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

In individual analytically oriented psychotherapy as a research method, observing a random sample of 34 schizophrenics with the symptoms of depressive syndrome, the author has found that depression in schizophrenia is determined by narcissistic injuries, by a collapse of narcissistic satisfactions through the loss of "ego" functions, completeness, competitiveness, and competence. The depressive model is most frequently encountered in florid schizophrenic psychosis, at the beginning of hospitalization, but depending on the intensity and depth of narcissistic traumas and losses, it can develop also in any phase of the therapeutic process and the course of illness. In the author's view, the depressive model in schizophrenia is not conditioned by the neuroleptic treatment. Its recognition is very important for the therapy of suicidal tendencies, and for their prevention in particular.
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PMID:[Narcissistic depression in schizophrenia]. 233 68

A challenging surgical problem is the correction of supra-tip depression of the nose following collapse of nasal septal support. Numerous materials have been used in augmentation rhinoplasties attempting to correct this deformity, all having certain disadvantages. A modified technique is described in which costal cartilage surrounded by perichondrium is grafted in such noses; the results of a small series is discussed. The problems of graft distortion and resorbtion appear to have been satisfactorily overcome by using this procedure.
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PMID:Chondroplastic graft augmentation rhinoplasty. 238 9

Many types of shock are characterized by profound hemodynamic alterations and depression of immune processes. Among the various mediators implicated in shock conditions, there is much evidence to suggest that, together with various cytokines, the inflammatory and chemotactic autacoid, platelet-activating factor (PAF), plays an important role. Studies on several animal models have shown that infusion of PAF mimicks the shock state, that markedly increased levels of PAF are produced in shock and that PAF antagonists afford significant protection against diverse forms of shock. The precise mechanism by which PAF antagonists protect against shock remains unclear; however, it is becoming apparent that in traumatic states a complex interaction occurs between PAF and cytokines, which leads to the acute phase reaction and circulatory collapse. We propose that PAF antagonists may be effective in counteracting shock because of their antiprotease activity and their ability to inhibit deleterious PAF/cytokine auto-generated feedback processes.
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PMID:Platelet-activating factor and cytokine interactions in shock. 255 74

The effects of i.c.v. administered dermorphin, a highly selective mu-opioid agonist, on cardiac function and renal, mesenteric and hindquarter blood flow were studied in conscious rats. Core temperature, blood gases, arterial plasma levels of norepinephrine, epinephrine, dopamine, 3,4-dihydroxyphenylalanine and dihydroxyphenylacetic acid (DOPAC) also were examined. Cardiac output was measured using a thermodilution technique and regional blood flows using directional pulsed Doppler velocimetry. Dermorphin, at doses of 0.1-100 nmol/kg, increased blood pressure and hindquarter blood flow, renal and mesenteric resistance, and core temperature. Higher doses (1-5 mumol/kg) caused respiratory depression, acidosis, and shock despite profound sympatho-adrenomedullary stimulation. Circulating levels of catecholamines were significantly increased at the dermorphin doses of 0.1-100 nmol/kg. At the 100 nmol/kg dose, plasma levels of epinephrine, norepinephrine, the dopamine metabolite dihydroxyphenylacetic acid and the catecholamine precursor 3,4-dihydroxyphenylalanine were increased by 2-15-fold. The data indicate that mu opioid receptor stimulation exerts potent effects on cardiorespiratory functions, activates the sympathoadrenomedullary system and produces a pattern of blood flow changes consistent with the stress-induced "defense" response (skeletal muscle vasodilation and splanchnic vasoconstriction). Excessive mu opioid receptor stimulation leads to shock due to respiratory and hemodynamic collapse.
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PMID:Mechanisms of central hemodynamic and sympathetic regulation by mu opioid receptors: effects of dermorphin in the conscious rat. 256 68

Tellurium is one of the rarest elements on earth. Intoxications are rare and almost exclusively occupationally exposed workers are affected. Only a few cases of non-occupational poisoning have been reported so far. Severe poisoning results in respiratory depression and circulatory collapse. After occupational exposure main symptoms and signs include loss of appetite, dryness of the mouth, suppression of sweating, a metallic taste in the mouth, and most notable, a sharp garlic odor of the breath, sweat and urine. We report our findings in a 37 year old, non-occupationally exposed woman with tellurium intoxication.
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PMID:Tellurium-intoxication. 258 20

A time sequence study was performed to study the early effects of radiation on the ultrastructure of the rat heart. Wistar rats were exposed to 20 Gy electron irradiation to a field including the heart and a third of the lung. The hearts were excised at varying time intervals (1 h-180 days), and the ultrastructure of perfusion-fixed subepicardium and subendocardium studied. Changes were observed in both myocytes and interstitium at all time intervals. The most pronounced change observed in the myocyte was that of intercalated disc damage which reached a peak at 30 days post-irradiation. Mitochondrial damage, characterized by swelling and fenestration in areas of myofibrillar contracture, was focal and relatively scarce. Swelling of the capillary endothelial cells and collapse of the capillaries were marked up to 60 days. Of significance was the observation that the damage to both myocytes and interstitium receded after 60 days and the hearts exhibited an almost normal ultrastructure from 100 to 180 days post-irradiation. Mechanical function of these hearts followed a similar pattern: maximal depression was observed 60 days after irradiation. Thereafter the work performance of these hearts improved significantly, almost reaching control levels after 180 days.
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PMID:Radiation-induced changes in the ultrastructure and mechanical function of the rat heart. 261 18

The long-term prognosis for 314 patients with hypertrophic cardiomyopathy (HCM) and 82 with dilated cardiomyopathy (DCM) was investigated in an attempt to elucidate clinical variables predicting sudden death (SD). In the patients with HCM, 68% of cardiac deaths occurred suddenly and unexpectedly. Variables associated with an increased risk to SD were young age (less than 30 years), reduced fractional shortening (less than 35%) and elevated left ventricular end-diastolic pressure (greater than or equal to 20 mmHg). Eight of the 10 patients who died suddenly during or immediately after strenuous exercise were less than 30 years old, and the collapse tended to be associated with exercise-induced ST-depression. In contrast, SD occurring during mild activities, resting or sleep was mainly observed in those aged 30 years or more. Ventricular tachycardia was observed on electrocardiographic monitoring in 24% of those 30 years or more, while it was rare in those under 30 years (5%). On the other hand, no SD was found in patients with apical hypertrophy nor in those 50 years or more. These observations suggest that HCM patients at a young age, with impaired left ventricular systolic and diastolic function, have an increased risk to SD. Since exercise-induced myocardial ischemia rather than ventricular arrhythmias appears to be the more likely mechanism for SD for those under 30 years old, restriction of strenuous exercise should be strongly advised for these patients. For those aged from 30 to 50 years, ventricular tachycardia should be controlled by antiarrhythmic agents for the prevention of SD. In patients with DCM, 24% of all cardiac deaths were attributed to SD. Although no variables reliably predicted SD, it was of note that only one patient out of 26 with SV1 + RV5 greater than or equal to 35 mm died suddenly. Whereas ventricular arrhythmias are known to be a contributing cause for SD, the prognostic significance of ventricular tachycardia on electrocardiographic monitoring in predicting SD has not yet been established. In addition, antiarrhythmic agents often precipitate hemodynamic deterioration. It therefore appears that use of antiarrhythmic agents is not a therapy of first choice and that primary treatment should be focused upon improvement in ventricular function in order to prevent SD in patients with DCM.
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PMID:Sudden death in hypertrophic and dilated cardiomyopathy. 263 25

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

In halothane-nitrous oxide-anesthetized pigs, the effect of the competitive adenosine antagonist, BW-A1433U (a derivative of 1,3-dipropyl-8-phenylxanthine), on postdefibrillation bradyarrhythmia and hemodynamic depression was investigated. In protocol 1, repetitive episodes of ventricular fibrillation lasting 15 seconds before transthoracic DC shock were performed in five animals, before (control) and after the administration of BW-A1433U (5 mg/kg i.v.). An unsuccessful initial shock was immediately followed by a rescue shock of 40 A. In ventricular fibrillation episodes requiring rescue shocks, nine of 19 episodes (47%) exhibited second- or third-degree atrioventricular block at 15 seconds postdefibrillation compared with only one of 16 BW-A1433U episodes (6%). In protocol 2, the effect of BW-A1433U was determined in the presence of dipyridamole, a nucleoside uptake blocker known to potentiate the cardiac actions of adenosine. To counter the hypotensive effect of dipyridamole, methoxamine was continuously infused at 0.015 mg/kg/min i.v. Sequential episodes of ventricular fibrillation lasting 45 seconds were terminated by shocks of 40 A in the presence of methoxamine alone, after dipyridamole (1.5-7.5 mg i.v.), and after BW-A1433U (5 mg/kg i.v.). Over the first 15 seconds postdefibrillation, BW-A1433U significantly (p less than 0.05) increased the number of spontaneous beats (31 +/- 2) and systolic/diastolic blood pressure (111 +/- 4/67 +/- 5 mm Hg; mean +/- SEM; n = 9) compared with both methoxamine (16 +/- 2 beats; 98 +/- 14/52 +/- 12 mm Hg; n = 5) and dipyridamole (8 +/- 3 beats; 58 +/- 11/27 +/- 6 mm Hg; n = 9), respectively. Rapid infusion of BW-A1433U during dipyridamole postdefibrillation periods raised heart rate and blood pressure to preventricular fibrillation levels within 30 seconds. Thus, BW-A1433U can reverse and prevent postdefibrillation bradyarrhythmia and hemodynamic depression. Endogenous adenosine may be an important mediator of postdefibrillation cardiovascular collapse.
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PMID:Role of endogenous adenosine in postdefibrillation bradyarrhythmia and hemodynamic depression. 273 45

Using position emission tomography (PET) and equilibrium imaging with oxygen-15 labelled gases, the cerebral blood flow (CBF), blood volume (CBV), oxygen extraction fraction (OEF) and oxygen consumption rate (CMRO2) were measured in multiple regions of interest over the cerebral cortex of 5 control subjects, 4 patients with strictly unilateral longstanding carotid artery occlusion, 1 patient with middle cerebral artery embolic stroke in the acute stage, and 4 patients with subcortical stroke and no cervical arterial disease. In each control subject, the regional CBV was linearly and positively correlated with both CBF and CMRO2, while the local mean transit time (t = CBV/CBF) was uniformly distributed, reflecting the local adaptation of both the vascular tone and the capillary density to the metabolic demand at constant cerebral perfusion pressure that characterizes the normal brain. In patients with subcortical stroke, cortical blood volume was reduced in proportion to the matched reduction in CBF and CMRO2, suggesting that the metabolic depression resulting from cortical deafferentation increases the resting tone of pial vessels. Unilateral carotid occlusion induced larger CBV and t, and steeper slopes of the CBV-CBF relationship, particularly on the occluded but also on the patent side. The assessment of the local cerebral perfusion pressure (CPP) as judged by the ratio CBF/CBV in 3 patients with focally raised OEF and preserved or reduced CMRO2, allowed the demonstration in multiple cerebral regions of single patients of two well-known physiological phenomena: the autoregulation of CBF, followed by the rise of the OEF as local CPP falls further. In addition, the depression of CMRO2 in the ischaemic cortex was associated with a trend for CBV to return towards normal values, compared with the maximally elevated CBV found in oligaemic but metabolically normal areas. This suggests that a process of metabolic vasoconstriction may participate, among other factors, in the vascular collapse that occurs, and would serve to regenerate some haemodynamic reserve, at very low CPP levels.
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PMID:Local brain haemodynamics and oxygen metabolism in cerebrovascular disease. Positron emission tomography. 278 86


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