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)

The effects of methylprednisolone, F(ab')2 fragments of human gamma globulins and rosmarinic acid, an inhibitor of complement activation, were tested on endotoxin-induced haemodynamic and haematological changes in the rabbit. Their effects were compared with complement depletion by cobra venom factor (CVF) pretreatment. The results provide further evidence for the role of complement activation and the concomitant triggering of the arachidonic acid cascade in the early phase of shock. The formation of vasoactive prostanoids (prostacyclin and thromboxane A2), the arterial hypotension and the thrombocytopenia were largely dependent on the presence of the intact complement system. F(ab')2 fragments (150 mg kg-1, i.v.) diminished the second fall in blood pressure to some extent but failed to alter any of the other endotoxin-induced changes. Methylprednisolone (40 mg kg-1, i.v.) given 10 min before endotoxin significantly reduced the activation of complement, the second rise of prostacyclin and the secondary hypotension, but was without effect on the early thromboxane peak of the haematological features of endotoxin shock. Rosmarinic acid (20 mg kg-1, i.v.) may be of potential interest for treatment of septic shock, since the drug suppressed the endotoxin-induced activation of complement, the formation of prostacyclin, both hypotensive phases, the thrombocytopenia and the concomitant release of thromboxane A2. The role of leukocytes and their arachidonic acid metabolites in plasma exudation deserves further investigation, because leukopenia and pulmonary oedema were not complement-dependent and were not affected by any of the treatments. Our results indicate that drugs, interfering with complement activation and/or prostaglandin biosynthesis, may be beneficial in endotoxin shock, provided that they are administered at an early stage.
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PMID:Modification of endotoxin-induced haemodynamic and haematological changes in the rabbit by methylprednisolone, F(ab')2 fragments and rosmarinic acid. 383 89

A thrombotic microangiopathy resembling the hemolytic uremic syndrome was diagnosed in 12 patients with adenocarcinoma, in whom the tumor was in complete or near-complete remission after treatment with mitomycin C-containing drug regimens. Microangiopathic hemolytic anemia, thrombocytopenia, and renal failure were initially present in all cases. All patients eventually developed pulmonary edema and systemic arterial hypertension, and three experienced neurologic complications. Blood transfusions exacerbated the syndrome in nine patients. High titers of platelet-aggregating plasma immune complexes were present in all six cases in which they were measured. The constituent antibody of each complex failed to react with mitomycin C antigen preparations, whereas in vitro reactivity to endodermally derived neoplasms was demonstrated. Plasmapheresis was associated with amelioration of the syndrome in only one patient. In patients receiving mitomycin C chemotherapy, the development of anemia and thrombocytopenia or azotemia may represent the initial manifestations of this newly defined thrombotic microangiopathy. A consistently effective form of management of this syndrome has not as yet been defined.
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PMID:Carcinoma-associated hemolytic-uremic syndrome: a complication of mitomycin C chemotherapy. 392 62

Twenty-eight peritoneovenous shunts were placed to relieve ascites in 26 patients with a variety of underlying malignancies. Nine of the patients had documented liver metastases and hyperbilirubinemia. Severe thrombocytopenia with laboratory evidence of disseminated intravascular coagulation (DIC) occurred in four of these nine patients following shunt placement. Relative or absolute thrombocytopenia was also commonly observed in this series. Other complications included pulmonary edema, ventricular tachycardia, culture-negative fever, pneumonia, and late shunt occlusion. Good palliation, with relief of abdominal pain or respiratory compromise, was achieved in 57% of these patients. Our experience suggests that DIC following peritoneovenous shunts in patients with malignancy may be more common than previously reported, although not as frequent as the incidence of DIC associated with shunt placement for cirrhotic ascites. Platelet aggregation or Factor X activation by ascitic fluid and failure of the liver to inactivate activated clotting factors may play a role in this coagulopathy. Because of the risk of potentially fatal DIC, palliative peritoneovenous shunts should be considered with caution in patients with liver metastases and hyperbilirubinemia.
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PMID:Thrombocytopenia and laboratory evidence of disseminated intravascular coagulation after shunts for ascites in malignant disease. 399 80

The case of a pregnant patient with diffuse scleroderma who died following Caesarean section under general anaesthesia is presented. The patient's postoperative course was complicated by pulmonary oedema and pulmonary hypertension, sepsis, thrombocytopenia and renal failure. Aspects of the disease which possess anaesthetic implications are reviewed.
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PMID:Scleroderma and pregnancy. Anaesthetic considerations. 405 5

alpha-Naphthylthiourea (ANTU) damages the pulmonary capillary endothelium producing a marked pulmonary edema. Since the pulmonary microvasculature regulates the circulating levels of serotonin (5-HT), the role of 5-HT in the pathophysiology of ANTU-induced pulmonary edema was examined. Mice treated with ANTU (10 mg/kg, ip) rapidly developed pulmonary edema which was maximal at 3 hr and was resolved by 12 hr. The lung content of both endogenous 5-HT and a tracer dose of 5-[3H]HT paralleled the time course of the development and resolution of the pulmonary edema. ANTU produced a significant thrombocytopenia (58 to 72%) at all time points, and an elevated platelet content of 5-HT and 5-[3H]HT during the resolution phase (6 to 12 hr). Drugs possessing select effects on 5-HT were shown to alter the edematogenic response to ANTU. Fluoxetine, a selective inhibitor of 5-HT uptake, potentiated the pulmonary edema, while clorgyline, an irreversible inhibitor of type A monoamine oxidase, was without effect. Reserpine which depletes 5-HT stores prevented both thrombocytopenia and pulmonary edema in response to ANTU. Reloading the lung and platelet 5-HT stores of reserpinized animals reestablished the normal response to ANTU. Pretreatment with the selective 5-HT2 receptor antagonist, ketanserin, prevented the thrombocytopenia, the increase in lung content of 5-HT and 5-[3H]HT, and prevented the edematogenic response to ANTU by 70%. These data indicate a major role for 5-HT in the pathophysiology of acute lung microvascular injury produced by ANTU.
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PMID:A role for serotonin in alpha-naphthylthiourea-induced pulmonary edema. 642 98

Hyperthermia is a totally different modality from existing treatment modalities. Systemic hyperthermia (S-HT) is effective against advanced tumors which make resistance to conventional cancer therapies. In S-HT, it is essential and very important to manage cardio-pulmonary function in good condition. Especially, PEEP (about 7 cm H2O) is very effective to prevent lung edema. Fifty-four patients with a variety of neoplasms were subjected to S-HT, alone or in combination with chemotherapy, radiotherapy, and immunotherapy. S-HT was performed under general anesthesia by using extracorporeal circuit in corporating a heat exchanger. Usually, S-HT was given for 4-8 hours with 41.5-42.0 degrees C at 2 weeks intervals. Out of 25 evaluable cases, response was obtained in 11 cases (44%) including 2 cases of complete response. Cardio-pulmonary performance was evaluated using a flow directed pulmonary artery catheter (Swan-Ganz catheter). At treatment temperature, all patients showed hyperdynamic conditions and developed a two-fold mean increase in cardiac index. Altogether 172 treatment sessions were associated with sinus tachycardia and a reduction in diastolic pressures. Laboratory abnormalities included thrombocytopenia without sign of D.I.C., moderate hyperglycemia, mild degree of hypophosphatemia, hypolcalemia and transient elevations in liver enzymes. Serum creatinine levels were elevated in all treatment sessions without elevation of serum BUN. Serum levels of calcium and magnesium were stable. All of abnormalities and toxicities were decreased within 1 to 2 weeks after treatments. It is suggested that with carefully monitored conditions S-HT be performed safely without heart failure.
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PMID:[Clinical practice of systemic hyperthermia therapy and physiological responses of the host]. 687 Feb 90

Bleeding, thrombocytopenia, and osteopenia are recognized as the side effects of heparin administration. We recently noted occurrence of pulmonary edema in a patient with myelofibrosis with myeloid metaplasia being treated with heparin for pulmonary embolism. The hypertensive episodes preceding left ventricular failure were considered related to serotonin released from the immunologically mediated lowering of platelets.
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PMID:Development of pulmonary edema related to heparin administration. 722 18

Intravenous injection of crude marijuana extract led to development of an acute illness with multisystem involvement. Gastrointestinal manifestations consisted of severe vomiting, diarrhea, and crampy abdominal pain. Hypotension, tachycardia, and peripheral vasodilation constituted the main cardiovascular manifestations of the disease. Moderate azotemia and oliguria, presumed to be of prerenal origin, were present and rapidly resolved with administration of intravenous fluids. Hematologic manifestations consisted of leukocytosis with a left shift, thrombocytopenia, prolonged partial thromboplastin time, increased fibrin degradation products, and positive protamine sulfate test. The observed coagulation abnormalities may suggest intravascular coagulation. C3, C4, and total hemolytic complement were reduced, suggesting possible activation of the complement system. Hyperventilation, hypoxemia, pulmonary edema, obstructive, and restrictive pulmonary function abnormalities and bilateral pleural effusions highlighted the pulmonary manifestations of the disease. Rhadbomyolysis and mild hepatic function abnormalities were also present. All observed abnormalities reversed in a few days with no significant sequelae.
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PMID:Toxicity with intravenous injection of crude marijuana extract. 723 64

A 2-year-old Old English Sheepdog had right-side congestive heart failure characterized by pericardial effusion, pleural effusion, ascites, and increased pulmonary wedge pressure. A diagnosis of atrial septal defect was made by means of cardiac catheterization and angiography. Surgical correction initially was deferred because of pulmonary hypertension. However, when congestive heart failure could not be managed adequately, surgical correction was attempted. Postsurgically, thrombocytopenia developed and that led to bleeding, oliguira, and pulmonary edema. The bleeding was controlled by whole blood transfusion, but the oliguria and pulmonary edema were not resolved, even with intensive diuretic therapy. The dog died 24 hours after surgery.
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PMID:Atrial septal defect (sinus venosus type) in a dog. 745 4

A patient with drug-induced thrombocytopenia who died because of massive pulmonary hemorrhage is described. The patient had a clinical picture of acute respiratory distress resembling pulmonary edema, but there was no hemoptysis. Chest x-ray films showed granular density in the pulmonary fields, and the electrocardiograms revealed a pattern of acute biatrial enlargement. The diagnosis was confirmed at autopsy.
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PMID:Lethal occult pulmonary hemorrhage in drug-induced thrombocytopenia. 747 71


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