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)

Recent work with isolated blood vessels has emphasized the importance of intact endothelium when the relaxation of vascular smooth muscle is induced by acetylcholine (ACh). However, the physiologic significance of this endothelial-dependent ACh response in a complete organ circulation is unclear. We questioned whether diminished ACh vasodilation would result from damage of lung vascular endothelium and whether this response could be used as an indication of endothelial injury. We therefore induced pulmonary endothelial cell injury in one rat model by repeated injections of alpha-naphthyl thiourea (ANTU) and in a second rat model by exposing rats for 52 h to 100% oxygen at a barometric pressure of 760 torr (hyperoxia). Rats injected with Tween 80, the solvent for ANTU, or exposed to ambient Denver air served as the respective control animals. The isolated lungs of these rats were perfused with a recirculating cell- and plasma-free, physiological salt solution to study the effect of ACh or NaCl infusion on pulmonary perfusion pressure and vascular responsiveness. ANTU-treated rats demonstrated an intact vasodilatory response after ACh infusion when compared with the solvent control animals. The immediate pulmonary vasodilation after ACh infusion was slightly enhanced in the hyperoxic rat lung when compared with the rats exposed to ambient air, but there was no difference between these groups in the prolonged depression of vascular responsiveness to hypoxia or angiotensin II. Thus, in both models of lung endothelial cell injury, the pulmonary vascular responses to ACh were intact.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acetylcholine-induced pulmonary vasodilation in lung vascular injury. 300 69

To evaluate whether alpha-naphthylthioura (ANTU) protects against hyperoxic injury to the pulmonary endothelium, we monitored survival and serotonin uptake by the lungs of ANTU-treated rats (5 mg/kg) and Tween 80-treated control rats exposed to 100% O2 or air at 1 atmosphere absolute. Exposure to 100% O2 for 24 h or 48 h significantly depressed serotonin uptake in control rats. Serotonin uptake in ANTU-treated rats compared with that in control rats exposed to air for 24 or 48 h was also significantly depressed. However, serotonin uptake by the lungs of ANTU-treated rats exposed to 100% O2 for 48 h was significantly greater than uptake by control lungs similarly exposed to O2. Nine of 14 ANTU-treated rats were alive after 7 days of exposure to 100% O2, and serotonin uptake by the lungs of survivors had returned to control values (3.29 +/- 0.25). In contrast, only 1 of 14 control rats survived and serotonin uptake was 1.17 in this lone survivor. These results indicate that ANTU injuries pulmonary endothelial cells but protects against subsequently hyperoxic injury. This protection may account for the reduced mortality in ANTU-treated rats exposed to hyperoxia.
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PMID:Alpha-naphthylthiourea (ANTU) protects against hyperoxic depression of pulmonary serotonin uptake. 621 77