Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The preparation of patients for reintervention should aim at the correction of: - states of shock and collapse, found in one out of three patients; - hydroelectrolytic disturbances (sodium depletion, hypochloremia, dyskaliemia); - and finally, re-establishment of the acid-base balance.
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PMID:[Preparation of the patient for reoperation]. 0 40

The authors report ten cases of renal insufficiency observed among a series of 43 cases of fat embolism. It is a matter of eraly oligoanuria (starting beween the 2nd and the 4th day). Its severity depends on the lesions involved : prolonged cardio-vascular collapse - cranio-encephalic lesion. The renal insufficiency does not seem typical of fat embolism. It must be essentially linked to a cardio-vascular collapse and/or to a disseminated intra-vascular coagulation.
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PMID:[Acute renal insufficiency and fat embolism]. 0 65

Leucomalacia or white matter necrosis is one of the major aspects of neonatal encephalopathies, especially in the premature baby. These necroses are found mainly in the deep periventricular white matter of the "semi-oval centre". Characteristically, they are ischaemic and their anatomical and histological progress is rapid: coagulation necrosis with rapid axonal fragmentation followed by polymorphic cellular reaction with glial cells and macrophages. Regeneration in the minor forms consists of glyosis process in severe forms; multiple cavities appear in a few weeks. Physiopathogenic hypotheses put forward are related to: 1 -- the very anatomic aite: special tissue and terminal arteries, 2 -- onset of myelinization process, 3 -- associated clinical and biological lesions such as hypoxia, acidosis and hypotention. These lesions are symptom-free during the neonatal period. One of us suggested in 1962 that these could be the anatomical basis of spastic monoplegia or diplegia (LITTLE's disease). All motor cerebral sequelae have disappeared since 10 years. This is particularly significant mainly in the case of spastic diplegia of the former premature baby under 2500 g. This decrease coincides with improvement in neonatal care, especially correction of hypoxia, acidosis and cardiovascular collapse. These findings seem to support the pathogenic hypotheses.
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PMID:[Leukomalacia and subsequent brain status in relation to intensive neonatal care]. 0 75

The study of 16 newborn of birthweight less than or equal to 2,200 g characterized by a common point: the presence of PLACENTA PRAEVIA IN THE MOTHER, enabled us to come to grips with the severe respiratory distress that these newborn can have. From the clinical standpoint: there is always early respiratory distress. From the radiological standpoint: by far the most dominant pathology was interstitial edema, giving rise to a WET LUNG. From the biochemical standpoint: the blood gases were characterized in a certain number of cases by hypoxemia which was refractory to the usual forms of treatment. From the mechanical standpoint: measurements carried out in 4 patients confirmed the extraordinary fall in these patients' compliance. The clinical, radiological, blood gas and mechanical analysis enabled one to differenciate 2 main types of indications for artificial ventilation: -- acute hypoxemia, -- the idea of an increased need for oxygen. In these 2 types of indications for artificial ventilation, it was apparent that the treatment of choice is constant positive pressure which may or may not be combined with intermittent positive pressure. With this treatment technique, none of the patients progressed to massive atelectasis. It can be said that with the advent of techniques of ventilation by high pressure combining IPP with CPP, one has definitively eliminated from this pathological picture, the principal cause of death: --anoxia due to massive alveolar collapse.
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PMID:[Severe respiratory distress with stubborn hypoxemia in newborn infants whose mothers had had placenta previa]. 0 84

Six cases of grave hypothermias are reported, having arisen during surgical interventions which necessitated a rapid and abundant transfusion of badly warmed blood. The role of favouring factors, surrounding cold due to the air-conditioning, anaesthesia, extent of the area of operation, seems important. The symptomatology permits the individualization of a hypothermic syndrom neighbouring the picture described in toxic accidental hypothermias. Accidents during the warming process associate collapse and disturbances in coagulation. It is therefore necessary to consider certain signs of alarm as important and generalize the conditions for prevention of thermolysis in the operating theatre.
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PMID:[Accidental peroperative hypothermia during rapid transfusion]. 0 5

The purple membrane of Halobacterium halobium acts as a light-driven proton pump, ejecting protons from the cell interior into the medium and generating electrochemical proton gradient across the cell membrane. However, the type response of cells to light as measured with a pH electrode in the medium consists of an initial net inflow of protons which subsides and is then replaced by a net outflow which exponentially approaches a new lower steady state pH level. When the light turned off a small transient acidification occurs before the pH returns to the original dark level. We present experiments suggesting that the initial inflow of protons is triggered by the beginning ejection of protons through the purple membrane and that the initial inflow rate is larger than the continuing light-driven outflow. When the initial inflow has decreased exponentially to a small value, the outflow dominates and causes the net acidification of the medium. The initial inflow is apparently driven by a pre-existing electrochemical gradient across the membrane, which the cells can maintain for extended times in the absence of light and oxygen. Treatments which collapse this gradient such as addition of small concentrations of uncouplers abolish the initial inflow. The triggered inflow occurs through the ATPase and is accompanied by ATP synthesis. Inhibitors of the ATPase such as N,N'-dicyclohexylcarbodiimide (DCCD) inhibit ATP synthesis and abolish the inflow. They also abolish the transient light-off acidification, which is apparently caused by a short burst of ATP hydrolysis before the enzyme is blocked by its endogenous inhibitor. Similar transient inflows and outflows of protons are also observed when anaerobic cells are exposed to short oxygen pulses.
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PMID:Light-driven proton translocations in Halobacterium halobium. 0 22

1. The TN-T and TN-I components of troponin both interact with tropomyosin and cause its precipitation in 0.1 M KC1 at neutral pH. The precipitate contains both end-to-end and side-by-side aggregates of tropomyosin molecules. 2. The TN-T and TN-I components change the band pattern of tropomyosin paracrystals formed in MgC1(2) solutions, although in different ways. TN-T causes the formation of hexagonal net structures, double-stranded net or paracrystals which result from the collapse of the double-stranded net. TN-I at pH 7.9 causes the formation of paracrystals with a 400 A periodic band pattern and a 200 A repeat. The same band pattern can also be seen in tropomyosin paracrystals formed at pH values below 6.0. 3. The TN-C component does not precipitate tropomyosin in 0.1 M KC1. The aggregates of tropomyosin obtained with either TN-T or TN-I can be solubilized by the addition of TN-C. No interaction of TN-C was observed with tropomyosin paracrystals formed in the presence of MgC12.
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PMID:Interaction of tropomyosin with troponin components. 0 83

The diagnosis of pheochromocytoms is still made only post mortem in a high percentage of the cases. It is important to know both the diversity of clinical forms (of the 16 cases investigated 13 (80%) presented permanent AH, of which 12 cases with paroxysmal attacks, followed by collapse only in one case, and 3 (20%) with paroxysmal AH on a normotensive background) and the severity of cardiovascular accidents, which increases twofold during crises (arrhythmias, left ventricular failure, coronary insufficiency, cerebrovascular strokes, secondary adrenalinic shocks). These complications are preceded by the "alarm syndrome". The preoperatory treatment is associated: blocking of adrenergic alpha-receptors and beta-receptors; correction of hypovolemia, also applied during the surgical phase I (until the venous ligature is made and the tumor excised) under continuous monitoring (ECG, ABP and central venous pressure). In phase II vasoplegin should be promptly corrected by nor. E+E, and corticoids.
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PMID:Disorders induced by pheochromocytoma in the cardiovascular system. A therapeutic approach. 0 88

Proposed since 1938 as a treatment for pulmonary edema, continuous positive pressure ventilation (PPP) still called teleexpiratory positive pressure in France (PPTE) and "Positive End Expiratory Pressure" (PEEP) or even "Continuous Pressure Breathing" (CPPB) in Anglo-Saxon countries, has taken a place in the first line of therapy in refractory hypoxia and particulary when the latter originate from lesional pulmonary edema. The aim of PPP is to open up the alveolar territories by calling on their elastic properties, to fight against micro-atelectasis and bronchial collapse, to diminish the closing volume, to increase the FRC, thereby improve VA/Qc, decrease Qs/Qt and increase PaO2. Furthermore, in the particular case of pulmonary edema, PPP acts against the hydrostatic pressure by increasing the external component of the transmural pressure and by evening out pulmonary capillary blood flow.
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PMID:[Justification, methods and indications for positive-pressure respiration in controlled and spontaneous ventilation in lesional pulmonary edeman]. 0 66

The alveolar wall on contact with air can be compared with a biological air-liquide interface. As with all interfaces, there are therefore superficial forces which tend to reduce the surface to a minimum. In the case of a pulmonary alveolus with a spherical surface, these forces are at the origin of an internal pressure excess dependent on the radius of the alveolus and on the superficial tension related to the nature of the interface. Owing to the disparity in the alveolar radii, under these conditions the smaller alveoli would collapse to the benefit of a larger one, the pressure being lower and lower in the latter. In addition, at any time in the respiratory cycles, this surpression must be negligible in order to avoid rupture of the equilibrium of the forces exerted on the alveolar wall. Consequently, it is necessary that this air-alveolar wall interface should have a superficial tension on the one hand variable with the surface, and on the other hand always very low. Owing to the demonstration of large concentrations of phospholipid in this area, it can be thought that a superficial film is substituted at the air-biological liquid interface and owing to this fact effectively has superficial properties necessary for alveolar stability. The "surface-tensio-active" effect of this film lead to the giving of the name of "surfactant" to these constituents as a whole.
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PMID:[Pulmonary surfactants. Generalities]. 0 71


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