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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary edema was induced by an intravenous infusion of bovine thrombin, 500 NIH/kg b.w., given in 5 min, in rats in which fibrinolysis had been inhibited by an intraperitoneal injection of the fibrinolysis inhibitor AMCA. Ninety minutes after termination of the thrombin infusion the lung weight was increased from 1.09 +/- 0.07 to 3.14 +/- 0.12 g due to edema. A high albumin concentration in the extravascular water indicated that the edema was a consequence of increased permeability in the microcirculation. In rats injected with the H1 histamine receptor antagonist mepyramine maleate and H2 receptor antagonist cimetidine after the thrombin infusion, the lung weight was significantly lower at 90 min (2.68 +/- 0.33 g), and the amount of edema as calculated morphometrically was slightly but significantly reduced. The concentration of albumin in the extravascular water (i.e. in the edema fluid) in rats subjected to histamine receptor blockade was unchanged, indicating that the slight decrease in edema was a result of decreased filtration pressure and not of an effect on microvascular permeability.
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PMID:Blockade of histamine receptors and thrombin-induced microembolic pulmonary edema in the rat. 383 50

This study examined the role of colloids versus crystalloids in pulmonary edema associated with the increased pulmonary microvascular permeability secondary to thrombin-induced pulmonary microembolism. Each of 23 healthy dogs received an intravenous injection of thrombin and a fibrinolysis inhibitor, which induced a microembolic state with increased (fivefold) pulmonary lymphatic flow and a lymph/plasma (L/P) protein ratio typical of a permeability change. Seven dogs received no treatment, eight received 15 ml/kg 10% dextran 40 (D40), and eight received 60 ml/kg Ringer's lactate solution (RL). Pulmonary water was measured serially by thermal conductivity and terminally by wet/dry weights. This preparation produced significant hemolysis; however, L/P ratios of hemoglobin approached unity in all groups. Initially there was hemoconcentration, which was reversed by RL and even more so by D40. Both D40 and RL temporarily raised the pulmonary artery and pulmonary artery wedge pressures to 15 mm Hg; D40 more than doubled the cardiac output of control or RL subjects--this was associated with a reduced pulmonary arteriolar resistance (P less than 0.05). In the early stage PaO2 was better maintained with D40 (P less than 0.02). Lymph flow increased and was comparable in all groups, as were lung water and lung weight, which tripled in all three groups. Results of this study indicated that in the presence of a pulmonary microvascular leak, colloids in doses that produced comparable microvascular pressures did not increase lung water and did not accumulate in the pulmonary interstitium. Colloids were superior to crystalloids in maintaining cardiac output, pulmonary vascular resistance, and oxygen tension in the early period after microembolism.U
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PMID:Pulmonary microvascular leakage after microembolization and hemodilution. 617 75

The Gaboon viper has acquired an impressive reputation which is at least partly unfounded. This handsome animal with such striking features is undoubtedly docile which accounts for the very low incidence of bite amongst humans. There are only six detailed clinical reports on the effect of bite and these are summarized in the review. The viper does indeed produce prodigious amounts of venom, but the toxicity, weight for weight, is rather low compared to other poisonous snakes. Venom extractions have been carried out on four snakes over a 13-year-period and the effects of this venom have been studied in a variety of experimental animals. Systemic envenomation is characterized by immediate abrupt hypotension, subsequent cardiac damage and dyspnoea. The individual venom components responsible for these effects have not been isolated but it seems likely that the two enzymes which have been studied extensively (phospholipase A2 and the thrombin-like enzyme, gabonase) do not contribute significantly to lethality. We propose three principal activities which give rise to the major signs of systemic envenomation. Haemorrhagin; causing widespread damage to microvasculature which leads to the pulmonary oedema and hence dyspnoea, and locally causes blistering. Cardiotoxin; a long-acting material causing cardiac muscle damage, arrhythmia and ultimately cardiac failure. Peripheral vasodilator; a short acting effect, operating either locally via bradykinin formation and/or unknown peptides or centrally on the vasomotor centre.
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PMID:The Gaboon viper (Bitis gabonica): its biology, venom components and toxinology. 639 43

Microembolic pulmonary oedema was induced by injection of thrombin (500 NIH units/kg body weight) i.v. in rats in which fibrinolysis had been inhibited by pretreatment with trans-4-aminomethyl-cyclohexanoid-carboxylic acid (AMCA). To evaluate the role of serotonin in this condition the effect of pretreatment with the antiserotonin compound methysergide (2.5 mg/kg body weight) on the amount of pulmonary oedema was studied. Pretreatment with methysergide resulted in a 20% decrease in lung weight in thrombin-treated rats. It caused a significant reduction of dilated lymph vessels, and of interstitial and alveolar oedema, as evaluated morphometrically. Methysergide pretreatment did not significantly alter the number of degranulated mast cells. Antiserotonin is thought to exert its effect by lowering the filtration pressure in the pulmonary microcirculation.
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PMID:Effect of methysergide pretreatment on thrombin-induced pulmonary oedema in the rat. 651 63

Solute and fluid compartments in the lungs were investigated following thrombin-induced intravascular coagulation in rats treated with the fibrinolysis inhibitor, Trans-4-(amino-methyl) cyclohexanecarboxalic acid. The lung weight was increased to almost three times normal due to accumulation of extravascular water with albumin and chloride concentrations similar to those in plasma. The blood content and dry weight were doubled. Microscopic sections were characterized by widespread fibrin-rich microemboli, thickened alveolar walls, distension of peribronchiolar and perivascular spaces with fluid, dilated lymph vessels and protein-rich alveolar oedema. An increased microvascular permeability to protein explains the findings. When the dose of thrombin was decreased to a point where no pulmonary oedema developed, supplementary infusion of low molecular weight fibrinogen degradation products induced oedema formation as verified microscopically.
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PMID:Pulmonary insufficiency in the rat after intravascular coagulation and inhibition of fibrinolysis. II. Investigations on oedema formation and morphology. 711 31

The effect of ibuprofen on thrombin-induced pulmonary edema was studied in rats. Thrombin infusion produced a significant increase in lung weight, wet weight/dry weight ratio and relative lung water content, a rise in mean pulmonary arterial pressure and a fall in mean systemic arterial pressure. It also caused a progressive decrease in PaO2 and a continuous increase in pH and PaCO2. Administration of either the S-isomer or R-isomer of ibuprofen at doses of 5 mg/kg body weight prior to thrombin infusion resulted in significant reduction in lung weight, wet weight/dry weight ratio and water content. The wet weight/dry weight ratio and the water content were somewhat lower after infusion of the S-isomer than of the R-isomer. Ibuprofen diminished the thrombin-induced increase in mean pulmonary arterial pressure and attenuated the early and late decrease in mean systemic arterial pressure caused by thrombin. Ibuprofen also stabilized thrombin-induced impairments in PaO2, PaCO2 and pH. The results thus indicate that ibuprofen effectively counteracts hemodynamic changes, stabilizes impairments in arterial blood gas variables and attenuates the increase in lung vascular permeability to protein with pulmonary edema caused by thrombin. The results also indicate a substantial R to S chiral inversion of ibuprofen in vivo in the rat.
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PMID:Effect of ibuprofen on thrombin-induced pulmonary edema in the rat. 754 27

The preventive effect of indomethacin on thrombin-induced pulmonary edema was studied in rats. Administration of thrombin caused a significant increase in lung weight, wet weight to dry weight ratio (WW/DW), and relative lung water content. During infusion of thrombin, mean pulmonary artery pressure rose and mean systemic artery pressure fell, PaO2 decreased progressively and there was a continuous rise in pH and PaCO2. An inhibitor of cyclooxygenase, indomethacin, at a dose of 1 mg/kg body weight, induced a significant further increase in lung weight (p < 0.05), and a tendency towards an increase in WW/DW and water content compared with animals given thrombin alone. Treatment with indomethacin, however, counteracted the elevated pulmonary artery pressure occurring in the early phase after thrombin infusion, but not that in the late phase. Systemic artery pressure was not affected by indomethacin. The increases in pH and PaCO2 after thrombin infusion were attenuated and remained stable almost at baseline level after indomethacin administration. Indomethacin did not prevent the hypoxemia induced by thrombin infusion. In conclusion, although indomethacin prevented the early increase in pulmonary artery pressure due to thrombin and the decrease in pH and the increase in PaCO2, it caused lung vascular permeability to protein to increase more than with thrombin alone.
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PMID:Effect of indomethacin on thrombin-induced pulmonary edema in the rat. 757 Nov 66

Liver pathology is one of the main features of HELLP syndrome and develops on the basis of a generalised activation of intravascular coagulation. Fibrin deposits and haemorrhagic necrosis predominantly develop in the periportal areas and may eventually lead to subcapsular haematomas or even rupture of the liver. While the compensated form of activation of intravascular coagulation, which is diagnosed by a decrease in antithrombin III and an increase in thrombin-antithrombin III complex (TAT) and the appearance of fibrin, monomers and D-dimers, is found in almost all cases of HELLP syndrome, the decompensated form of intravascular coagulation with prolonged bleeding time (PT, PTT) and drop in fibrinogen is found only in the most severe forms. The development of a decompensation of coagulation correlates with the appearance of severe complications such as liver haematoma, abruptio placentae, renal failure and pulmonary oedema. The best prophylaxis against the development of life-threatening complications is early diagnosis and termination of pregnancy after stabilisation of the maternal condition, consisting of magnesium sulphate infusion, antihypertensive treatment with dihydralazine or calcium antagonists, steroids etc. Severe complications of HELLP syndrome have occasionally been observed in the postpartum period. As prophylaxis against postpartal worsening of HELLP syndrome, curettage of the uterus and continuation of the treatment with calcium antagonists and dexamethasone have been recommended.
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PMID:[Liver pathology within the scope of HELLP syndrome]. 784 9

Neonatal respiratory distress syndrome (RDS) is an acute lung injury believed to result primarily from surfactant deficiency in the immature lung. Although surfactant replacement therapy has improved the outcome of this disease, RDS remains a major cause of neonatal mortality and morbidity. Preliminary experimental evidence suggests that unopposed intravascular thrombin activity may contribute to the progression of RDS by promoting high permeability pulmonary oedema and pulmonary hypertension. In the extravascular lung compartment, polymerizing fibrin may inhibit surfactant function. In addition, interstitial and alveolar thrombin formation and resulting fibrin deposition may contribute to the development of chronic lung disease through amplification of inflammation and fibrosis. There is good evidence that extravascular coagulation occurs during the course of RDS. Fibrin is a major component of the hyaline membranes, which are a hallmark of acute lung injury, and which can be regarded as locally produced clots. It has been less certain whether neonatal RDS is also associated with intravascular activation of the coagulation system. Although low levels of antithrombin III (AT III) have been reported in infants with RDS, direct evidence of increased intravascular thrombin formation has been lacking. However, recently, plasma concentrations of thrombin-antithrombin III (TAT) complexes have been measured in infants with RDS and correlated with RDS severity. TAT formation was significantly increased in severe neonatal RDS, while free AT III activity was decreased. These data are consistent with increased thrombin generation and resulting AT III consumption. Therefore, to regulate thrombin activity, infants with severe RDS may benefit from replacement therapy with AT III concentrate. This hypothesis has been strengthened by experiments that have demonstrated the efficacy of thrombin inhibition in several animal models of acute lung injury. However, controlled clinical trials will be required to determine whether thrombin is just a coincidental marker of neonatal RDS, or whether unopposed thrombin activity exacerbates the disease process.
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PMID:Antithrombin III deficiency in neonatal respiratory distress syndrome. 818 52

The effect of a synthetic leukocyte elastase inhibitor on thrombin-induced pulmonary edema was studied in rats. The chloromethylketone human neutrophil elastase inhibitor, ICI 200,355, blunted rat leukocyte elastase activity in rat lung tissue. Administration of thrombin produced a significant increase (p < .01) in lung weight. The wet weight to dry weight ratio (WW/DW) and relative water contents were also significantly elevated (p < .01). Pretreatment with ICI 200,355 (200 micrograms/kg h-1) resulted in significant reductions (p < .05) in lung weight and a tendency to decrease WW/DW and water content compared with animals given thrombin alone. It is possible that the elastase inhibitor effectively reduced the rate of thrombin-induced pulmonary edema by attenuation of increased vascular permeability.
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PMID:Effect of a synthetic leukocyte elastase inhibitor on thrombin-induced pulmonary edema in the rat. 846 58


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