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)

Ten patients with hemolytic uremic syndrome (HUS) were admitted to our ICU during the last 7 years. The mean age at entry was 26 month old. Only one child was more than 2 years of age. A greater incidence of this illness was noted during the summer season. Almost all cases (90%), were severe with arterial hypertension and requiring peritoneal dialysis. HUS is a multisystemic disorder with early renal involvement, but the possibility of other sites being affected must be kept in mind. Half of the patients presented extrarenal manifestations of disease, including: seizures (30%), colonic ischemia requiring intestinal resection, and heart failure with lung edema due to severe hypertension. The two parameters that were helpful in determining the prognosis were the interval of renal insufficiency (greater than 14 days) and neurologic impairment, with the later being of most importance.
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PMID:[Hemolytic uremic syndrome. Evaluation of clinical and prognostic factors]. 828 50

An in-vivo rat lung model for ischemia-reperfusion injury was prepared. The left lung was collapsed after hilar stripping, and the left main pulmonary artery and bronchus were clamped. After the determined period of clamping the left main pulmonary artery and bronchus were declamped and the right main pulmonary artery was clamped. Arterial gas analyses were performed, 1, 10, and 20 minutes after reperfusion. The wet/dry lung eight ratio was calculated and lungs were histologically examined. Before clamping, PaO2 was 102-155 mmHg in all animals. The experimental animals were divided into 4 groups; Group I: temperature 19 degrees C, humidity 55% and duration of clamping 120 minutes (n = 2); Group II: 23 degrees C, 55% and 120 minutes (n = 4); Group III: 23 degrees C, 55% and 90 minutes (n = 5); Group IV: 23 degrees C, 65% and 75 minutes (n = 9). In Group IV, PaO2 decreased significantly in all 9 animals immediately after reperfusion, and at 1, 10, and 20 minutes it was 53.2 +/- 6.1 mmHg, 53.4 +/- 10.2 mmHg, and 67.0 +/- 10.2 mmHg, respectively. Pulmonary edema was observed histologically in 7 of the 9 animals. In-vivo rat lung models for ischemia-reperfusion injury are affected by the surrounding conditions. We established a stable model by setting ischemic time, temperature, and humidity at 75 minutes, 23 degrees C, and 65%, respectively.
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PMID:Preparation of in-vivo rat lung model for ischemia-reperfusion injury. 830

Exposure of isolated perfused rabbit lungs (IPL) to ischemia-reperfusion causes a transient increase in pulmonary arterial (PA) pressure at the onset of reperfusion. Because thromboxane A2 (TxA2) is a potent vasoconstrictor, we hypothesized that it may contribute to the ischemia-reperfusion-induced pressor response. To evaluate this hypothesis, we exposed IPL perfused with a cell-free solution to 40 min of warm ischemia followed by reperfusion and measured perfusate immunoreactive thromboxane B2 (iTxB2) and 6-ketoprostaglandin F1 alpha (i6-keto-PGF1 alpha). We observed that ischemia-reperfusion IPL compared with controls had an increase in PA pressure (40.2 +/- 4.8 vs. 9.3 +/- 0.3 mmHg, P < 0.05), lung edema (29.3 +/- 6.3 vs. -0.2 +/- 0.2 g, P < 0.05), iTxB2 perfusate levels (155 +/- 22 vs. < 50 pg/ml, P < 0.05), and i6-keto-PGF1 alpha (436 +/- 33 vs. 61 +/- 16 pg/ml, P < 0.05). In ischemia-reperfusion IPL, infusion of SQ 29548 (10(-6) M), a specific TxA2/prostaglandin H2 receptor antagonist, attenuated the PA pressor response and the degree of edema. We conclude that pulmonary hypertension associated with ischemia-reperfusion results in part from pulmonary release of TxA2. Furthermore, TxA2 directly through membrane effects or indirectly through hydrostatic mechanisms increases the severity of ischemia-reperfusion-induced lung edema.
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PMID:Thromboxane contributes to pulmonary hypertension in ischemia-reperfusion lung injury. 844 95

Acute cardiac failure, pulmonary edema, and ischemia of the brain, cord, and other structures pose special problems with trauma to the aortic arch and its branches. Data on 93 such cases are reported. Diagnosis was made by clinical examination in hemodynamically unstable patients and led to immediate operation in 61.3%. Patients in stable condition had angiography, which localized the injury and allowed planning of incision and bypass shunts. In left subclavian artery injuries, anterior thoracotomy was best for proximal control regardless of wound entry sites; midline sternotomy with sternocleidomastoid extension was usually adequate for other vessels. Flow was reestablished in all carotid injuries; there were no neurological complications. Temporary or permanent bypass shunts during periods of proximal aortic occlusion were valuable in decreasing cardiac afterload, maintaining circulation to the brain, and allowing an unhurried methodical approach to the hematoma. Occlusion of one or more venae cavae alleviated acute cardiac dilatation during brief periods of ascending aortic clamping. Associated trauma contributed to the high mortality.
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PMID:Penetrating injuries of the aortic arch and its branches. 845 17

Sporadic cases of inexplicable noncardiogenic pulmonary edema occur after operations requiring total cardiopulmonary bypass (CPB). Prostaglandins, such as thromboxane (Tx) A2, have been implicated in this form of pulmonary pathology in many clinical and experimental settings. Because Tx generation has been demonstrated in association with ischemia of solid organs, we postulated that total CPB, which decreases pulmonary tissue perfusion and oxygenation, would stimulate local Tx synthesis. Total CPB was examined in 7 sheep. The level of TxB2 (a stable metabolite of the active, unstable A2) was measured in the left and right atria before, during, and after 105 minutes of total CPB. Significant increases in TxB2 concentrations occurred in the left atrium compared with the right (p < 0.05) during CPB. Immediately after reperfusion, both the left atrial and right atrial TxB2 concentrations increased significantly over the baseline values (p < 0.05), but this increase and the atrial gradient were rapidly abolished with continued pulmonary perfusion. To determine the effect of extracorporeal circulation without significant (< 30%) alteration in pulmonary perfusion, we evaluated the effect of partial CPB in 5 sheep. Increased TxB2 concentrations were noted at 15 and 30 minutes after the onset of partial CPB (left atrium increased significantly over baseline; p < 0.05), but this elevation spontaneously diminished to insignificance after 15 and 30 additional minutes of extracorporeal circulation. These data establish that total CPB stimulates Tx generation in the lung, and although the effect of partial CPB is transient, that of total CPB is progressive and abolished by reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiopulmonary bypass and pulmonary thromboxane generation. 845 38

A novel active-site directed specific inhibitor of phospholipase A2 (PLA2), 1-hexadecyl-3-trifluoroethylglycero-sn-2-phosphomethanol (MJ33), administered endotracheally co-dispersed in liposomes, significantly reduced the formation of thiobarbituric acid reactive substances (TBARS) in isolated rat lungs subjected to ischemia-reperfusion. Elevated conjugated dienes were unaffected. This contrasts with the effects of the cyclo-/lipoxygenase inhibitor 5,8,11,14-eicosatetraynoic acid (ETYA), which decreased formation of both TBARS and conjugated dienes (CD). The effects of MJ33 plus ETYA were additive for TBARS but results for CD were similar to ETYA alone. A similar dissociation of inhibition of TBARS and CD formation by MJ33 was observed with t-butyl hydroperoxide induced lipid peroxidation of isolated lung microsomes. Assay of lung homogenate with phosphatidylcholine as substrate showed that MJ33 selectively inhibited the Ca(2+)-independent acidic PLA2. MJ33 had no effect on thromboxane B2 release by the isolated lung, indicating the effects of acidic PLA2 inhibition do not involve the arachidonate cascade. MJ33 also partially prevented lung edema and lactate dehydrogenase release associated with ischemia-reperfusion. The observations show that this PLA2 inhibitor can be delivered to oxidant-sensitive lung sites by its co-dispersal in liposomes, and that oxidant-induced lipid peroxidation in this model of lung injury occurs in a complex lipid prior to PLA2 activity.
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PMID:A phospholipase A2 inhibitor decreases generation of thiobarbituric acid reactive substance during lung ischemia-reperfusion. 846 33

Over the past century, the treatment of various forms of circulatory shock has included fluid resuscitation with either crystalloidal or colloidal solutions. Despite decades of investigation, there still is considerable controversy over the beneficial and adverse effects of each fluid type. Most authors agree that the initial resuscitation of any form of shock should be performed with crystalloid solutions. Trauma resuscitation uses crystalloid therapy almost exclusively. Much controversy exists when the shock state involves increased microvascular permeability, such as seen in sepsis, anaphylaxis, and burns. Concerns involve increased permeability pulmonary edema and whether colloid or crystalloid therapy may contribute to its formation. Regardless of fluid type used for resuscitative efforts, it is essential to ensure adequate invasive and noninvasive monitoring to guide therapy. Endpoints to resuscitation should include stabilization of vital signs, adequate urine output, adequate cardiac output, and evidence of supply-independent oxygen consumption. Side effects of aggressive fluid loading are frequent and include intravascular volume overload, pulmonary edema, increased myocardial water content, brain swelling, gastrointestinal ischemia, and massive systemic edema. These complications can best be minimized by careful fluid titration, using physiologic and hemodynamic endpoints.
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PMID:Fluid resuscitation in circulatory shock. 849 Jul 65

The purpose of the present study was to clarify the role of endothelin-1 (ET-1) in the pathogenesis of ischemia/reperfusion lung injury and to determine whether pretreatment with an ET receptor antagonist prevents such injury. The left lung of Sprague-Dawley rats was subjected to 60 min of no-flow warm ischemia followed by 90 min of reperfusion. The plasma ET-1 concentration increased significantly after reperfusion compared with before and after ischemia (p < 0.05). Arterial oxygen tension was reduced, and the lung tissue wet/dry weight ratio increased in post-reperfusion lungs compared with both pre-ischemia and post-ischemia lungs. Histologic study showed pulmonary edema, hemorrhage, hyaline membrane formation, and a significant increase in lung tissue neutrophils after reperfusion. In addition, the expression of ET-1 mRNA was determined by Northern blot analysis. Although ischemia did not significantly alter ET-1 expression, reperfusion increased expression in the left lung markedly and in the right lung moderately. Pre-infusion of FR139317, an ETA receptor antagonist, prevented post-reperfusion damage to the lung. These results suggest that ET-1 contributes to the ischemia/reperfusion injury of the rat lung, mediated by an ETA receptor, and that an ETA receptor antagonist may inhibit ischemia/reperfusion lung injury.
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PMID:Contribution of endothelin-1 to warm ischemia/reperfusion injury of the rat lung. 852 Jul 82

A 38-year-old patient underwent left single-lung transplantation for end-stage histiocytosis with secondary pulmonary hypertension and polycythemia. Despite use of an optimal lung graft and a total ischemia limited to 250 minutes, major pulmonary edema developed postoperatively. Hemodilution resulted in a quick recovery of lung function. We speculate that blood hyperviscosity was a major factor of pulmonary edema in this patient.
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PMID:Hemodilution is an effective treatment for reperfusion edema after lung transplantation. 861 Feb 92

Pulmonary edema following reperfusion is a major clinical problem. Changes in endothelial cell shape induced by oxidant injury may account for immediate capillary leakage associated with reperfusion injury. In these experiments we examined the role of tumor necrosis factor-alpha (TNF-alpha) in acute endothelial cell injury following ischemia-reperfusion. Sprague-Dawley rats were treated with a neutralizing antisera directed against TNF-alpha prior to production of distal ischemia. These rats demonstrated a significant reduction (P < 0.05) in acute lung edema in response to 4 hr of ischemia and 30 min of reperfusion when compared to rats undergoing the same procedure without antisera treatment. An in vitro model was developed to determine if TNF-alpha had a direct effect on endothelial cell response to ischemia-reperfusion. The effects of TNF-alpha and oxidant stress on the integrity of cultured endothelial cell monolayers was measured. Rat pulmonary artery endothelial cell monolayers reacted in vitro to oxidant stress by an increase in permeability. The cells changed shape and an increase in diffusion of 125I-albumin across cell monolayers resulted when these cells were exposed to 50 microM hydrogen peroxide (H2O2) or plasma from the ischemic hind limb of a Sprague-Dawley rat (50 microliters/ml). Pretreatment of cultured cells with low levels of recombinant mouse TNF-alpha significantly affected both the cell shape change and the increase in permeability (P < 0.05). Increased permeability of cell monolayers in vitro was not due to cell lysis as determined by media lactate dehydrogenase levels. The effect appeared to be due to cellular rounding and contraction seen using video time lapse microscopy. These data suggest a direct effect of TNF-alpha on endothelial cells, whereby the cells are rendered more susceptible to oxidant injury accompanying reperfusion.
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PMID:TNF-alpha potentiates oxidant and reperfusion-induced endothelial cell injury. 876 63


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