快速减压后大鼠模型视网膜电生理的变化

目的 观察快速减压(RD)后大鼠视网膜电图(ERG)的变化,并探讨减压病造成视网膜早期功能损伤的特点。方法 20只大鼠按数字表法随机分为4组,分别为正常对照(NC)组、安全减压(SD)组、快速减压处理后0 h(RD0)组和6 h(RD6)组,SD组、快速减压处理各组大鼠暴露于加压舱内,舱内气压在30 s内升至1.0 MPa,维持5.5 min,快速减压各组打开放气阀用55 s减至常压,SD组采用动物安全减压方案减到常压。按照国际临床视觉电生理学会的标准化方案,采用国特医疗系统和银-氯化银角膜电极以及银针电极对大鼠进行暗视视网膜电图(Scot-ERG)、振荡电位(OPs)、明视视网膜电图(L-ERG)记录。结果 快速减压后大鼠ERGa、b波以及OPs O2波幅值降低,潜伏期明显延长。快速减压后6h,Scot-ERG b波和OPs O2波幅值增加,RD6组[b波(134.5±27.9) μV,O2波(27.1±9.2)μV]较RD0组[b波(56.5±21.1) μV,O2波(8.1±1.9) μV]高(P＜0.05)。SD组比RD0组和RD6组视网膜电活动受抑制程度轻,SD组Scot-ERG b波和OPs O2波幅值[b波(266.5±25.2) μV,02波(44.1±5.6) μV]高于快速减压后RD0组和RD6组(P＜0.05)。结论 快速减压会造成大鼠视网膜电生理异常,安全减压可有助于减轻这种功能损伤。     

模拟大深度潜艇艇员快速上浮脱险致减压病大鼠模型的建立

目的 建立稳定的模拟大深度潜艇艇员快速上浮脱险致减压病大鼠模型.方法 雄性SD大鼠80只,采用数字表法随机分为4组:正常对照组,高压暴露2、4、8 min组,每组20只.高压暴露各组置于空气加压舱内以2t/8指数速率加压至150 m,分别停留2、4、8 min后,以3m/s匀速减压至常压出舱.观察各组大鼠行为学和肺、脑、脊髓组织病理结果.结果 高压暴露2、4、8 min组大鼠出舱后均出现竖毛、搔抓、行动迟缓、反应性差等行为状态.病理结果显示,大鼠肺泡和肺间质及脊髓组织出血明显,细胞水肿,脑组织未见明显改变.暴露2、4、8 min组大鼠发病率分别为20.0％、55.0％、10.0％,死亡率分别为0、20.0％、85.0％,3个高压暴露组大鼠发病率及死亡率差异均有统计学意义(P＜0.01).由于8 min方案暴露时间过长,制备的大鼠模型出舱后死亡率较高,而2 min方案高压下停留时间不够,制备的大鼠模型发病率较低,高压暴露4 min方案大鼠死亡率低且减压病发病率高.结论 本实验以高压暴露4 min方案成功地建立了大深度潜艇艇员快速上浮脱险致减压病动物模型.     

神经减压病

综述了神经减压病的临床表现、诊断与治疗方法，讨论了Ⅰ型与Ⅱ型减压病的划分标准及对曾患过Ⅱ型减压病的飞行人员永久停飞处理的问题。     

Dehydration effects on the risk of severe decompression sickness in a swine model

BACKGROUND: Several physiological factors have been suspected of affecting the risk of decompression sickness (DCS), but few have been thoroughly studied during controlled conditions. Dehydration is a potential factor that could increase the risk of DCS. It has been suggested that hydration may enhance inert gas removal or increase surface tension of the blood. HYPOTHESIS: Dehydration increases DCS risk. METHODS: Littermate pairs of male Yorkshire swine (n=57, mean +/- 1 SD 20.6 +/- 1.7 kg) were randomized into two groups. The hydrated group received no medication and was allowed ad lib access to water during a simulated saturation dive. The dehydrated group received intravenous 2 mg x kg(-1) Lasix (a diuretic medication) without access to water throughout the dive. Animals were then compressed on air to 110 ft of seawater (fsw, 4.33 ATA) for 22 h and brought directly to the surface at a rate of 30 fsw x min(-1) (0.91 ATA x min(-1)). Outcomes of death and non-fatal central nervous system (CNS) or cardiopulmonary DCS were recorded. RESULTS: In the hydrated group (n=31): DCS=10, cardiopulmonary DCS=9, CNS DCS=2, Death=4. In the dehydrated group (n=26): DCS=19, cardiopulmonary DCS=19, CNS DCS=6, Death=9. Dehydration significantly increased the overall risk of severe DCS and death. Specifically, it increased the risk of cardiopulmonary DCS, and showed a trend toward increased CNS DCS. In addition, dehydrated subjects manifested cardiopulmonary DCS sooner and showed a trend toward more rapid death (p < 0.1). CONCLUSION: Hydration status at the time of decompression significantly influences the incidence and time to onset of DCS in this model.     

Factitious decompression sickness

The diagnosis of decompression sickness is made largely by history; there are few physical findings and no radiographic or laboratory tests to support the diagnosis. We present three cases of factitious decompression sickness in which patients fabricated an appropriate history and underwent compression therapy. Due to the potential severity of decompression sickness and the relative safety of compression therapy, the initiation of therapy must not be delayed in a case of decompression sickness. Once therapy is begun, investigation into the particulars of a suspicious case can be made.     

Spinal cord decompression sickness: a comparison of recompression therapies in an animal model

Somatosensory evoked potentials (SEP) were used in an animal model to measure spinal cord electrophysiological function. Animals were submitted to a dive profile resulting in spinal cord decompression sickness (DCS). The animals were treated after a delay allowing the lesion to consolidate. Serial measurements of SEP documented the onset, duration, and outcome of treatment. Physiological data were recorded throughout each experiment. Group A (n = 10) was recompressed to 60 fsw (feet of sea water) breathing 100% oxygen (2.8 ATA) and Group B (n = 8) was treated at 66 fsw breathing 66% oxygen (2.0 ATA). No differences were found between groups in the severity, surface interval before treatment, or the maximum effect of treatment. The maximum effect of treatment was seen by 25 min of treatment. Animals were regrouped into responders and nonresponders. The latter displayed a more rapid onset, a more severe insult, and more adverse physiological effects than the responders. The possibility of a different etiology was considered together with the failure to differentiate between the treatment groups. It was concluded that treatment B was safer but the problems of introducing a new therapeutic table outweighed the safety advantage.     

Application of a bubble formation model to decompression sickness in rats and humans.

Although decompression sickness results from bubble formation in blood or tissue, pressure schedules currently in use are essentially empirical and contain little input from cavitation theory. The recent convergence of three lines of investigation suggests that a synthesis of practice and theory may now be possible. The data consist of pressure reduction limits for gelatin, rats, and humans following steady-state exposures. From the gelatin studies, a model has been developed in which bubble formation is initiated by spherical gas nuclei stabilized by surface-active skins of varying gas permeability. We demonstrate that the model is also in good agreement with data on rats and humans over a wide range of pressures and that the model parameters assume sensible values in each case. This suggests that cavitation theory can provide a rationale for current diving practice and can serve to secure, consolidate, and extend this practice.     

高空减压病研究工作的若干进展

对高空减压病加压治疗的新经验及减压气泡检测方法的新成就进行了综述，并对下述几种情况的处理提出了相应的建议：高空上升时在空中求发病；空中发病、下降至地面时症状已消除以及下降至地面后发病的病例。对体表心前区多普勒超声气泡检测的假阳性与假阴性问题，以及视觉辅助系统与计算机辅助系统在提高检测方法的敏感性与特异性方面的作用进行了讨论。     

静脉注射全氟化碳乳剂对大鼠减压病防治作用的研究

目的 观察静脉注射全氟化碳乳剂(perfluorocarbon emulsion,PFCE)对大鼠减压病(decompression sickness,DCS)的防治作用.方法 以"700 kPa-60 min空气暴露、3 min减压"方案制备SD大鼠减压病模型,在高气压暴露前或暴露后即刻静脉注射PFCE(7 ml/kg),观察大鼠行为学(包括发病和死亡)以及肺、大脑和脊髓组织的病理变化.高气压暴露后以生理盐水处理,或者不经任何处理作为对照.结果 高气压暴露后即刻静脉注射PFCE的动物发病率(21.7%)显著低于生理盐水组(60.0%)(P<0.05)和空白对照组(66.7%)(P<0.01),死亡率(13.0%)显著低于空白对照组(42.9%)(P<0.05);大部分行为学及病理学指标显著改善(P<0.05).高气压暴露前静脉注射PFCE的动物发病率(80.0%)和死亡率(45.0%)与生理盐水组、空白对照组相比差异无统计学意义.结论 高气压暴露后即刻静脉注射PFCE对大鼠急性DCS具有良好的防治作用.     

The treatment of decompression sickness

The initial event in decompression sickness is the separation of gas from solution because of supersaturation. If this event gives rise to immediate symptoms, recompression is remarkably effective. This end-point is characteristic of joint pain, that is, Type 1 decompression sickness. Unfortunately the onset of serious Type 2 decompression sickness may be insidious and the delay may be associated with blood-brain barrier dysfunction. Pressure is less effective in the resolution of this problem than a raised partial pressure of oxygen. Standard therapy using oxygen may be associated with worsening of symptoms and air tables with recurrence. Recompression to 4 ata and the use of a mixture of 50% oxygen and 50% helium offers a good working compromise in the treatment of both serious decompression sickness and gas embolism arising in air diving, avoiding the need for a differential diagnosis. Only oxygen or helium and oxygen mixtures should be used in the therapy of decompression sickness in helium and oxygen diving. When therapy has been delayed, intravenous fluids and steroids are important adjuncts.     

Threshold altitude resulting in decompression sickness

A review of case reports, hypobaric chamber training data, and experimental evidence indicated that the threshold for incidence of Altitude Decompression Sickness (DCS) was influenced by various factors such as prior denitrogenation, exercise or rest and period of exposure, in addition to individual susceptibility. Fitting these data with appropriate statistical models has the potential for estimating the frequency of occurrence of DCS at various altitudes under different experimental conditions and allows us to examine the influence of various factors on the threshold for DCS. This approach was illustrated by logistic regression analysis on the incidence of DCS below 9,144 m (30,000 ft). Estimations using these regressions showed that under a noprebreathe, 6-h exposure, simulated extravehicular activity profile, the threshold for symptoms occurred at approximately 3,353 m (11,000 ft); while under a no-prebreathe, 2-h exposure profile with knee-bends exercise, the threshold occurred at 7,925 m (26,000 ft). These examples showed that definition of threshold altitude should be qualified by the particular combination of experimental variables under which it was observed.     

Electrocardiographic changes in serious decompression sickness

Electrocardiographic changes observed in 21 dogs suffering from spinal cord decompression sickness (DCS) are described. Changes seen included P wave peaking and P-R depression compatible with right heart strain; S-T segment and T wave changes suggestive of myocardial ischemia; and ventricular arrhythmias ranging from unifocal premature ventricular contractions to ventricular tachycardia. Compression therapy did not always restore the ECG changes promptly to normality. The changes are discussed in association with concurrent physiological events. These included pulmonary hypertension, systemic hypertension and hypotension, and cerebral DCS. Possible mechanisms ranging from local cardiac DCS or coronary gas embolism to autonomic nervous system disturbances arising from cerebral and spinal cord DCS are reviewed. It is concluded that ECG recordings should be made more often when treating clinical DCS.     

脊髓减压病大鼠神经细胞凋亡及神经生长因子的保护作用

目的探讨脊髓减压病对大鼠脊髓神经细胞凋亡的影响及神经生长因子的保护作用。方法SD大鼠随机分为正常对照组、安全减压组、生理盐水组和神经生长因子治疗组，建立大鼠脊髓减压病模型．于出舱后0，10，30，60，120min经蛛网膜下腔各注入20μl生理盐水或神经生长因子，在6，24，48，72h用TUNEL法标记脊髓神经细胞凋亡，免疫组织化学方法检测TNF-α蛋白表达。结果脊髓减压病大鼠出舱后6h组出现少量脊髓神经细胞凋亡及TNF—α蛋白表达，24h组阳性染色明显增强，48h组达到高峰，神经生长因子治疗后神经细胞凋亡及TNF—α蛋白表达明显减少，与生理盐水组比较差异有统计学意义（P〈0．05）。TNF—α蛋白表达与神经细胞凋亡存在正相关（P〈0．05）。结论神经细胞凋亡是脊髓减压病大鼠的重要病理变化，TNF—α可能参与了脊髓减压病继发损伤，神经生长因子可以减轻脊髓减压病的神经细胞损伤。     

Probabilistic model of decompression sickness based on stochastic models of bubbling in tissues

BACKGROUND: Decompression sickness (DCS) is caused by gas bubbles formed from pre-existing and new microscopic gas nuclei in blood and tissues. Assuming a random pattern of bubbling processes in living tissues, we developed a probabilistic model of DCS. We hypothesized that symptoms of DCS in an individual exposed to decompression appear when the total volume of bubbles in a unit volume of any tissue, w(t), exceeds the critical specific volume of a free gas phase, wcr. Therefore, one may consider the expectation of w(t)/wcr as a measure of the dynamic risk of gas bubble lesion of a given tissue segment. METHODS: Using the standard approach to estimation of various risks and the sum rule of probabilities of joint events, we defined the cumulative probability of DCS onset by the equation Pcum(t) = 1 - exp[Fcum(t)], where Fcum(t) = sigmaVnQnMnc(t), Qn = 1/wncr, where Vn is the volume of a tissue n. The function Mnc(t) coincides with the function Mn(t), defining a time history of the expectation of wn(t) until it achieves its maximum and then becomes a constant. Evaluating Pcum(t) for particular altitude decompressions, we identified the additive cumulative risk function of development of any DCS symptoms, Fcum-tot(t), with the function defining the cumulative risk of any bubble lesion of the "worst" virtual tissue (WVT) of Type A. On the other hand, we identified the additive cumulative risk function of development of intolerable DCS symptoms, Fcum-int(t), with the function defining the cumulative risk of acute bubble lesion of the WVT of Type phi. RESULTS: We found parameters of the curves Pcum-tot(t) and Pcum-int(t) that fit the known empirical curves for the cumulative probability of DCS onset. For men performing mild exercise at 30 kPa after preoxygenation, our estimated parameters for curves Pcum-tot(t) indicate that the WVTs of Type A have nitrogen washout half-times of 260 and 290 min for preoxygenation times of 75 and 135 min, respectively. On the other hand, the parameters of curves Pcum-int(t) show that the WVTs of Type phi in men performing mild exercise at 20-40 kPa after preoxygenation during 0-6 h are virtual tissues with nitrogen washout half-times of 400 to 615 min. CONCLUSION: Our model provides a new approach to predicting DCS risk for various decompression profiles. By demonstrating the dependence of DCS risk on body tissue parameters, the model explains why resistance to DCS in mammals increases with a lower body mass and greater specific blood flow in tissues.