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 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper summarizes the role of the renal pressure natriuresis and diuresis mechanisms in maintaining sodium and water balance in hypertension. In all forms of chronic hypertension studied to date, the renal pressure natriuresis and diuresis mechanisms are abnormal, since increased arterial pressure is required to maintain normal excretion of sodium and water, and therefore fluid balance. When renal perfusion pressure is prevented from increasing in various forms of experimental hypertension, caused by infusion of mineralocorticoids, angiotensin II, vasopressin, or norepinephrine and adrenocorticotrophic hormone (ACTH), sodium and water retention continues until ascites, pulmonary oedema and circulatory collapse occur within a few days. Thus, chronic hypertension appears to be an essential homeostatic response that permits sodium and water balance to be maintained despite various abnormalities which tend to decrease renal excretory capability. The intrarenal mechanisms by which increased renal perfusion pressure maintains sodium and water balance in hypertension have not been fully elucidated, but appear to involve small changes in glomerular filtration rate (GFR) and reductions in fractional sodium reabsorption, due either to the direct hydraulic effects of pressure or to various indirect effects, such as changes in angiotensin II formation.
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PMID:Mechanisms of sodium balance in hypertension: role of pressure natriuresis. 302 42

Thoracic CT for patients in intensive care is cumbersome but provides important additional information in the presence of complicated lung changes. Total opacification of a lung field visualised on conventional portable films may be due to infiltration and/or fluid and/or collapse by using the clinical information in conjunction with densitometric measurements. CT may help in the differentiation of pulmonary oedema, particularly in the presence of ARDS and its complications. It is also possible to accurately localise abscesses and empyemas in the presence of extensive consolidation. This makes it possible to drain abscesses or empyemas, or pleural fluid in unusual situations, which has become loculated, or to aspirate a pneumothorax.
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PMID:[Computerized tomography of the thorax in intensive care patients]. 303 34

Unilateral reexpansion pulmonary edema (RPE) is a rare complication of the treatment of lung collapse secondary to pneumothorax, pleural effusion, or atelectasis. Although RPE generally is believed to occur only when a chronically collapsed lung is rapidly reexpanded by evacuation of large amounts of air or fluid, in this review 15 of 47 cases of RPE available for assessment occurred when the pulmonary collapse was of short duration or when the lung was reexpanded without suction. The pathogenesis of RPE is unknown and is probably multifactorial. Implicated in the etiological process of RPE are chronicity of collapse, technique of reexpansion, increased pulmonary vascular permeability, airway obstruction, loss of surfactant, and pulmonary artery pressure changes. Since the outcome of RPE was fatal in 11 of 53 cases reviewed (20%), physicians treating lung collapse must be aware of the possible causes and endeavor to prevent the occurrence of this complication.
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PMID:Reexpansion pulmonary edema. 327 31

A successful emergency operation for a 75-year-old man with aorto-caval fistula secondary to rupture of the abdominal aortic aneurysm is reported. A definite diagnosis of aorto-caval fistula was made by echography with characteristic engorgement of the caval vein. Clinical signs and symptoms characterized by lung edema, sudden onset, and circulatory collapse were also noticeable. In the operation, the fistula was closed via inside of the aneurysm with several mattress sutures following control of aortic flow and opening of the aneurysm. Back-flow of the blood through the fistula was readily controlled by finger tip. The aneurysm was replaced conventionally by a vascular prosthesis. There might be several suitable surgical selection available properly to individual case. No delay in surgical treatment depending on definite diagnosis by echography in such urgent condition should be stressed.
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PMID:[Aorto-caval fistula due to a ruptured abdominal aortic aneurysm--an emergency operation following echoic diagnosis]. 328 24

Hybridoma cells were obtained by fusing spleen cells from mice, immunized against the 15 kDa porcine surfactant apoprotein, with a myeloma cell line. Adult mice were inoculated intraperitoneally with this hybridoma; mice that were not inoculated or were inoculated with myeloma cells served as controls. Lung-thorax compliance was measured at various intervals after inoculation. The animals were then killed for histologic-morphometric evaluation of alveolar air expansion, inflammatory reaction in the pulmonary parenchyma, and intraalveolar edema. In the hybridoma group, the mice developed respiratory failure 9 days after inoculation, with markedly reduced lung-thorax compliance, lung congestion, alveolar collapse, hemorrhagic pulmonary edema, and hyaline membranes. Morphometric data from the same animals showed reduced volume density of alveolar air, and increased volume densities of intraalveolar "fluid" (edema) and tissue components. These lung lesions are similar to those in the adult respiratory distress syndrome.
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PMID:Respiratory failure in mice caused by a hybridoma making antibodies to the 15 kDa surfactant apoprotein. 339 79

The importance of the renal pressure natriuresis and diuresis mechanisms in long-term control of body fluid volumes and arterial pressure has been controversial and difficult to quantitate experimentally. Recent studies, however, have demonstrated that in several forms of chronic hypertension caused by aldosterone, angiotensin II (AngII), vasopressin, or norepinephrine and adrenocorticotropin, increased renal arterial pressure is essential for maintaining normal excretion of sodium and water in the face of reduced renal excretory capability. When renal arterial pressure was servo-controlled in these models of hypertension, sodium and water retention continued unabated, causing ascites, pulmonary edema, or even complete circulatory collapse within a few days. Apparently, other mechanisms for volume homeostasis, such as the various natriuretic and diuretic factors that have been postulated, are not sufficiently powerful to maintain fluid balance in the absence of increased renal arterial pressure when renal excretory function is reduced in these forms of hypertension. The intrarenal mechanisms responsible for pressure natriuresis and diuresis are not entirely clear, but they seem to involve small increases in glomerular filtration rate and filtered load as well as reductions in fractional reabsorption in proximal and distal tubules. During chronic disturbances of arterial pressure additional factors, especially changes in AngII and aldosterone formation, act to amplify the effectiveness of the basic renal pressure natriuresis and diuresis mechanisms in regulating arterial pressure and body fluid volumes.
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PMID:Regulation of arterial pressure: role of pressure natriuresis and diuresis. 353 87

A fatal case of sodium azide poisoning in which exchange blood transfusions, charcoal hemoperfusion, hemodialysis and potent vasopressor agents failed to prevent the development of circulatory collapse associated with a wide complex cardiac rhythm is presented. The cellular toxin sodium azide resulted in the development of an altered mental status, profound metabolic acidosis, cardiac arrhythmia (atrial fibrillation and terminal wide complex arrhythmias), a relative decrease in cardiac output, hypotension and non-cardiogenic pulmonary edema. Further animal studies are needed to gain new approaches for the treatment of this rare cause of human poisoning.
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PMID:A case of fatal sodium azide ingestion. 374 89

Improved survival of patients receiving high-dose steroid therapy in sepsis and adult respiratory distress syndrome (ARDS) has been reported, but such therapy and its benefits remain controversial. Recently research has been directed toward manipulation of the arachidonic acid cascade. Improved survival and hemodynamics with administration of nonsteroidal anti-inflammatory drugs (NSAID) have been reported in animal models of sepsis and ARDS. The purpose of this study was to compare the effects of steroids (methylprednisolone) and NSAID (ibuprofen) in a porcine model of septic ARDS induced by a continuous infusion of live Pseudomonas aeruginosa. Cardiopulmonary parameters were monitored in animals intubated, paralyzed, and ventilated at a 250 ml tidal volume and 0.5 Fio2. Pigs were randomly assigned to one of five groups: groups I and II received respective doses of 12.5 mg/kg ibuprofen and 30 mg/kg methylprednisolone at 20 and 210 minutes after baseline; group III had P. aeruginosa only; groups IV and V received respective doses of ibuprofen and methylprednisolone at 20 and 210 minutes of sepsis. Significant pulmonary edema, increased intrapulmonary shunting, hypoxemia, hemoconcentration, and systemic hypotension occurred with P. aeruginosa infusion. In septic animals treated with ibuprofen normal systemic arterial pressure was maintained, hemoconcentration was decreased, and oxygenation was improved with a significant decrease in shunting and pulmonary edema. Administration of methylprednisolone improved hemoconcentration and cardiac index, but no significant effect on pulmonary edema, intrapulmonary shunting, or oxygenation was observed. The results of this study demonstrated a significant beneficial effect of ibuprofen and we would encourage controlled clinical trials of this drug in the management of sepsis and ARDS. On the other hand, methylprednisolone was found to be relatively ineffective in treatment of circulatory collapse and ARDS associated with sepsis.
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PMID:A critical comparison of the hematologic, cardiovascular, and pulmonary response to steroids and nonsteroidal anti-inflammatory drugs in a model of sepsis and adult respiratory distress syndrome. 376 92

Acute lung disease is commonly associated with interstitial pulmonary edema and a tendency towards partial or total alveolar collapse. To counteract this tendency mechanical ventilation is successfully used in most cases. Mechanical ventilation, however, leads to a harmful retention of water and salt, which may worsen interstitial pulmonary edema and further impair gas exchange. This problem seems to be less known. A survey of the effects of currently used modes of mechanical ventilation on excretory function and hemodynamics of the kidneys is given together with a short review of the possible afferent and efferent mechanisms which mediate the renal response to mechanical ventilation. Some clinical suggestions are made to break through the vicious cycle between mechanical ventilation and kidney function.
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PMID:[Artificial respiration and kidney function disorder--a vicious circle?]. 389 Jun 7

Severe head trauma patients frequently develop pulmonary failure. The aetiology of this respiratory distress may be central (neurogenic pulmonary oedema, delayed neurogenic pulmonary dysfunction, abnormal respiratory patterns) or peripheral, due to chest trauma, multiple trauma or lung infection. Hypoxia and hypercarbia alter cerebral haemodynamics, increase intracranial pressure and cause secondary deterioration of neurological function. Ventilatory support is of utmost importance in supportive care of head trauma patients. Continuous mechanical ventilation and intermittent mandatory ventilation are most frequently employed. Hyperventilation is used to lower intracranial pressure and positive end-expiratory pressure (PEEP) is applied in lung disorders characterized by interstitial oedema and alveolar collapse. The effects of PEEP on cerebral perfusion pressure and on intracranial pressure depend on the interaction of pulmonary compliance, cerebral pressure/volume relationship and cerebral vascular autoregulation. High levels of PEEP may be deleterious in patients with altered cerebral autoregulation. High frequency ventilation theoretically has less influence on intrathoracic pressures and on cerebral haemodynamics but has not been shown superior in the respiratory support of severe head trauma patients.
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PMID:Ventilatory support for pulmonary failure of the head trauma patient. 389 Sep 90


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