Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension-hypervolemia therapy (HHT) is widely employed for treatment against vasospasm after subarachnoid hemorrhage (SAH). A few investigations have been reported to establish the fact that HHT results in a high incidence of congestive heart failure and pulmonary edema as well as deterioration of brain edema. From the point of view that the cerebral circulation is not independent of the systemic circulation, the authors investigated the effect of HHT on the systemic circulation of patients with SAH. In 72 patients, intracranial pressure (ICP), pulmonary catheter wedge pressure (PCWP), pulmonary arterial pressure (PA), central venous pressure (CVP), arterial pressure (AP), cardiac index (CI), arterial blood gas (ABGS), electrocardiogram (ECG), serum and urine electrolytes were monitored postoperatively. Furthermore, among these patients, the flow (Flow), volume (Volume) and velocity (Velocity) of the cortical vessels were monitored by means of a Laser Doppler in 25 patients. A cisternal or spinal drain was placed in all of the patients. Elevation of PCWP and CVP and Flow were observed when 300ml of 10% glycerol was administered within a period of 30 minutes, whereas administration of the same dose of glycerol over a period of 60 or 120 minutes caused no significant changes on these parameters. Elevation of PCWP and CVP and decrease of CI and Flow, occasionally associated with premature ventricular contraction (PVC), were observed in some patients when 100ml of 25% albumin was administered. However, administration of the same dose of albumin over a period of 120 or 240 minutes did not cause deterioration of the cardiac function. These facts could be explained by Guyton's law in which massive transfusion causes cardiac dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Serious pitfalls which can be encountered in a course of hypertension-hypervolemia therapy for vasospasm]. 157 56

Negative consequences of the impact of alpine factors on the body of man are described. Alpine acute lung edema is one of the dangerous diseases that may develop under alpine conditions. This may affect not only beginners but also aborigines of the mountains, who return to the places they come from after a temporary stay in lowlands. Acute brain edema is regarded as no less severe condition. It may occur in about 1.2% of the people who climb to a height of 4500-5000 m. Primary alpine pulmonary arterial hypertension and chronic alpine cor pulmonale are fairly prevalent under alpine conditions.
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PMID:[The effect of altitude factors on the human body]. 158 27

A case of high altitude pulmonary edema with high altitude cerebral edema was reported. A young Japanese male complained of severe palpitation and shortness of breath on the third day of climbing at 3,000 m above sea level. During the next 2 d at altitude, the following symptoms occurred: cough with foamy sputum, cyanosis, and loss of consciousness. Soon after evacuation, he showed severe hypoxemia and deep coma with decerebrate rigidity; electroencephalogram showed diffuse alpha waves, indicating "alpha wave coma." Brain computerized tomography revealed brain edema, showing small compressed ventricles and diffuse low density of the cerebrum. Pulmonary edema on chest roentgenogram disappeared by the fifth hospital day, and his consciousness recovered gradually during the next 2 weeks after the admission. He was examined serially by electroencephalography and brain computerized tomography. He recovered fully, but there were transient psychological abnormalities soon after discharge and mild brain atrophy was observed by brain computerized tomography 6 years later.
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PMID:A case of high altitude pulmonary edema followed by brain computerized tomography and electroencephalogram. 320 90

11C-methylated inulin, supposedly useful for imaging of brain edema and pulmonary edema, was prepared using cyclotron produced 11CO2. The synthesis consists of the production of 11C-methyl iodide and its coupling with inulin alkoxide sodium in dimethylsulfoxide as solvent. 11C labeled inulin was purified by alcohol precipitation. The radiochemical yield of pure 11C-inulin was 34% of 11CO2 30 min after the end of bombardment. The blood clearance and body distribution of 11C was observed in rabbits after i.v. injection of 11C-inulin. The blood clearance curve was composed of a sum of three exponential functions. The gamma camera image showed that the 11C activity in blood moved quickly to kidneys and urine and a small dose of radioactivity remained persistently in edematous tissues, i.e. the edematous lung tissues produced by oleic acid treatment.
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PMID:Synthesis of 11C-methylated inulin as a radiopharmaceutical for imaging brain edema and pulmonary edema. 326 13

22 patients with severe preeclampsia-eclampsia were treated in our Intensive Care Unit from 1972 to 1978. Control of convulsions was achieved by diazepam, diphenylhydantoin and phenobarbital. In 11 comatose patients brain monitoring was carried out by frequent neurological examination and use of computerized x-ray tomography; aspiration of gastric contents was prevented by nasotracheal intubation. Brain oedema therapy included controlled hyperventilation, steroids and mannitol (7 patients). 10 patients with respiratory failure (due to pulmonary oedema, "shock lung" or aspiration pneumonitis) were treated by mechanical ventilation. Diastolic blood pressure above 100 mm Hg was reduced by hydralazine. Diuresis was induced by normalization of hypovolaemia with albumin and plasma expanders. Six patients died (27%); main causes of death included intracerebral haemorrhage, brain oedema, heart failure, acute pulmonary thromboembolism and bleeding from DIC.
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PMID:[Intensive care of severe preeclampsia-eclampsia. A report on 22 cases (author's transl)]. 742 60

The acute complications of diabetic ketoacidosis in children and adolescents are well recognized but not completely understood. Clinical studies have focused primarily on brain edema. We have investigated the prevalence and course of interstitial pulmonary edema in patients with severe diabetic ketoacidosis all of whom had uneventful clinical courses. High resolution computed tomography scans of the lungs were analyzed by determining the Hounsfield attenuation level and then converting to physical density values. All seven patients had evidence of interstitial pulmonary edema on the first scan, which was performed within 1 h of hydration and prior to receiving insulin; six of the seven patients had increased pulmonary density 6-8 h into treatment, and all had complete resolution of the interstitial changes at discharge. Our study suggests that subclinical interstitial pulmonary edema may be a frequent occurrence in children and adolescents with severe diabetic ketoacidosis and may very well be present prior to treatment. The study also supports the philosophy of cautious rehydration and the close monitoring of children and adolescents with diabetic ketoacidosis until a more complete understanding of this pathophysiologic event is achieved.
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PMID:Interstitial pulmonary edema in children and adolescents with diabetic ketoacidosis. 987 65

Activated peripheral T-lymphocytes are increased in both pre-insulin-dependent diabetes mellitus (IDDM) patients and in recently diagnosed IDDM patients, as well as in various forms of acute stress. We studied the in vivo T-lymphocyte activation in six patients in severe diabetic ketoacidosis (DKA) prior to treatment, after 24 h of treatment and > or =5 days after admission. Five of the six patients showed an increased percentage of activated T-lymphocytes based on the expression of HLA-DR at 24 h of treatment when compared to the admission percentage of activation (P<.05). There was no correlation to the admission serum glucose, osmolality, or electrolytes. Serum pH showed a trend toward an inverse correlation, but was not statistically significant. We speculate that T-lymphocyte activation plays a role in the progression of the acute complications of subclinical brain edema and interstitial pulmonary edema of DKA. This process could also be another factor in the progression of the chronic complications of IDDM in addition to the well-established effects of hyperglycemia and hypertension.
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PMID:Acute activation of peripheral lymphocytes during treatment of diabetic ketoacidosis. 1135 83

DMSO is an amphipathic molecule with a highly polar domain and two apolar methyl groups, making it soluble in both aqueous and organic media. It is one of the most common solvents for the in vivo administration of several water-insoluble substances. Despite being frequently used as a solvent in biological studies and as a vehicle for drug therapy, the side-effects of DMSO (undesirable for these purposes) are apparent from its utilization in the laboratory (both in vivo and in vitro) and in clinical settings. DMSO is a hydrogen-bound disrupter, cell-differentiating agent, hydroxyl radical scavenger, intercellular electrical uncoupler, intracellular low-density lipoprotein-derived cholesterol mobilizing agent, cryoprotectant, solubilizing agent used in sample preparation for electron microscopy, antidote to the extravasation of vesicant anticancer agents, and topical analgesic. Additionally, it is used in the treatment of brain edema, amyloidosis, interstitial cystitis, and schizophrenia. Several systemic side-effects from the use of DMSO have been reported, namely nausea, vomiting, diarrhea, hemolysis, rashes, renal failure, hypertension, bradycardia, heart block, pulmonary edema, cardiac arrest, and bronchospasm. Looking at the multitude of effects of DMSO brought to light by these studies, it is easily understood how many researchers working with DMSO (or studying one of its specific effects) might not be fully aware of the experiences of other groups who are working with it but in a different context.
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PMID:Multidisciplinary utilization of dimethyl sulfoxide: pharmacological, cellular, and molecular aspects. 1266 39

The objectives of this study were to monitor plasma cytokines as markers of cellular activation and as potential markers for the progression of the acute complications of diabetic ketoacidosis (DKA). Blood samples were obtained prior to, during and after treatment of severe DKA (pH < 7.2) in six children and adolescents. Plasma IL-10, IL-1beta, TNF-alpha, IL-6, IL-8 and IL-2 cytokine levels were assayed by ELISA at each of the time points. Prior to treatment, elevations of multiple cytokines were found, the highest being IL-10. Treatment of DKA resulted in a significant decrease of IL-10 at 6-8 h (p = 0.0062), and further increases in the inflammatory cytokines at 6-8 h and/or 24 h vs 120 h (baseline): IL-1beta (p =.0048); TNF-alpha (p =.0188) and IL-8 (p =.0048). This study strengthens the hypothesis that the metabolic crisis of DKA, and its treatment, have differential effects on cellular activation and cytokine release. The time frame for the increase in inflammatory cytokines correlates with the reported progression of subclinical brain edema, interstitial pulmonary edema and the development of clinical brain edema.
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PMID:Cytokine response to diabetic ketoacidosis and its treatment. 1449 40

There is a paucity of studies, clinical and experimental, attesting to the benefit of cerebral perfusion pressure (CPP) directed pressor therapy following traumatic brain injury (TBI). The current study evaluates this therapy in a swine model of TBI and hypotension. Forty-five anesthetized and ventilated swine received TBI followed by a 45% blood volume bleed. After 1 h, all animals were resuscitated with 0.9% sodium chloride equal to three times the shed blood volume. The experimental group (PHE) received phenylephrine to maintain CPP > 80 mm Hg; the control group (SAL) did not. Outcomes in the first phase (n = 33) of the study were as follows: cerebro-venous oxygen saturation (S(cv)O(2)), cerebro-vascular carbon dioxide reactivity (DeltaS(cv)O(2)), and brain structural damage (beta-amyloid precursor protein [betaAPP] immunoreactivity). In the second phase (n = 12) of the study, extravascular blood free water (EVBFW) was measured in the brain and lung. After resuscitation, intracranial and mean arterial pressures were >15 and >80 mm Hg, respectively, in both groups. CPP declined to 64 +/- 5 mm Hg in the SAL group, despite fluid supplements. CPP was maintained at >80 mm Hg with pressors in the PHE group. PHE animals maintained better S(cv)O(2) (p < 0.05 at 180, 210, 240, 270, and 300 min post-TBI). At baseline, 5% CO(2) evoked a 16 +/- 4% increase in S(cv)O(2), indicating cerebral vasodilatation and luxury perfusion. By 240 min, this response was absent in SAL animals and preserved in PHE animals (p < 0.05). Brain EVBFW was higher in SAL animals; however, lung EVBFW was higher in PHE animals. There was no difference in betaAPP immunoreactivity between the SAL and PHE groups (p > 0.05). In this swine model of TBI and hypotension, CPP directed pressor therapy improved brain oxygenation and maintained cerebro-vascular CO(2) reactivity. Brain edema was lower, but lung edema was greater, suggesting a higher propensity for pulmonary complications.
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PMID:Cerebral perfusion pressure directed therapy following traumatic brain injury and hypotension in swine. 1457 61


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