急性暴露于3atm腹肌空气中的人对直立倾斜的心血管反应。

Undersea biomedical research Pub Date : 1992-03-01
S Sagawa, K Miki, F Tajima, K Shiraki
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引用次数: 0

摘要

为了研究急性高压暴露对心血管直立反应的影响,对8名男性受试者在环境温度为31℃(热中性)的3个大气压的模拟压缩空气高压环境中进行了15分钟的被动70度平头倾斜(HUT)试验。在HUT前、中、后15 min测量心率(HR)、血压、心输出量(CO)、闭塞容积描记术测量前臂血流量(FBF)、激光多普勒皮肤血流量(BFLD)。连续记录食管温度和心率。在29摄氏度(热中性)的正常大气条件下进行相同的测试。在两种环境下,没有受试者在HUT期间出现晕厥的迹象。两种大气压下,3atm时基线HR显著降低(P < 0.05), HUT期间HR (δ HR)增加幅度相同(15次/分)。两种环境下收缩压(δ收缩压)的降低是相同的。因此,对HUT (δ HR/ δ收缩压)的变时反应是相同的。显著减少CO (P小于0.05)是由于减少中风的体积在小屋,和减少更大(P小于0.05)3 atm abs。没有与压力有关的变化在巴西利亚足协收入囊中的小屋,前臂血管阻力,BFLD除了更增加(P小于0.05)在总外周阻力3 atm abs。这些观测结果表明,直立的宽容是保持在较低的公司在3 atm abs,可能是由内脏区域的血管收缩反应引起的。我们得出的结论是,3atm腹肌时发生的严重心动过缓并不会干扰人体对直立的正常反应,因为3atm腹肌HUT期间发生的氧压升高引起的外周血管收缩和总外周阻力的增强。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cardiovascular responses to upright tilt in man during acute exposure to 3 atm abs air.

To examine the effect of acute hyperbaric exposure on cardiovascular response to orthostasis, a passive 70 degrees head-up tilt (HUT) test was performed for 15 min in a simulated compressed-air hyperbaric environment of 3 atm abs at ambient temperature of 31 degrees C (thermoneutral) on 8 male subjects. Heart rate (HR), blood pressure, cardiac output (CO) by impedance cardiography, forearm blood flow (FBF) by the occlusion plethysmography, and laser-Doppler skin blood flow (BFLD) on the thigh were measured for 15 min before, during, and after HUT. Esophageal temperature and HR data were recorded continuously. An identical test was performed in a 29 degrees C (thermoneutral) normal atmospheric condition. None of the subjects showed signs of syncope during HUT in either environment. Baseline HR was significantly lower (P less than 0.05) at 3 atm abs, and the increase in HR (delta HR) during HUT was of the same magnitude (15 beats/min) at both atmospheric pressures. The reduction of systolic blood pressure (delta SBP) was identical in both environments. Thus, the chronotropic response to HUT (delta HR/delta SBP) was the same. A marked reduction in CO (P less than 0.05) was attributed to a reduction of stroke volume during HUT, and the reduction was greater (P less than 0.05) at 3 atm abs. There were no pressure-dependent changes during HUT in FBF, forearm vascular resistance, and BFLD except for a greater increase (P less than 0.05) in total peripheral resistance at 3 atm abs. These observations suggest that orthostatic tolerance was maintained in the presence of lower CO at 3 atm abs, probably by a greater vasoconstrictor response in the splanchnic areas. We conclude that the substantial bradycardia which occurred at 3 atm abs did not interfere with a normal response to orthostasis in humans because of a peripheral vasoconstriction caused by the elevated oxygen pressure and an enhanced increase in total peripheral resistance which occurred during HUT in 3 atm abs.

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