Blood-brain barrier opening after explosive decompression from hyperbaric N2-O2 mixtures.
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Biomedical subjects
Publications and source records attributed to S P Gruenau.
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The effects of adaptation to cold, hypoxia, or exercise on hyperbaric decompression tolerance were investigated in two factorial experiments. For either 14 or 28 days, groups of mice were handled (control); exposed discontinuously for 4 h to cold (4 degrees C) or hypoxia (P approximately 379 or 320 Torr); or exercised by swimming (15 min at 31 degrees C) or treadmill excursion (8.1 m/min for 1 or 1.5 h). The animals were divided into subgroups, exposed to one of three hydrostatic pressures (7.6--11.1 ATA) for 30 min, decompressed, and observed to determine survival rate or bends incidence (type II decompression sickness). Decompression sickness was significantly reduced (P less than 0.05) in the treadmill-trained animals, was unchanged in cold-exposed and swim-exercised mice, and tended to increase in animals adapted to hypoxia. Enhanced tolerance by treadmill training is presumably due to lean body conformation, which could reduce nitrogen saturation of tissues, and greater muscle capillarization and cardiovascular fitness, which may improve nitrogen elimination. Reduced tolerance with adaptation to hypoxia may be attributed to rheological changes associated with polycythemia, which facilitate bubble production.
The adrenocortical endocrine subsystem has been demonstrated to enhance mammalian tolerance to harsh environmental conditions, including hypoxia and temperature extremes. In a series of factorial experiments, mice were exposed to one of three elevated hydrostatic pressures for 30 min and then decompressed (0.75 atm/s). It was demonstrated that 1) tolerance to decompression does not differ significantly (P greater than 0.3) in surgically intact, sham adrenalectomized, or in adrenalectomized animals; 2) intraperitoneal administration of pharmacologic doses (0.4, 1.0, and 2.0 mg/mouse) or corticosterone or deoxycorticosterone acetate does not significantly enhance (P greater than 0.1) survivorship when compared to vehicle-injected controls; and 3) the incidence of decompression sickness (DS) does not fluctuate with time of day (P greater than 0.4). In a fourth study, the plasma concentration of corticosterone was quantitated in 1) colony control mice, 2) mice exposed to the 1-ATA chamber environment (chamber control), or 3) mice compressed to 3, 5, 7, 9, or 11 ATA and then decompressed. In general, plasma corticosterone in symptom-free mice was elevated approximately threefold (P less than 0.05) by exposure to the 1-ATA chamber environment and by decompression from 3 to 11 ATA. At 11 ATA, plasma corticosterone levels in decompressed mice exhibiting decompression sickness symptoms were significantly elevated (P less than 0.05) compared to the levels observed in decompressed symptom-free mice. These studies indicate that adrenocortical function does not enhance tolerance to decompression in mice.
Previous studies have demonstrated two tremorgenic systems that involve separate brain mechanisms and exhibit different peak frequencies. One system (the thalamo-cortical) generates low frequency (4--8 Hz) tremor; the other (the olivo-cerebellar) produces high frequency (10--18 Hz) tremor. Based on this evidence, the present study focused on determining whether one or both of these tremor systems is involved in the high pressure nervous syndrome (HPNS). Specifically, the concern was to identify and to quantify amplitude and frequency characteristics of HPNS tremor in 8 guinea pigs breathing helium-oxygen during compression (40 ft/min) in a chamber dive to 61.6 ATA (2000 fsw) with a bottom time of 1 h. Rectal temperature was recorded and maintained at 39 degrees C +/- 1 degree. Leg tremor was recorded by magnetic inductance and stored on magnetic tape for power spectral analysis. Frequency histograms of the tremor data revealed development of a biphasic response. From surface to about 31.3 ATA (1000 fsw), a low-power, single, 4- to 6-Hz component was evident, which resembled fine or moderate tremor. Between 34.3 ATA (1100 fsw) and 61.6 ATA, a 12- to 18-Hz component emerged abruptly with a dramatic increase in power, which reflected coarse, uncontrollable tremors. In the first 5 to 10 min after the animals arrived at maximum pressure, relative power of the high frequency component dropped to and remained near base-line levels. These results support the hypothesis that HPNS tremor consists of two components and possibly two separate tremor systems.
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Visual evoked responses (VER'S) were recorded from the cortex of immature Weddel seals, 3-365 days of age. Results indicated a high degree of maturity at birth evident from the multiphasic array of waveforms and the comparatively short onset latency of the VER. At low intensities, single flashes evoked an immature secondary response. Topographical distribution of VER's were confined largely to the gyrus immediately adjacent to midline, from the posterior aspect near lambda to the vertex. Recordings from CI-744 dosed seals displayed a well-demarcated developmental sequence of VER's, contrary to VER's recorded in flaxedilized seals. Onset latency and waveform configuration changed concomitantly as a function of age. During the postnatal period from birth to weaning, VER changes were related to major behavioral events such as the seal's first encounter with swimming and diving at 2 weeks of age and weaning at 6 weeks of age.