Mekjavić I B, Kakitsuba N
School of Kinesiology, Simon Fraser University, Burnaby, British Columbia, Canada.
Undersea Biomed Res. 1989 Sep;16(5):391-401.
Temperature of the tissue affects the many components involved in the formation of tissue gas phase formation: diffusion, perfusion, and inert gas solubility. Since the effects of perfusion and inert gas solubility may be counteracting in terms of enhancing growth of gas bubbles, the optimal thermal status of divers throughout a dive remains unresolved. To elucidate the role of peripheral body temperature on gas phase formation, four subjects were exposed to a 10 degree and 40 degree C environment for 3 h on two separate occasions, after a no-stop decompression from a 12-h dive to 9.14 m (30 fsw) on air. The 3-hour exposures to either a cold or warm air environment resulted in a significant difference in mean skin temperature (P less than or equal to 0.01) with no alteration in rectal temperature. Total peripheral resistance during the 10 degree C exposure was 13.8 +/- 1.9 mmHg.liter-1.min-1 and significantly higher than that observed during the 40 degree C exposure (10.4 +/- 3.5 mmHg.liter-1.min-1). Gas bubbles in the venous return were monitored with a Doppler ultrasonic transducer placed in the precordial region, both at rest and after a deep knee bend. Venous bubbles were only detected in 1 subject following the warm air exposure, whereas 3 of the 4 subjects developed Doppler-detectable bubbles during the cold air exposure. Although both the cold and warm air exposures (3 h postdecompression) were uneventful, a hot shower taken by the subjects on completion of the cold air exposure (6 h postdecompression) precipitated mild type I symptoms of decompression sickness. These symptoms were not present after a hot shower following the warm air exposure. The present results indicate that despite the assumed greater inert gas solubility of tissues expected during cold air exposure, the decrease in the perfusion may have played a more significant role in the observed levels of detectable venous gas bubbles. Development of type I symptoms following a 12-h saturation, a 3-h cold exposure, and a subsequent hot shower suggests that a rapid rise in peripheral temperature may cause a significant rise in tissue gas tension. This increase in tension does not seem to be sufficiently reduced by increased perfusion to the tissues to prevent bubble formation.
扩散、灌注以及惰性气体溶解度。由于灌注和惰性气体溶解度在促进气泡生长方面的作用可能相互抵消,潜水过程中潜水员的最佳热状态仍未明确。为了阐明外周体温对气相形成的作用,四名受试者在两次分别的情况下,在从12小时潜水至9.14米(30英尺海水深度)并进行无停留减压后,暴露于10摄氏度和40摄氏度的环境中3小时。在3小时内暴露于冷空气或暖空气环境导致平均皮肤温度出现显著差异(P小于或等于0.01),而直肠温度没有变化。在10摄氏度暴露期间,总外周阻力为13.8±1.9 mmHg·升⁻¹·分钟⁻¹,显著高于在40摄氏度暴露期间观察到的数值(10.4±3.5 mmHg·升⁻¹·分钟⁻¹)。使用置于心前区的多普勒超声换能器在静息状态和深膝弯曲后监测静脉回流中的气泡。在暖空气暴露后,仅在1名受试者中检测到静脉气泡,而在冷空气暴露期间,4名受试者中有3名出现了多普勒可检测到的气泡。尽管冷空气和暖空气暴露(减压后3小时)均无异常情况,但在冷空气暴露结束时(减压后б小时)受试者洗热水澡引发了轻度I型减压病症状。在暖空气暴露后洗热水澡则未出现这些症状。目前的结果表明,尽管在冷空气暴露期间预计组织中惰性气体溶解度会更高,但灌注的减少可能在观察到的可检测静脉气泡水平中发挥了更重要的作用。在12小时饱和、3小时冷暴露以及随后洗热水澡后出现I型症状表明,外周温度的快速升高可能导致组织气体张力显著升高。这种张力的增加似乎没有通过增加组织灌注充分降低以防止气泡形成。