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)

Aggregate anaphylaxis was induced in seven ovalbumin-sensitized monkeys, with high tires of ovalbumin specific haemagglutinating antibodies. After pretreatment with an intravenous (i.v.) injection of 0.25 mg/kg terbutaline (n = 6) or an infusion of isoprenaline (n = 1), anaphylactic shock was induced by i.v. challenge with specific antigen. Haemodynamics, regional blood flows, respiratory mechanics, blood gases and haematological changes were studied during the following 30 min. Severe shock developed following ovalbumin challenge and the cardiac output was reduced by a mean of 74%. Pulmonary vascular resistance increased 11-fold. Pulmonary dynamic compliance decreased, but there was only a minor increase in pulmonary resistance. Hypoxaemia and severe metabolic acidosis developed. Circulating platelets and leucocytes decreased markedly. Three animals died with fulminant pulmonary oedema. In conclusion, the reaction pattern was similar to that found in studies of monkeys that received no prior treatment. However, the occurrence of pulmonary oedema suggests that the effects of large doses of terbutaline on the heart, combined with the high pulmonary vascular resistance, resulted in more severe pulmonary changes than took place in untreated animals.
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PMID:Anaphylaxis in the monkey: pulmonary oedema after pre-treatment of beta-receptor stimulants. 11 19

Acute pulmonary edema developed in two young, previously healthy women immediately after the intravenous administration of contrast media. The pulmonary edema, rare in young persons, could not be explained by classical anaphylaxis, contrast media overdose, sodium and fluid overload, or acute myocardial infarction. A nonimmunologic osmotic mechanism causing reversible pulmonary capillary leak might explain the clinical events observed in both patients. Both responded to continuous positive airway pressure (CPAP), indicating the possible utility of CPAP in treating pulmonary capillary-leak contrast reactions.
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PMID:Acute pulmonary edema after the intravenous administration of contrast media. 38 41

Evidence from isolated bovine pulmonary vessels and respiratory smooth muscles suggests that bovine slow-reacting substance of anaphylaxis (SRS-Abov) may contribute to bronchoconstriction and pulmonary oedema during anaphylaxis in cattle. Bovine bronchus is sensitive to low concentrations of SRS-Abov and is considerably more sensitive than trachea. Contraction of the calf bronchus to SRS-Abov can be antagonized by sodium meclofenamate, suggesting prostaglandins may be involved in the contraction. Bovine pulmonary artery did not contract to SRS-A at any of the concentrations examined. None of the proposed SRS-A receptor antagonists, FPL 55712, PR-D-92-EA, or sodium meclofenamate, inhibit the effects of bovine SRS-A in bovine pulmonary vein.
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PMID:Effects of bovine SRS-A (SRS-Abov) on bovine respiratory tract and lung vasculature in vitro. 88 66

We studied systemic anaphylaxis induced by the administration of 200 mug of horseradish peroxidase into 11 anesthetized rabbits known to be producing anti-horseradish peroxidase antibodies only of the IgE class. Ventilatory changes included a transient, abrupt decrease in breathing frequency followed by increased minute ventilation; lung mechanical changes included decreased dynamic lung compliance and increased total pulmonary resistance; cardiovascular changes included pulmonary hypertension, systemic hypotension, and, frequently, a transient bradycardia. Recovery from these physiologic changes took place within 60 min. After recovery, the administration of 2 mg of horseradish peroxidase into 6 of the rabbits induced a second reaction indistinguishable from the first with respect to ventilatory and circulatory alterations; however, lung mechanical changes were less prominent. No histologic evidence of pulmonary edema or intraluminal plugging of the pulmonary edema or intraluminal plugging of the pulmonary circulation was observed by light microscopy. Although the first anaphylactic reaction was accompanied by disappearance of stainable basophils from the circulating blood, the second reaction occurred despite the absence of circulating basophils. These studies characterize further the effects of antigen challenge in rabbits producing detectable concentrations of IgE, but not other classes of antibody to the antigen.
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PMID:IgE-induced respiratory and circulatory changes during systemic anaphylaxis in the rabbit. 98 86

Thromboxanes (Txs) were implicated as possible participants in the altered microvascular permeability of acute lung injury when the Tx synthase inhibitor, OKY-046, was reported to prevent pulmonary edema induced by phorbol myristate acetate (PMA). Recently, however, we found that OKY-046, at a dose just sufficient to block Tx synthesis in intact dogs, did not prevent PMA-induced pulmonary edema but rather merely reduced it modestly. The present study was designed to explore other mechanisms whereby OKY-046 might prevent PMA-induced pulmonary edema. The finding that 5-lipoxygenase (5-LO) metabolites of arachidonic acid were increased within the lung after PMA administration, coupled with the report that OKY-046 inhibited slow-reacting substance of anaphylaxis formation, permitted formulation of the hypothesis that OKY-046, at a dose in excess of that required to inhibit Tx synthesis, inhibits the formation of a product(s) of 5-LO and, thereby, prevents edema formation. In vehicle-pretreated pentobarbital-anesthetized male mongrel dogs (n = 4), PMA (20 micrograms/kg i.v.) increased pulmonary vascular resistance (PVR) from 4.4 +/- 0.3 to 26.3 +/- 8.8 mmHg.l-1 x min (P < 0.01) and extravascular lung water from 6.7 +/- 0.5 to 19.1 +/- 6.2 ml/kg body wt (P < 0.05). Concomitantly, both TxB2 and leukotriene B4 (LTB4) were significantly increased in the lung. Pretreatment with OKY-046 (100 mg/kg i.v., n = 8) prevented PMA-induced increases in TxB2, LTB4, and pulmonary edema formation but did not prevent the increase in PVR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:OKY-046 prevents increases in LTB4 and pulmonary edema in phorbol ester-induced lung injury in dogs. 133 76

We determined changes in vascular resistance and microvascular permeability during anaphylactic reaction in isolated canine lungs perfused at constant pressure with autologous blood. In lungs with anaphylaxis induced by an intra-arterial injection of Ascaris suum antigen (10 mg), pulmonary vascular resistance and capillary pressure assessed as double occlusion pressure increased transiently by 10 times and 6.3 mmHg, respectively. Pre- to postcapillary vascular resistance ratio decreased from 0.89 +/- 0.05 to 0.21 +/- 0.06, suggesting predominant pulmonary venoconstriction. In lungs perfused in the antidromic direction from the pulmonary vein to the artery, anaphylaxis caused marked precapillary vasoconstriction, consistent with pulmonary venoconstriction. Vascular permeability assessed using the capillary filtration coefficient and isogravimetric capillary pressure did not change significantly for 3 h in either group. No changes were found in any variables in the saline-injected control lungs. The final weight of the anaphylactic lungs was significantly greater than that of the control lungs. Thus we conclude that anaphylaxis in isolated canine lung produces an increase in capillary pressure due to pulmonary venoconstriction without significant changes in vascular permeability. Pulmonary edema accompanied by anaphylactic hypotension may result from an increase in pulmonary hydrostatic intravascular pressure but not an increase in pulmonary vascular permeability.
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PMID:Pulmonary vascular response to anaphylaxis in isolated canine lungs. 144 18

Immunopathological studies of SIDS share the problems of all necropsy based studies of this syndrome: the extent of autolytic changes in the material under study; and the lack of appropriate controls. Despite these problems, several studies have been performed on serum, bronchoalveolar lavage, and pulmonary tissue. Many of these studies have been inspired by the modified anaphylaxis hypothesis, based on the experiments of Coombs and coworkers. Lightly anaesthetised guinea-pigs, which had been sensitised to cows' milk protein, were shown to die after intratracheal challenge. Studies of serum IgE concentrations in SIDS initially indicated raised specific IgE for Dermatophagoides pteronyssinus, Aspergillus fumigatus, and bovine beta-lactoglobulin, but subsequent studies have not sustained these findings. Raised immunoglobulin concentrations in bronchoalveolar lavage fluid have been found in association with SIDS but this probably reflects plasma leakage rather than local secretion. Immunocytochemical analysis of lavage cells performed by the same group revealed no major difference between SIDS cases and controls, although these were limited to four cases. To date, there have been no comprehensive studies of the inflammatory cell content of the pulmonary parenchyma in SIDS. In our own studies, we have examined the mast cell and eosinophil populations in the lungs of 49 cases of infants with SIDS and in 33 infants dying of non-pulmonary causes in the first 18 months of life. We found no difference in mast cell numbers between the groups but there was a striking excess of eosinophils in the lungs of infants dying of SIDS. Because eosinophils can secrete oxygen free radicals and cytotoxic cationic proteins, we regard this as evidence of a potential mechanism for the pulmonary oedema that is characteristic of SIDS. A viral infection which might otherwise have been trivial could therefore prove fatal.
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PMID:Immunopathology of SIDS. 147 58

Hyskon (32 per cent dextran 70 in 10 per cent dextrose in water), a useful distension medium for hysteroscopic surgery, has significant side effects. A case of pulmonary edema following transcervical myoma resection is presented. Additional known side effects of Hyskon discussed include coagulation defects, spurious laboratory results, and anaphylaxis. Prevention and management of complications are described.
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PMID:Hyskon complications in hysteroscopic surgery. 170 73

Intravenous fluorescein angiography is a commonly performed and extraordinarily valuable diagnostic procedure. The frequency of adverse reactions after angiography has varied considerably in previous reports. In a prospective study of 2789 angiographic procedures in 2025 patients, the authors found that the percentage of adverse reactions depended strongly on the patient's angiographic history. Overall, adverse reactions followed 4.8% of the angiographic procedures. These reactions included nausea (2.9%), vomiting (1.2%), flushing/itching/hives (0.5%), and other reactions (dyspnea, syncope, excessive sneezing) (0.2%). No cases of anaphylaxis, myocardial infarction, pulmonary edema, or seizures occurred. The percentage of reactions was 1.8% for patients who had had previous angiography without ever having had an adverse reaction. In contrast, the percentage of reactions was 48.6% for patients who had had an adverse reaction to angiography previously.
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PMID:Frequency of adverse systemic reactions after fluorescein angiography. Results of a prospective study. 189 Dec 25

A 27-year-old woman undergoing autologous bone marrow transplantation for relapsed, refractory Hodgkin's disease developed acute non-cardiogenic pulmonary edema immediately after transfusion of autologous bone marrow. A few similar cases in the literature are identified. Although the precise mechanisms for these rare reactions are not clear, several possibilities including anaphylaxis due to dimethylsulfoxide, leukoagglutination, complement activation, and transient left ventricular dysfunction are proposed and discussed. Features which might allow patients at risk for similar events to be identified include the presence of active pulmonary tumor, and a history of dyspnea and pulmonary infiltrates following transfusion of homologous blood products.
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PMID:Cardiac arrest after autologous marrow infusion. 207 Jan 52


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