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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have developed a model of reperfusion injury in Krebs buffer-perfused rabbit lungs, characterized by pulmonary vasoconstriction, microvascular injury, and marked lung edema formation. During reperfusion there was a threefold increase in lung superoxide anion (O2-) production, as measured by in vivo reduction of nitroblue tetrazolium, and a twofold increase in the release of O2- into lung perfusate, as measured by reduction of succinylated ferricytochrome c. Injury could be prevented by the xanthine oxidase inhibitor allopurinol, the O2- scavenger SOD, the hydrogen peroxide scavenger catalase, the iron chelator deferoxamine, or the thiols dimethylthiourea or N-acetylcysteine. The protective effect of SOD could be abolished by the anion channel blocker 4,4'-diisothiocyano-2,2'-stilbene disulfonic acid, indicating that SOD consumes O2- in the extracellular medium, thereby creating a concentration gradient favorable for rapid diffusion of O2- out of cells. Our results extend information about the mechanisms of reperfusion lung injury that have been assembled by studies in other organs, and offer potential strategies for improved organ preservation, for treatment of reperfusion injury after pulmonary thromboembolectomy, and for explanation and therapy of many complications of pulmonary embolism.
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PMID:Role of reactive oxygen species in reperfusion injury of the rabbit lung. 246 23

Ischemia/reperfusion mechanisms contribute to lung injury after transplantation, pulmonary embolism, and resolution of atelectasis. Alveolar tissue becomes hypoxic and deprived of substrate only when both ventilation and perfusion are interrupted, a situation modeled in vivo by complete, unilateral lung collapse. Because previously hypoxic mitochondria may be an important intracellular source of superoxide and hydrogen peroxide (H2O2) during reperfusion and re-oxygenation, the authors, in this study, investigated whether mitochondrial H2O2 release changed as a result of lung hypoxia/hypoperfusion resulting from collapse. Mitochondria were isolated from hypoxic (previously collapsed) right or contralateral left rabbits' lungs and from control rabbits' lungs. Mitochondrial H2O2 release, a marker of superoxide production, was measured fluorometrically after incubation with or without 1 mmol/L cyanide and 0.1 mmol/L nicotinamide adenine dinucleotide. Mitochondrial recovery was determined by assaying succinate dehydrogenase activity in mitochondrial preparations and lung homogenates. Lung succinate dehydrogenase activity and mitochondrial recovery were comparable among groups. Calculated lung mitochondrial content did not change (control subjects: left 7.9 +/- 0.5, right 13.8 +/- 1.7; hypoxic: left 10.3 +/- 1.3, right 10.5 +/- 2.4, all mg mitochondrial protein/lung). Mitochondria released hydrogen peroxide at approximately 5.6 nmol/h/mg pro in buffer alone and 14.8 nmol/h/mg pro in buffer with cyanide and nicotinamide adenine dinucleotide. However, lung collapse and resulting hypoxia caused no change in mitochondrial number or capacity to release H2O2 in vitro. Based on these findings, it is suggested that other sources of reactive oxygen metabolites, including xanthine oxidase and activated neutrophils, contribute to the oxidant injury observed in this model.
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PMID:Hydrogen peroxide release by mitochondria from normal and hypoxic lungs. 794 83

A male patient, who had had a conservatively treated hemorrhagic peptic ulcer 12 years earlier, underwent gastrocystoplasty after radical cystoprostatectomy for carcinoma of the urinary bladder. After operation the patient suffered urinary incontinence and dysuria which he found so bothersome that the gastric bladder was converted to diversion using the same gastric segment as a tube. Postoperatively there were clots of blood in stomal urine and after the kidneys had been drained intestinal fluid oozed from the stoma. On the 14th postoperative day the patient died of pulmonary embolism. The autopsy showed a perforated peptic ulcer in the gastric segment resulting in a closed fistula to the small bowel. Most probably the reason for development of the peptic ulcer was stress caused by the operation and it might have been avoided by using hydrogen-blocking agents. This case seriously questions whether a gastric segment should be used in the urinary tract at all, and at least it should never be used as a conduit.
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PMID:Ulcer perforation in gastric urinary conduit: never use a gastric segment in the urinary tract if there are other options available. 1081 Feb 73

Hydrogen peroxide is widely used for irrigation of surgical wounds. However, its administration has been associated with gas embolism. We report a case of gas embolism after wound irrigation with hydrogen peroxide in a 11-year-old boy undergoing extraction of the extra-traumatic splint under general anesthesia. When 3% hydrogen peroxide 12 ml was applied to wound of the left femur after extraction of the splint, the patient showed clinical signs of pulmonary embolism. Symptomatic treatment was initiated immediately. When the patient awoke from anesthesia, he showed tonic convulsion. But he recovered without any complications. The administration of hydrogen peroxide into a closed tissue is contraindicated during surgery.
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PMID:[Oxygen embolism after intraoperative use of hydrogen peroxide]. 1260 76