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

Cytokines are recognized as critical early mediators of organ injury. We attempted to determine whether or not severe hepatic ischemia/reperfusion injury results in tumor necrosis factor-alpha (TNF-alpha) release with subsequent local and systemic tissue injury. After 90 min of lobar hepatic ischemia, TNF was measurable during the reperfusion period in the plasma of all 14 experimental animals, with levels peaking between 9 and 352 pg/ml. Endotoxin was undetectable in the plasma of these animals. Pulmonary injury, as evidenced by a neutrophilic infiltrate, edema and intra-alveolar hemorrhage developed after hepatic reperfusion. The neutrophilic infiltrate was quantitated using a myeloperoxidase (MPO) assay; this demonstrated a significant increase in MPO after only 1 h of reperfusion. Anti-TNF antiserum pretreatment significantly reduced the pulmonary MPO after hepatic reperfusion. After a 12-h reperfusion period, there was histologic evidence of intra-alveolar hemorrhage and pulmonary edema. Morphometric assessment showed that pretreatment with anti-TNF antiserum was able to completely inhibit the development of pulmonary edema. Liver injury was quantitated by measuring serum glutamic pyruvic transaminase which showed peaks at 3 and 24 h. Anti-TNF antiserum pretreatment was able to significantly reduce both of these peak elevations. These data show that hepatic ischemia/reperfusion results in TNF production, and that this TNF is intimately associated with pulmonary and hepatic injury.
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PMID:Role of tumor necrosis factor-alpha in the pathophysiologic alterations after hepatic ischemia/reperfusion injury in the rat. 216 33

Reactive oxygen species are a major cause of damage occurring in ischemic tissue after reperfusion. During reperfusion transitional metals such as iron are required for reactive oxygen species to mediate their major toxic effects. Xanthine oxidase is an important source of reactive oxygen species during ischemia-reperfusion injury, but not in all organs or species. Because cytochrome P-450 enzymes are an important pulmonary source of superoxide anion (O2-.) generation under basal conditions and during hyperoxia, and provide iron catalysts necessary for hydroxyl radical (.OH) formation and propagation of lipid peroxidation, we postulated that cytochrome P-450 might have a potential role in mediating ischemia-reperfusion injury. In this report, we explored the role of cytochrome P-450 enzymes in a rabbit model of reperfusion lung injury. The P-450 inhibitors 8-methoxypsoralen, piperonyl butoxide, and cimetidine markedly decreased lung edema from transvascular fluid flux. Cimetidine prevented the reperfusion-related increase in lung microvascular permeability, as measured by movement of 125I-albumin from the vascular space into lung water and alveolar fluid. P-450 inhibitors also prevented the increase in lung tissue levels of thiobarbituric acid reactive products in the model. P-450 inhibitors did not block enhanced O2-. generation by ischemic reperfused lungs, measured by in vivo reduction of succinylated ferricytochrome c in lung perfusate, but did prevent the increase in non-protein-bound low molecular weight chelates of iron after reperfusion. Thus, cytochrome P-450 enzymes are not likely a major source of enhanced O2-. generation, but serve as an important source of iron in mediating oxidant injury to the rabbit lung during reperfusion. These results suggest an important role of cytochrome P-450 in reperfusion injury to the lung and suggest potential new therapies for the disorder.
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PMID:Role of cytochrome P-450 in reperfusion injury of the rabbit lung. 217 18

A series of 62 femorofemoral bypass grafts (FFBG) is reported. The indication for this operation was unilateral iliofemoral occlusion with severe ischemia of the lower limb in poor-risk patients. Severe ischemia presented as rest pain and/or minor necrotic lesions to the foot fingers, while patients were defined poor-risk for aging and concomitant diseases advising major surgical procedures and general anaesthesia. Claudication was not considered as an indication for this operation, and this statement is discussed in detail reviewing the literature. Operative death rate was approximately 6.4% (4 subjects), due to acute renal failure, revascularization syndrome, cardiac arrest and pulmonary oedema. Twenty subjects had had a total of 33 previous vascular reconstructive procedures; this occurrence did not reveal any statistically significant consequences on long-term patency rate, although a difference was seen in favour of the patients who had not undergone previous vascular reconstructive procedures. In the group of patients who underwent FFBG as the first vascular procedure, five early occlusions occurred: three Fogarty catheter thrombectomies were successful. Cumulative patency rate was then 77% at 36 months in the series of 58 survivors. Rest pain was relieved in any instances and a satisfactory improvement of claudication was obtained.
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PMID:The femorofemoral bypass graft. Report of a 11-year experience. 225 Sep 77

A technique of orthotopic liver transplantation using a segmental graft from living donors was developed in the dog. Male mongrel dogs weighing 25-30 kg were used as donors and 10-15 kg as recipients. The donor operation consists of harvesting the left lobe of the liver (left medial and left lateral segments) with the left branches of the portal vein, hepatic artery and bile duct, and the left hepatic vein. The grafts are perfused in situ through the left protal branch to prevent warm ischemia. The recipient operation consists of two phases: total hepatectomy with preservation of the inferior vena cava using total vascular exclusion of the liver and veno-venous bypass, implantation of the graft in the orthotopic position with anastomosis of the left hepatic vein to the inferior vena cava and portal, arterial and biliary reconstruction. Preliminary experiments consisted of four autologous left lobe transplants and nine non survival allogenic left lobe transplants. Ten survival experiments were conducted. There were no intraoperative deaths in the donors and none required transfusions. One donor died of sepsis, but all the other donor dogs survived without complication. Among the 10 grafts harvested, one was not used because of insufficient bile duct and artery. Two recipients died intraoperatively of air embolus and cardiac arrest at the time of reperfusion. Three dogs survived, two for 24 hours and one for 48 hours. They were awake and alert a few hours after surgery, but eventually died of pulmonary edema in 2 cases and of an unknown reason in the other. Four dogs died 2-12 hours postoperatively as a result of hemorrhage for the graft's transected surface. An outflow block after reperfusion was deemed to be the cause of hemorrhage in these cases. On histologic examination of the grafts, there were no signs of ischemic necrosis or preservation damage. This study demonstrates the technical feasibility of living hepatic allograft donation. It shows that it is possible, in the dog, to safely harvest non ischemic segmental grafts with adequate pedicles without altering the vascularization and the biliary drainage of the remaining liver. We propose that this technique is applicable to human anatomy.
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PMID:Segmental liver transplantation from living donors. Report of the technique and preliminary results in dogs. 227 16

The incidence and clinical significance of silent myocardial ischemia occurring in the early period after acute myocardial infarction (AMI) was studied in 59 patients who had an uncomplicated early course after admission for AMI. Calibrated 2-lead ambulatory electrocardiographic monitoring performed for 39 +/- 2 hours starting 4 +/- 1 days after AMI identified silent myocardial ischemia, defined as greater than or equal to 1 mm ST-segment change lasting greater than or equal to 2 minutes, in 27 patients. These patients had 5 +/- 1 episodes lasting a median of 11 minutes/episode (range 2 to 36 minutes/episode). Patients with and without silent ischemia had comparable baseline demographics, were receiving similar anti-ischemic medications and had similar severity of coronary disease by angiography. No reinfarctions occurred during the in-hospital period. Fourteen of 27 patients (52%) with silent ischemia had greater than or equal to 1 in-hospital clinical ischemic event (pulmonary edema, n = 5, cardiac death, n = 1, and postinfarction angina, n = 11). In contrast, only 7 of 32 patients without silent ischemia (22%) had greater than or equal to 1 in-hospital event (pulmonary edema, n = 1, cardiac death, n = 1, and postinfarction angina, n = 6). The frequency of ischemic events was significantly greater in patients with silent ischemia compared to those without silent ischemia, p less than 0.02. Silent ischemia occurs frequently very early after AMI and identifies a group of patients who are at increased risk for adverse in-hospital clinical outcomes.
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PMID:Frequency and importance of silent myocardial ischemia identified with ambulatory electrocardiographic monitoring in the early in-hospital period after acute myocardial infarction. 230 Dec 53

The large mass of fixed macrophages resident in the liver make it a potentially rich source of cytokines. We have previously demonstrated that an isolated and severe ischemia/reperfusion injury to the liver results in cytokine release, specifically tumor necrosis factor alpha, and that TNF is then involved in the development of pulmonary pathology. This study was designed to determine the kinetics of TNF release following varying periods of hepatic ischemia and to further investigate the acute lung injury that follows. Suprahepatic blood samples were obtained at serial time points following a 45-, 60-, 75-, or 90-min ischemic insult to a segment of the rat liver with subsequent reperfusion. Using a bioassay based on the WEHI 164 cell line, plasma TNF levels were measured in all experimental animals; sham-operated control animals had undetectable levels. Changes in pulmonary capillary permeability were then measured using a standard 125I-labeled albumin washout technique following a 90-min ischemic insult with subsequent reperfusion. A significant increase in the mean permeability index was observed 9 to 12 hr following hepatic reperfusion (.601 +/- 102 as compared with .114 +/- .085 in sham-operated controls, P less than 0.005). Animals treated with anti-TNF antiserum prior to the induction of hepatic ischemia had a significantly reduced pulmonary capillary leak compared to animals pretreated with rabbit serum without TNF-blocking properties (.184 +/- .029 versus .694 +/- 052 for the control serum, P less than 0.005). TNF release follows both moderate and severe ischemic injury to the liver and the results reported here implicate TNF as an important mediator of increased pulmonary capillary permeability. These experiments confirm previous histologic studies that demonstrated pulmonary edema and intra-alveolar hemorrhage following hepatic ischemia/reperfusion, with subsequent blockade of the histologic injury by pretreatment with anti-TNF antiserum.
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PMID:The production of tumor necrosis factor alpha and the development of a pulmonary capillary injury following hepatic ischemia/reperfusion. 230 55

Obstruction of pulmonary arterial blood flow results in minimal biochemical and/or morphological changes in the involved lung. If the lung is reperfused, a syndrome of leukopenia and lung edema occurs. We used the radiolabeled microsphere technique to measure the response of the bronchial circulation in rabbits to acute pulmonary artery occlusion (PAO) and to pulmonary artery reperfusion. We found that the bronchial blood flow (Qbr) decreased from a base line of 0.37 +/- 0.10 to 0.09 +/- 0.04 (SE) ml.min-1.g dry lung-1 (P less than or equal to 0.05) after 4 h of PAO. In a separate group of animals, Qbr 24 h after PAO remained low (0.20 +/- 0.07 ml.min-1.g dry lung-1, P = 0.06). Qbr during PAO was inversely correlated with the wet-to-dry ratio after reperfusion (r = -0.68, P = 0.06). Qbr did not change during 4 h of reperfusion. We speculate that a critical level of Qbr may be necessary during PAO to prevent ischemia/reperfusion injury from occurring.
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PMID:Bronchial circulation in pulmonary artery occlusion and reperfusion. 231 50

In order to know the regularity of forming edema after thermal injury, we performed experiments of pulmonary edema in isolated lobes with steam and obtained direct continuous measurements of transudation as it occurs. Transvascular flux (Qf) and gain weight (Gw) of the lobe increased immediately and the peak value of exudation occurred within half an hour after inhalation injury. Studies in protein content, colloid osmotic pressure of bronchus exudate and water content of lung, reconfirmed increase in pulmonary capillary permeability. Marked hemoconcentration was revealed. Plasma leaked 145 ml (32.5%), plasma protein leaked 2.9 g (15%) during the experiment. According to pressure of artery (Pa), vein (Pv), arterial occlusion (Pao), venous occlusion (Pvo), double occlusion (Pdo) and blood flow through the lobe (QT), the total vascular (Rt) arterial (Ra), middle compartment (Rmid), and venous (Rv) resistances were calculated. All the resistances indicated an increase and QT showed a decrease after inhalation injury. The experimental results suggested that tissue ischemia is significant after thermal injury and resuscitation should be started as early as possible and should include whole blood or plasma in resuscitation regimes during burn shock phase.
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PMID:[Pulmonary edema in an isolated lobe after inhalation injury]. 239 33

Pulmonary hypoperfusion/ischemia-reperfusion (I/R) may initiate ARDS (nonhydrostatic pulmonary edema). Endothelial damage via xanthine oxidase (XO)-derived oxygen radicals (O2*) may mediate I/R injury. We previously documented Factor VIII antigen (F8) as a marker for endothelial injury. The purpose of this study was to (1) document I/R-induced nonhydrostatic pulmonary edema, (2) identify whether XO or O2* mediates nonhydrostatic edema, and (3) identify the site of injury (? endothelium). Rat lungs were isolated, ventilated, and perfused (100 min, control, or 40 min at 37 degrees C, I (static vent.), + 60 min, R). Effluent was analyzed for F8 release (ELISA: data relative to control). Tungsten-fed rats had negligible lung XO vs rats fed standard diet (3.6 vs 34.5 mU/g, (P less than 0.05). Catalase (CAT) 50 micrograms/ml) was added to perfusate prior to R. Sectioned lungs were fluorescein anti-F8 photographed (IF) and qualitatively assessed. (Table: see text). We conclude that (1) pulmonary hypoperfusion (I/R) leads to nonhydrostatic pulmonary edema, and (2) the edema results in part from XO-generated O2* directed at the capillary endothelium.
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PMID:Xanthine oxidase-derived oxygen radicals induce pulmonary edema via direct endothelial cell injury. 249 87

The reimplantation response after lung transplantation may critically impair the function of transplanted lungs in the early postoperative period. The purpose of this study is to evaluate the factors which cause this reimplantation response. Using canine left lungs, four groups were studied. Group I underwent complete hilar stripping (n = 6). Group II underwent complete hilar stripping and kept in warm ischemia for 60 min. by clamping left pulmonary artery and veins (n = 6). Group III underwent the same surgery as Group II and administered superoxide dismutase (SOD) (12000 U/kg/h) during reperfusion (n = 7). Group IV underwent autotransplantation of left lung (n = 6). To evaluate the function of left lung, arterial blood gas, pulmonary arterial pressure, aortic pressure, cardiac output and left extravascular lung water (liter EVLW) were measured in a transient contralateral pulmonary arterial occlusion before operation and 60 min. after reventilation and reperfusion. The measurement of EVLW was performed by thermal-green dye double indicator dilution method. The results obtained were as follows. 1) The values of liter EVLW measured in rt. pulmonary arterial occlusion were extremely well correlated with those of both lung EVLW. (r = 0.943 p less than 0.001). 2) The ratios of postoperative-liter EVLW: preoperative-liter EVLW and postoperative-total pulmonary resistance (TPR): preoperative-TPR were as follows: Group I; 1.29 +/- 0.19 and 1.23 +/- 0.36, Group II; 1.85 +/- 0.49 and 1.69 +/- 0.36, Group III; 1.28 +/- 0.17 and 1.50 +/- 0.36 Group IV; 2.28 +/- 0.40 and 1.70 +/- 0.34. These data indicate that the most important factor of reimplantation response at the time of this acute phase is the oxygen free radical-induced reperfusion injury. Hilar stripping, ischemic injury and surgical trauma are also important factors of reimplantation response. Vascular anastomosis is not so important when it is done well technically. 3) Administration of SOD provides protection against lung edema after lung transplantation.
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PMID:[Experimental studies on reimplantation response after lung transplantation]. 250 45


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