350m氦氧模拟饱和潜水中肺呼吸功能的变化

在350m氦氧模拟饱和及370m巡回潜水实验中,观察了16项肺功能指标及其衍生指标的定期监测结果。通过监测试图对暴露于高气压环境中人员的安全性、作业能力作出客观的评价,以加强医学保障,同时对大深度氦氧环境所导致的呼吸功能改变进行实验研究。     

3.6MPa氦氧饱和潜水对潜水员心功能的影响

为了使我国大深度饱和潜水向纵深发展,适应未来海洋开发的需要,我所建成了500m饱和潜水设备系统,结合验收该设备的性能,进行了3.6MPa(350m)氦氧饱和潜水模拟实验的医学保障研究,心血管功能监测是实验研究的一部分。 1 材料和方法 500m(5.1MPa)饱和潜水设备系统由居住舱(17m~3)、过渡舱(8m~3)和巡潜水舱(19m~3)三部分组成。本次实验的模拟压力为3.6MPa。呼吸氦氧混合气,其中Po_2为40±2kPa,P_(N2)为90kPa,P_(co2)—     

模拟65msw氦氧饱和潜水对人体氧化应激的影响

目的：探讨模拟65 msw饱和潜水暴露对机体氧化应激的影响。方法：7名健康男性潜水员参加65 msw饱和潜水,在暴露前、中、后取24 h尿检测超氧化物歧化酶（SOD）、丙二醛（MDA）、总氨基酸（T-AA）、总抗氧化能力（T-AOC）含量,同时监测24 h尿量及体重变化。结果：总氨基酸含量在减压末期比基础值显著增高,减压后1周恢复至正常水平;SOD、MDA、T-AOC在各时间点无明显变化。进舱后第1天尿量比进舱前基础值明显减少,随后逐渐恢复。加压后第2天开始体重逐渐增高,减压结束时比进舱前体重明显增高。结论：模拟65 msw饱和潜水暴露未造成参试潜水员明显氧化损伤。在饱和潜水试验中实时监测24 h尿量及氧化应激程度对防止机体损伤具有重要意义。     

海上150 m氦氧饱和-182 m巡回潜水对潜水员血浆和尿液CRH、β-EP含量的影响

目的 :探讨海上大深度饱和潜水对潜水员血浆和尿液中CRH、β EP含量的影响。 方法 :用放射免疫法检测潜水员饱和前后血浆CRH、β EP含量和潜水员在饱和潜水前、加压后、饱和暴露期间及减压后尿中CRH和 β EP的含量。 结果 :血浆CRH含量在饱和潜水后显著高于饱和潜水前 (P <0 .0 1 )。尿液中的CRH、β EP含量在加压后、饱和期间及减压后均显著高于饱和潜水前 (P <0 .0 5)。结论 :大深度饱和潜水能引起潜水员血浆和尿液中CRH、β EP含量的改变 ,CRH、β EP参与了大深度饱和潜水引起的机体应激反应     

模拟350m饱和潜水中尿17—羟,17—酮甾体及儿茶酚胺含量的变化

本实验在我国首次进行的350m氦氧模拟饱和潜水试验中研究了人体肾上腺皮质及髓质功能的变化,这对潜水员的选拔及健康保障具有重要意义。 对象及方法 讲究对象 男性海军现役潜水员4名,经严格体检除外各种疾病。年龄20～22岁、身高169～173cm.体重64.5～68kg,潜水工龄2～4年。试验前均经过2.5个月严格适应性训练。     

氦氧潜水呼吸介质转换时内耳减压病发病机理探讨

氦氧潜水减压时间长。Ｋｅｌｅｒ利用转换呼吸气体成分的方法大大地缩短了减压时间,在减压中,以氦氧混合气（Ｈｅ－Ｏ２）转为空气最常见,但是,这种方式的气体转换后,有时会发生内耳减压病,其症状为眼震、耳呜、耳聋、恶心、呕吐,重者出现运动平衡失调。本研究旨在...     

200米氦氧模拟饱和潜水对人心血管功能影响

本实验观察了潜水员的左心室功能、心电图和阻抗心动图,以了解200m(21ATA)氦氧饱和潜水巾、及以后人体血流动力学变化。 方法 受试潜水员共4名,平均年龄23.3±0.5岁,体重66.1±4.1kg,身高173.8±3.9cm,体表面积1.75±0.07m~2。模拟深度200m,饱和停留53小时,呼吸氦氧混合气,其中Po_2444.4     

350m氦氧模拟饱和潜水过程中潜水员坐位踏车时心缩间期的变化

在350m氦氧模拟饱和潜水过程中,对4名男性潜水员采用耳密度图导数图方法观察坐位踏车时心缩间期变化。在压力(300、230、135m)下和减压后的主要变化是等容收缩期、射血前期(PEP)和PEP/左室射血时间加大,与加压前比较有显著差异,尤其在踏车负荷加重时更为明显。提示心肌收缩力受高气压的影响而降低。     

Gas bubbles in rats after heliox saturation and different decompression steps and rates.

Effects of pressure reduction, decompression rate, and repeated exposure on venous gas bubble formation were determined in five groups (GI, GII, GIII, GIV, and GV) of conscious and freely moving rats in a heliox atmosphere. Bubbles were recorded with a Doppler ultrasound probe implanted around the inferior caval vein. Rats were held for 16 h at 0.4 MPa (GI), 0.5 MPa (GII and GIII), 1.7 MPa (GIVa), or 1.9 MPa (GIV and GV), followed by decompression to 0.1 MPa in GI to GIII and to 1.1 MPa in GIV and GV. A greater decompression step, but at the same rate (GII vs. GI and GIVb vs. GIVa), resulted in significantly more bubbles (P < 0.01). A twofold decompression step resulted in equal amount of bubbles when decompressing to 1.1 MPa compared with 0.1 MPa. The faster decompression in GII and GVa (10.0 kPa/s) resulted in significantly more bubbles (P < 0.01) compared with GIII and GVb (2.2 kPa/s). No significant difference was observed in cumulative bubble score when comparing first and second exposure. With the present animal model, different decompression regimes may be evaluated.     

Diving response and arterial oxygen saturation during apnea and exercise in breath-hold divers.

This study addressed the effects of apnea in air and apnea with face immersion in cold water (10 degrees C) on the diving response and arterial oxygen saturation during dynamic exercise. Eight trained breath-hold divers performed steady-state exercise on a cycle ergometer at 100 W. During exercise, each subject performed 30-s apneas in air and 30-s apneas with face immersion. The heart rate and arterial oxygen saturation decreased and blood pressure increased during the apneas. Compared with apneas in air, apneas with face immersion augmented the heart rate reduction from 21 to 33% (P < 0.001) and the blood pressure increase from 34 to 42% (P < 0.05). The reduction in arterial oxygen saturation from eupneic control was 6.8% during apneas in air and 5.2% during apneas with face immersion (P < 0.05). The results indicate that augmentation of the diving response slows down the depletion of the lung oxygen store, possibly associated with a larger reduction in peripheral venous oxygen stores and increased anaerobiosis. This mechanism delays the fall in alveolar and arterial PO(2) and, thereby, the development of hypoxia in vital organs. Accordingly, we conclude that the human diving response has an oxygen-conserving effect during exercise.     

Cell-cell adhesion molecules in Dictyostelium

Multicellularity in the cellular slime mold Dictyostelium discoideum is achieved by the expression of two types of cell-cell adhesion sites. The EDTA-sensitive adhesion sites are expressed very early in the development cycle and a surface glycoprotein of 24,000 Da is known to be responsible for these sites. The EDTA-resistant contact sites begin to accumulate on the cell surface at the aggregation stage of development. Several glycoproteins have been implicated in the EDTA-resistant type of cell-cell binding and the best characterized one has an Mr of 80,000 (gp80). gp80 mediates cell-cell binding via homophilic interaction and its cell binding site has been mapped to an octapeptide sequence. The mechanism by which gp80 mediates cell-cell adhesion will be discussed.     

Changes in fibrinolytic activity in diving grey seals

In order to test the hypothesis that enhanced fibrinolytic activity is a factor which prevents the blood of diving seals from clotting, we instrumented two female grey seals (Halichoerus grypus) with subcutaneous electrodes for measurements of heart rate (HR) and an extradural intravertebral venous catheter for collection of blood samples before, during and after simulated dives of 10 min duration. Blood samples were used for in vitro determination of clot lysis time (CLT), which is a measure of the level of fibrinolytic activity, and for analyses of plasma levels of cortisol, noradrenaline and adrenaline (A). The seals displayed profound diving bradycardia indicative of a substantial reduction in blood flow rates (pre-dive HR: 78 (63–98) bpm; dive HR: 8 (7–10) bpm; (median (range); n=2)) and elevated catecholamine levels (pre-dive A: 121 (98–184) pg·ml⁻¹; peak dive/post-dive A: 3510 (447–6181) pg·ml⁻¹), both of which are factors which promote blood coagulation. Nevertheless, we found that CLT always increased in connection with diving (pre-dive CLT: 436 (356–568) min; peak CLT during diving: 1380 (640–1800) min), which implies a reduced, rather than enhanced, fibrinolytic activity in this situation. These results show that enhanced fibrinolytic activity is not part of the defence system which prevents fatal clotting from occurring in diving grey seals.