The effect of varying the pressure/time profile upon development of tremors and convulsions of the high-pressure neurological syndrome was studied in adult mice and squirrel monkeys and in baby mice. Two distinct response patterns were observed. In the adults rapid compression produces early onset of convulsions; convulsions subside rapidly when animals are held at constant pressure just above the convulsion point; and interrupted compression schedules show that total compression time rather than instantaneous compression rate at the moment seizures develop is the controlling parameter. Baby mice up to 12 days of age, by contrast, fail to show any perceptible relation between compression rate and convulsion threshold pressure (Pc); their seizures continue for a considerable period of time after a constant pressure level just above the convulsion threshold has been reached; and interrupted compressions of type a fail to change their convulsion threshold. Together with supplementary data regarding tremor thresholds and the transient increase of convulsion thresholds by prior seizures these results lead to a proposed schema describing these phenomena in terms of a pressure-dependent primary event predisposing to tremors and convulsions; a time-dependent event counteracting the convulsions (absent in baby mice); and a transient effect of prior convulsions, raising subsequent Pc.
An interrupted compression profile technique was used to develop data to separate the effects of time and pressure factors governing increase of high-pressure neurological syndrome (HPNS) convulsion threshold pressures (the compression rate effect) during different compression profiles. A single differential equation fits all data available to date for compression rate effect on convulsion thresholds of CD-1 mice (three distinct types of compression profile; mean compression rates 12-1,000 atm/h). The process leading to increase in HPNS convulsion pressure is initiated at the very beginning of compression, proceeds at increasingly rapid rates as higher pressures are attained, and approaches a limiting upper convulsion pressure. The convulsion threshold pressure in any given experiment is independent of the compression rate prevailing during the time immediately preceding onset of the seizure. The magnitude of the compression rate effect in the CD-1 mouse is independent of chamber temperature over a range of 27-36 degrees C, and rectal temperatures of 29.2-37.5 degrees C. The bearing of these results on the design of optimal compression schedules and on the analysis of the neurological mechanisms underlying the HPNS is discussed.
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