of SK&F 101926 have suggested that death is associated with respiratory failure and/or cardiovascular collapse. To define the relationships between respiratory failure, cardiovascular collapse, and death, respiratory and cardiovascular parameters were monitored in anesthetized rats following the intravenous administration of SK&F 101926 at a dosage (3 mg/kg) which resulted in 70% mortality. Within 5 min after receiving this dosage, mean arterial blood pressure was reduced to values between 30 and 40 mm Hg in all rats. This degree of hypotension was well tolerated by some rats and, consequently, was not considered to be the cause of death. Deaths occurred between 9 and 58 min after dosing and were preceded by respiratory depression involving marked reductions in respiratory rate and the lack of compensatory increases in tidal volume. At the time of respiratory arrest, heart rates remained above 200 beats/min, mean arterial blood pressure remained between 30 and 40 mm Hg, and there were no consistent changes in dynamic lung compliance or total pulmonary resistance. Pretreatment of rats with a mast cell stabilizing agent (disodium cromoglycate), a mast cell degranulating agent (compound 48/80), or a histamine/5-hydroxytryptamine blocking agent (cyproheptadine) prevented the reductions in respiratory rate and death caused by SK&F 101926. These pretreatments also reduced the effect of SK&F 101926 on blood pressure, but were not able to completely prevent the hypotension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Respiratory and cardiovascular changes associated with toxic doses of a peptide antagonist of vasopressin in the rat. 160 Dec 32

Cardiovascular collapse following intravascular bupivacaine may be resistant to treatment. The effect of amrinone on recovery from bupivacaine-induced severe cardiovascular depression was evaluated in 20 pigs (13-26 kg) in a placebo-controlled randomized double-blind study. Under 0.7% isoflurane anesthesia at FIO2 0.21, 0.5% bupivacaine 2 mg.kg-1.min-1 was infused until mean arterial pressure was 40% of the baseline. Cardiac output and heart rate decreased 75% and 50% from the baseline, respectively. The total dose of bupivacaine was 17 +/- 6 (SD) mg.kg-1 in the control and 19 +/- 5 mg.kg-1 in the amrinone group, resulting in mean plasma concentrations of 42 +/- 6 and 53 +/- 19 micrograms.ml-1, respectively. A bolus of amrinone 4 mg.kg-1 (n = 10) was given immediately after cardiovascular depression, followed by an infusion of 0.6 mg.kg-1.min-1. The control animals received corresponding volumes of physiologic saline (n = 10). After cardiovascular depression, the lungs were ventilated with FIO2 1.0 without anaesthetics or sympathomimetic support. Electric activity of the heart ceased in all control animals in 3.9 +/- 2 min after cardiovascular depression despite atropine and external cardiac compression. All animals in the control group and 5 of 10 animals in the amrinone group were given atropine (P less than 0.01). The animals receiving amrinone survived without cardiac compression (P less than 0.0001). During bupivacaine infusion, all animals developed burst suppression in the electroencephalogram. At the time of cardiovascular depression, in 8 of 10 control and in 6 of 10 amrinone animals, the electroencephalogram was isoelectric.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of amrinone on recovery from severe bupivacaine intoxication in pigs. 164 51


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