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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Daily resting and exercise electrocardiograms from 81 healthy subjects taking part in eight different air saturation chamber experiments at depths of 2-132 ft sea water gauge (fswg) were recorded and interpreted. Scalar and planar characteristics were measured and analyzed in addition to noting changes in rhythm. Of the measured variables, only the heart rate and QT-interval changed significantly in the majority of exposures. Heart rate decrements of 14%-23% were observed, generally with normalization after several days at depth, and in some cases a rebound immediately postexposure. The observed increase in QT-interval can be explained entirely by the bradycardia, which seems to be due to a combination of pressure, hyperoxia, and a chamber effect. Further distinction among these factors was not possible. Associated with the decrements in heart rate were asymptomatic supraventricular arrhythmias, generally AV-nodal escape rhythms or beats, in 10% of the subjects. One incident of symptomatic ventricular tachycardia was noted 20 h after surfacing during an exercise test. Otherwise, only infrequent, isolated premature ventricular beats were detected at depth, but were not more frequent than in the predive periods. These findings are consistent with the premise that exposure to hyperbaric air and other nitrogen-oxygen mixtures causes an increase in parasympathetic tone of sufficient magnitude to cause cardiac arrhythmias. That autonomic imbalance in diving activities may cause more malignant arrhythmias is discussed.
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PMID:Cardiac arrhythmias and heart rate changes in prolonged hyperbaric air exposures. 608 26

VEGF signaling inhibition decreases alveolar and vessel growth in the developing lung, suggesting that impaired VEGF signaling may contribute to decreased lung growth in bronchopulmonary dysplasia (BPD). Whether VEGF treatment improves lung structure in experimental models of BPD is unknown. The objective was to determine whether VEGF treatment enhances alveolarization in infant rats after hyperoxia. Two-day-old Sprague-Dawley rats were placed into hyperoxia or room air (RA) for 12 days. At 14 days, rats received daily treatment with rhVEGF-165 or saline. On day 22, rats were killed. Tissue was collected. Morphometrics was assessed by radial alveolar counts (RAC), mean linear intercepts (MLI), and skeletonization. Compared with RA controls, hyperoxia decreased RAC (6.1 +/- 0.4 vs. 11.3 +/- 0.4, P < 0.0001), increased MLI (59.2 +/- 1.8 vs. 44.0 +/- 0.8, P < 0.0001), decreased nodal point density (447 +/- 14 vs. 503 +/- 12, P < 0.0004), and decreased vessel density (11.7 +/- 0.3 vs. 18.9 +/- 0.3, P < 0.001), which persisted despite RA recovery. Compared with hyperoxic controls, rhVEGF treatment after hyperoxia increased RAC (11.8 +/- 0.5, P < 0.0001), decreased MLI (42.2 +/- 1.2, P < 0.0001), increased nodal point density (502 +/- 7, P < 0.0005), and increased vessel density (23.2 +/- 0.4, P < 0.001). Exposure of neonatal rats to hyperoxia impairs alveolarization and vessel density, which persists despite RA recovery. rhVEGF treatment during recovery enhanced vessel growth and alveolarization. We speculate that lung structure abnormalities after hyperoxia may be partly due to impaired VEGF signaling.
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PMID:Recombinant human VEGF treatment enhances alveolarization after hyperoxic lung injury in neonatal rats. 1590 74

Bronchopulmonary dysplasia is a chronic lung disease of extreme preterm infants and results in impaired gas exchange. Although bronchopulmonary dysplasia is characterized histologically by alveolar-capillary simplification in animal models, it is clinically defined by impaired gas diffusion. With the use of a developmentally relevant model, we correlated alveolar-capillary structural simplification with reduced functional gas exchange as measured by the diffusing factor for carbon monoxide (DFCO). Neonatal mouse pups were exposed to >90% hyperoxia or room air during postnatal days 0 to 7, and then all pups were returned to room air from days 7 to 56. At day 56, DFCO was measured as the ratio of carbon monoxide uptake to neon dilution, and lungs were fixed for histologic assessment of alveolar-capillary development. Neonatal hyperoxia exposure inhibited alveolar-capillary septal development as evidenced by significantly increased mean linear intercept, increased airspace-to-septal ratio, decreased nodal density, and decreased pulmonary microvasculature. Importantly, alveolar-capillary structural deficits in hyperoxia-exposed pups were accompanied by a significant 28% decrease in DFCO (0.555 versus 0.400; P < 0.0001). In addition, DFCO was highly and significantly correlated with structural measures of reduced alveolar-capillary growth. Simplification of alveolar-capillary structure is highly correlated with impaired gas exchange function. Current mechanistic and therapeutic animal models of inhibited alveolar development may benefit from application of DFCO as an alternative physiologic indicator of alveolar-capillary development.
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PMID:Relationship of structural to functional impairment during alveolar-capillary membrane development. 2566 Nov 10