Ornhagen H C
Undersea Biomed Res. 1979 Mar;6(1):27-39.
The beating frequency (BF) reducing effect of 150 atm of hydrostatic pressure on mammalian cardiac pacemaker tissue (hyperbaric bradycardia) was counteracted by dissolved gas only if the gas was added after hydrostatic compression. The effect on BF seemed to be related to the narcotic potency of the gas and the effect was reversible. The gases tested were N2O, N2, Ne, and He, in decreasing order of potency. If N2O was added at a moderately raised ambient pressure prior to hydrostatic compression to 150 atm, there was no difference in the degree of hyperbaric bradycardia, compared to compression without gas. During decompression, however, experiments performed with gas showed a significantly higher gain in BF compared to experiments without gas. Autonomic blockade seemed to eliminate the difference between decompression with and without N2O. The results demonstrate that N2O, N2, and Ne, and to a small extent He, may counteract the retarding effect that increased hydrostatic pressure has on cardiac pacemaker activity. These effects on the cardiac pacemaker are similar both to the effects of increased hydrostatic pressure and of gases at elevated pressures on the central nervous system, but some important differences remain to be explained.
只有在静水压力压缩后添加溶解气体时,150个大气压的静水压力对哺乳动物心脏起搏器组织的心跳频率(BF)降低作用(高压性心动过缓)才会被抵消。对BF的影响似乎与气体的麻醉效力有关,且这种影响是可逆的。所测试的气体为N2O、N2、Ne和He,效力依次降低。如果在静水压力压缩至150个大气压之前,在适度升高的环境压力下添加N2O,与无气体压缩相比,高压性心动过缓的程度没有差异。然而,在减压过程中,有气体参与的实验显示,与无气体实验相比,BF的增加幅度显著更高。自主神经阻滞似乎消除了有N2O和无N2O减压之间的差异。结果表明,N2O、N2和Ne,以及在较小程度上的He,可能抵消静水压力增加对心脏起搏器活动的延迟作用。这些对心脏起搏器的影响与静水压力增加以及高压下气体对中枢神经系统的影响相似,但一些重要差异仍有待解释。