Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether altered airway smooth muscle contractility contributes to airway hyperreactivity resulting from hyperoxic exposure, in vitro contractile responses of airways to two physiological constrictors, acetylcholine (10(-9) to 10(-4) M) and histamine (10(-8) to 10(-4) M), were examined. Extrathoracic trachea, intrathoracic trachea, and bronchus from 1- to 2-day-old (newborn) guinea pigs exposed to 85% oxygen for 84 h were compared with tissues obtained from newborns reared in room air. Responses in the presence and absence of aspirin (ASA; 10(-3) M) were compared. Hyperoxic exposure did not affect the histology of the airway epithelia. Contractile responses to acetylcholine and histamine were similar. Without ASA, maximal tensions generated were higher in both extrathoracic and intrathoracic trachea obtained from hyperoxia-exposed neonates than in trachea from newborns reared in room air. ASA caused maximal tensions of trachea from newborns reared in room air to increase but did not affect the already increased contractility of trachea from hyperoxia-exposed animals; the tensions achieved in hyperoxic tissues with and without ASA were similar to the hyperactive responses induced by ASA in tissues from animals reared in room air. Bronchi showed responses similar to those seen in tracheal segments. Thus, despite no apparent histological effect on the airway epithelium, hyperoxic exposure seems to increase airway smooth muscle contractility, is nonspecific for different constricting agents, and shows no regional differences in airway reactivity.
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PMID:Hyperoxic exposure enhances airway reactivity of newborn guinea pigs. 836 64

A giant hemangioma of the tongue was resected in a 16-year-old otherwise healthy young man (ASA I). Despite a total blood loss of 4,300 ml, corresponding to 105% of the patients intravascular blood volume, no allogeneic red blood cells had to be transfused intraoperatively. Besides minimization of intraoperative blood loss with preoperative alcohol injections into the tumor, ligation of large tumor-perfusing arteries, application of fibrin glue, skillful surgical technique, positioning of the surgical field above the level of the heart, controlled hypotension and maintenance of normothermia, acute normovolemic hemodilution (augmented by preoperative administration of recombinant human erythropoetin - rhEpo) and autotransfusion of lost blood were used for recovery of autologous blood. Under the protection of hyperoxia, a decrease of the hemoglobin (Hb) concentration to 4.2 g/dl was bridged by extreme normovolemic hemodilution. No signs of immanent or manifest tissue hypoxia were encountered. Retransfusion of autologous red blood cells was only started when surgical control of bleeding was achieved. Additionally a total of 4 units of fresh frozen plasma were infused for stabilization of plasma coagulation. After a 9-hour surgical duration, the patient was transferred to the intensive care unit, normotensive (with low-dose infusion of norepinephrin) and normothermic with a Hb concentration of 5.6 g/dl. In the face of an increasing lactacidosis 2 units of packed red blood cells were transfused on post surgical day 1.
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PMID:[Giant hemangioma of the tongue: combined use of perioperative blood conservation procedures]. 1239 34

The synthesis of adrenal steroids requires molecular oxygen. Because arterial hypoxemia is a common clinical condition, the purpose of the present study was to examine steroidogenesis in vitro under physiological changes in O(2) tension (Po(2)) in cells from human adrenal glands with aldosterone-secreting adenomas (ASA; n=3) or with bilateral adrenal hyperplasia causing Cushing's syndrome (n=4). A decrease in Po(2) from 150 mmHg (mild hyperoxia) to 80 mmHg had minimal effect on steroid production. A reduction to 40 mmHg (still well within the physiological range) significantly inhibited cAMP- and ACTH-stimulated aldosterone, cortisol, and dehydroepiandrosterone (DHEA) production from ASA. Furthermore, cortisol and DHEA production in cells from histologically normal tissue, adjacent to ASA and from bilateral adrenal hyperplasias, was also inhibited under a Po(2) of 40 mmHg. We conclude that physiological decreases in Po(2) to levels typical for adrenal venous Po(2) under mild hypoxia inhibit steroidogenesis. These studies may have implications for oxygen therapy in critically ill patients with functional adrenal insufficiency, as well as for therapeutic options in patients with adrenal neoplasms.
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PMID:Steroidogenesis in human aldosterone-secreting adenomas and adrenal hyperplasias: effects of hypoxia in vitro. 1610 60