Alteration of Striatal Dopamine Levels Under Various Partial Pressure of Oxygen in Pre-convulsive and Convulsive Phases in Freely-Moving rats

The purpose of this study was to investigate the change in the striatal dopamine (DA) level in freely-moving rat exposed to different partial pressure of oxygen (from 1 to 5 ATA). Some works have suggested that DA release by the substantia nigra pars compacta (SNc) neurons in the striatum could be disturbed by hyperbaric oxygen (HBO) exposure, altering therefore the basal ganglia activity. Such changes could result in a change in glutamatergic and GABAergic control of the dopaminergic neurons into the SNc. Such alterations could provide more information about the oxygen-induced seizures observed at 5 ATA in rat. DA-sensitive electrodes were implanted into the striatum under general anesthesia. After 1 week rest, awaked rats were exposed to oxygen–nitrogen mixture at a partial pressure of oxygen of 1, 2, 3, 4 and 5 ATA. DA level was monitored continuously (every 3 min) by in vivo voltammetry before and during HBO exposure. HBO induced a decrease in DA level in relationship to the increase in partial pressure of oxygen from 1 ATA to 4 ATA (?15 % at 1 ATA, ?30 % at 2 ATA, ?40 % at 3 ATA, ?45 % at 4 ATA), without signs of oxygen toxicity. At 5 ATA, DA level strongly decreases (?75 %) before seizure which occurred after 27 min ± 7 HBO exposure. After the epileptic seizure the decrease in DA level disappeared. These changes and the biphasic effect of HBO were discussed in function of HBO action on neurochemical regulations of the nigro striatal pathway.     

Pressure (< or=4 ATA) increases membrane conductance and firing rate in the rat solitary complex.

Neuronal sensitivity to pressure, barosensitivity, is illustrated by high-pressure nervous syndrome, which manifests as increased central nervous system excitability when heliox or trimix is breathed at >15 atmospheres absolute (ATA). We have tested the hypothesis that smaller levels of pressure (相似文献   

Effects of increased ambient pressure and nitrogen on man's monosynaptic reflexes.

Neurological signs during dives may result from altered excitability of central neurons. The present study assesses the effect of an increase in pressure from 1 to 3 ATA on the excitability of muscle spindles and alpha motoneurons by comparing the EMG amplitudes of the mechanically and electrically elicited monosynaptic reflexes of the gastrocnemius-soleus muscle in 10 normal adults breathing a normoxic oxygen-nitrogen gas mixture. At the surface the amplitude of the electrically elicited H response was matched to that of the mechanically elicited Achilles tendon reflex (ATR), but at depth these amplitudes became significantly different. In every subject the amplitude of the ATR, which depends upon the excitability of both muscle spindles and the alpha motoneurons, was reduced on an average of 38% (with a range of 12-75%). The H response bypasses the muscle spindles and hence, depends primarily upon alpha motoneuron excitability. Its amplitude was unaltered in four, reduced in three, and increased in three subjects. Since the ATR was always depressed despite the direction of change in the H response, we have concluded that an increase in ambient pressure (i.e., pressure per se, or nitrogen, or both) must have decreased the responsiveness of muscle spindles to the tendon tap via a reduction in fusimotor activity.     

Continuous intracellular recording from mammalian neurons exposed to hyperbaric helium, oxygen, or air.

We developed a hyperbaric chamber for intracellular recording in rat brain stem slices during continuous compression and decompression of the tissue bath with the inert gas helium. Air, rather than helium, was also used as the compression medium in some cases to increase tissue nitrogen levels. An important feature is the chamber door, which opens or closes rapidly at 1 atmosphere absolute (ATA) for increased accessibility of the microelectrode. The door also closes and seals smoothly without disrupting the intracellular recording. Hyperbaric oxygen was administered during helium compression using a separate pressure cylinder filled with perfusate equilibrated with 2. 3-3.3 ATA oxygen. Measurements of tissue/bath PO(2) and pH confirmed that the effects of compression using helium or air could be differentiated from those due to increased PO(2). One hundred and thirteen neurons were studied during 375 compression cycles ranging from 1 to 20 ATA (mode 3.0 ATA). We conclude that it is technically feasible to record intracellularly from the same mammalian neuron while changing ambient pressure over a physiologically important range. These techniques will be useful for studying how various hyperbaric environments affect neurophysiological mechanisms.     

Free radical generation in the brain precedes hyperbaric oxygen-induced convulsions.

We tested the hypothesis that hyperbaric oxygenation (HBO) generates free radicals in the brain before the onset of neurological manifestations of central nervous system (CNS) oxygen poisoning. Chronically cannulated, conscious rats were individually placed in a transparent pressure chamber and exposed to (1) 5 atmospheres absolute (ATA) oxygen for 15 min (n = 4); (2) 5 ATA oxygen for 30 min (n = 5), during which no visible convulsions occurred; (3) 5 ATA oxygen for 30 min with recurrent convulsions (n = 6); (4) 5 ATA oxygen until the appearance of the first visible convulsions (n = 5); (5) 4 ATA oxygen for 60 min during which no convulsions occurred (n = 5); and (6) 5 ATA air for 30 min (n = 5, controls). Immediately before compression, 1 mL of 0.1 M of alpha-phenyl-N-tert-butyl nitrone (PBN) was administered intravenously (iv) for spin trapping. At the termination of each experiment, rats were euthanized by pentobarbital iv and decompressed within 1 min. Brains were rapidly removed for preparation of lipid extracts (Folch). The presence of PBN spin adducts in the lipid extracts was examined by electron spin resonance (ESR) spectroscopy. ESR spectra from unconvulsed rats exposed to 5 ATA oxygen for 30 min revealed both oxygen-centered and carbon-centered PBN spin adducts in three of the five brains. One of the five rats in this group showed an ascorbyl signal in the ESR spectrum.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of hyperbarism on collagenous protein metabolism in granulation tissue.

Rats with subcutaneously implanted polyurethane sponges were exposed 6 hours daily for 7 days to high ambient atmospheric pressures (1.5, 2, 2.5 and 3 ATA). Another group was exposed 4 hours daily for 4 weeks to 3 ATA before inducing granulation tissue formation. 14C-proline was administered 16 hours before terminating the experiment. Free hydroxyproline, soluble and insoluble collagen and total noncollagenous protein were isolated from the 7-day granuloma and the amount and radioactivity of 14C-hydroxyproline and 14C-proline were determined. Seven days' graduated hyperbarism did not affect collagen synthesis; the maturation of collagen to insoluble forms was inhibited at 2 and 2.5 ATA, but not at 3 ATA. Stimulated degradation of collagen (free hydroxyproline) was observed at 2, 2.5 and 3 ATA. In animals subjected to long-term exposure at 3 ATA pressure, the collagen in the granuloma matured to insoluble forms more quickly. Biochemical changes were correlated with changes in the fine structure of the granulation tissue. The appearance of the fibroblast proteosynthetic apparatus was not influenced by hyperbarism. Progressive spherical transformation, fusion of mitochondria and lysosomal activation in the pericapillary fibroblasts occurred at 2, 2.5 and 3 ATA. In short-term experiment, the formation of cytosegresomes and cellular necrosis also contributed to the effect at 3 ATA, which is thus already a toxic pressure for granulation tissue.     

Measurement of Free Radicals from Smoke Inhalation and Oxygen Exposure by Spin Trapping and Esr Spectroscopy

Research in smoke inhalation has established that free radicals are produced from gases released during combustion and these species impair lung function. Using spin traps and their adducts in an animal model free radicals were measured. Various hyperbaric oxygen regimens were tested in an attempt to attenuate pulmonary damage caused by free radical reactions. Our data demonstrated that persistent oxygen- and carbon-centered free radicals are detectable in intravascular fluids after smoke inhalation. The smoke inhalation model showed however, clearing of spin trap adducts one hour after smoke exposure. Other researchers have found that when 100% oxygen is given at 1 atmosphere absolute (ATA) for 1 h, free radicals were not detectable. However, oxygen given at 2.5 ATA does produce detectable free radicals. With continued exposure at this pressure, the levels of free radicals increase for up to 60min. This study suggests that the level of free radical induced oxygen toxicity may be a function of oxygen pressure and duration of oxygen exposure.     

Effects of hydrostatic pressure and inert gases on platelet aggregation in vitro

A novel cuvette was used to subject citrated platelet-rich plasma (PRP) to high hydrostatic pressure with negligible contamination by He (used for compression of the apparatus). Aggregation was induced at pressure by ADP and quantified turbidimetrically. The maximum degree of aggregation (MDA) was reduced from a control level of 82.2 to 53.6% by exposure to 101 ATA. Because decompression bubbles did not form, aggregation was also measured immediately after a compression cycle. After exposure to 101 ATA hydrostatic pressure, platelets responded normally to ADP at 1 ATA. In a matching apparatus, PRP was equilibrated with high partial pressures of inert gases. Normal physiological plasma Po2 and pH were maintained during equilibration. N2O (5 ATA) reduced the MDA from 86.5 (control) to 58.1%. N2 (51 ATA) reduced the MDA from 74.7 (control) to 51.6%, and 101 ATA Pn2 reduced the MDA from 78.0 (control) to 32.3%. He (100 ATA) reduced the MDA from 83.6 to 38.6%. It was concluded that platelet aggregation was relatively sensitive to hydrostatic pressure and less sensitive to inert gases than predicted from their anesthetic potency ratios.     

0.7 MPa(7ATA)高气压下大鼠脊髓突触体甘氨酸摄取的变化

目的:研究氮麻醉时甘氨酸神经递质功能变化。方法:制备脊髓突触体,用同位素方法观察0.7MPa(7ATA)高压空气环境中大鼠脊髓突触体摄取甘氨酸的情况。结果:0.7MPa(7ATA)时甘氨酸摄取速度减慢,达到饱和摄取量时间延长,最大饱和摄取量下降。甘氨酸摄取的Vm减小,Km增加。在加入10-7mol.L-1皮质酮后,可增加0.7MPa(7ATA)高压空气时甘氨酸摄取Vm。结论:在高气压下发生氮麻醉时,甘氨酸摄取转运体的功能降低,与甘氨酸亲和力下降;皮质酮有助于高亲和力甘氨酸转运体功能恢复。     

Inhibition of toxin production inClostridium perfringens in vitro by hyperbaric oxygen

Since 1960, gas gangrene has been treated by the administration of pure oxygen at 3 atmospheres absolute (3 ATA).Small animals are useless for research at this pressure because of oxygen intoxication.In vitro, the growth ofClostridium perfringens (C. welchii) was not arrested by 1 1/2 hr of hyperbaric oxygen at 3 ATA, but the production of toxin is inhibited during this period. It is not inhibited at 2 ATA. If the results of the conservative treatment of patients with hyperbaric oxygen depend upon a comparable process, such treatment at less than 3 ATA would probably be ineffective.     

一氧化氮合成酶在不同压力氧气导致的肺型氧中毒中的表达变化

目的：临床上过量使用氧气可导致肺型氧中毒的发生,目前有文献认为常压氧和高压氧导致的肺型氧中毒具有不同的发病机制。本实验拟探讨一氧化氮合成酶在不同压力氧气导致的肺型氧中毒中的表达变化。方法：60只雄性SD大鼠,随机分为6组（n=10）,分别暴露于1绝对压（atmosphere absolute,ATA）、1．5ATA、2ATA、2．5ATA、3ATA,100％氧气中56、20、10、8、6h,暴露于空气组作为对照。出舱后测定各组大鼠肺组织湿干比、支气管肺泡灌洗液蛋白含量。收集肺组织,裂解提取蛋白。行Western blot检测内皮一氧化氮合酶（eNOS）、神经型一氧化氮合酶（eNOS）的表达变化。结果：相对于正常对照组,1．0ATA组肺湿干比、支气管肺泡灌洗液蛋白量表达明显增高。随着氧分压的增高,这种改变减弱。和1．0ATA组相比,高压氧组的肺湿干比、肺泡灌洗液蛋白含量显著降低。各个氧气压力暴露组大鼠肺组织中nNOS的含量没有明显改变。而eNOS含量则在氧气压力为2ATA时明显降低（P〈0．05）,氧气压力为2．5ATA及3ATA时明显增高（P〈0．05）。结论：eNOS在肺中的表达量随着氧气压力的变化而改变。     

Catecholamine content (as measured by the HPLC method) in brain and blood plasma of the eel: effects of 101 ATA hydrostatic pressure

The catecholamine content (noradrenaline, NA; adrenaline, A; dopamine, DA, and its metabolite, DOPAC) was measured, by the HPLC method, in brain and blood plasma of eels studied at atmospheric pressure (1 ATA) or at 101 ATA of hydrostatic pressure (HP). In the brain, HP induces a slight but significant increase (P less than 0.05) in A and DA contents but NA and DOPAC levels are not modified at 101 ATA when compared to 1 ATA. In the plasma, only A and NA are detected, adrenaline being the predominant amine. In eels exposed to 101 ATA HP, A and NA are strongly increased (+100%; P less than 0.01). The significance of the catecholamine increase in brain and plasma of the eels under HP is discussed.     

Stimulation of perivascular nitric oxide synthesis by oxygen

We hypothesized that elevated partial pressures of O(2) would increase perivascular nitric oxide (*NO) synthesis. Rodents with O(2)- and.NO-specific microelectrodes implanted adjacent to the abdominal aorta were exposed to O(2) at partial pressures from 0.2 to 2.8 atmospheres absolute (ATA). Exposures to 2.0 and 2.8 ATA O(2) stimulated neuronal (type I) NO synthase (nNOS) and significantly increased steady-state.NO concentration, but the mechanism for enzyme activation differed at each partial pressure. At both pressures, elevations in.NO concentration were inhibited by the nNOS inhibitor 7-nitroindazole and the calcium channel blocker nimodipine. Enzyme activation at 2.0 ATA O(2) appeared to be due to an altered cellular redox state. Exposure to 2.8 ATA O(2), but not 2.0 ATA O(2), increased nNOS activity by enhancing nNOS association with calmodulin, and an inhibitory effect of geldanamycin indicated that the association was facilitated by heat shock protein 90. Infusion of superoxide dismutase inhibited.NO elevation at 2.8 but not 2.0 ATA O(2). Hyperoxia increased the concentration of.NO associated with hemoglobin. These findings highlight the complexity of oxidative stress responses and may help explain some of the dose responses associated with therapeutic applications of hyperbaric oxygen.     

Effects of hyperbaric oxygen in circulatory shock induced by splanchnic artery occlusion and reperfusion in rats

We studied the effects of hyperbaric oxygen in a severe model of circulatory shock induced by occlusion and reperfusion of major splanchnic arteries (splanchnic artery occlusion (SAO) shock). Pentobarbital-anesthetized rats subjected to total occlusion of the superior mesenteric and the celiac arteries for 40 min developed a severe shock state, resulting in a uniformly fatal outcome after release of the occlusion. Exposure to hyperbaric oxygen at 2 ATA (atmosphere absolute) (1 ATA = 0.1 MPa) was initiated immediately after reperfusion. SAO shock rats exposed to hyperbaric oxygen maintained mean arterial blood pressure at significantly higher values throughout the postreperfusion period compared with untreated SAO shock rats (p less than 0.01), with final mean arterial blood pressures of 88 +/- 9 and 51 +/- 4 mmHg, respectively. Treatment with hyperbaric oxygen attenuated the increase in plasma activities of the lysosomal hydrolase cathepsin D (p less than 0.05), and diminished the increase of hematocrit (p less than 0.01 from untreated shock rats). Splanchnic occlusion shock rats treated with hyperbaric oxygen also exhibited a significantly higher survival rate than the untreated shock group (77 vs. 0%, respectively; p less than 0.01). Our results suggest that the beneficial effects of exposure to hyperbaric oxygen immediately after reperfusion of the splanchnic region outweigh its possible deleterious effect.     

Does hyperbaric oxygen exposure affect high-intensity, short-duration exercise performance?

Hyperbaric oxygen (HBO) exposure involves the breathing of 100% oxygen under conditions of elevated atmospheric pressure and is used to increase the oxygen content of the plasma fraction of arterial blood. The purpose of this study was to determine the effects of acute HBO exposure on selected physiological responses and performance in response to maximal lower extremity or upper extremity short-term, high-intensity exercise. The study was performed with 2 separate experiments incorporating double-blinded and randomized protocols. In experiment 1, 9 subjects ran on a treadmill at a speed of 268 m x min(-1) with a predetermined grade. In experiment 2, 9 different subjects performed a repetitive bench press exercise. Both exercise protocols were designed to induce fatigue within 1-2 minutes. Within each experiment, subjects received either a 1-hour HBO exposure inspiring 100% O2 at 202.6 kPa (2.0 atmospheres absolute pressure [ATA]) or a 1-hour sham exposure inspiring ambient air at 121.5 kPa (1.2 ATA) before exercise. No significant differences (p > or = 0.05) were observed in postexercise blood lactate concentrations, peak heart rate, ratings of perceived exertion, or performance as determined by treadmill running time or number of completed lifts. Unlike other methods that elevate oxygen content of the blood, acute HBO exposure appears to have no significant effect on subsequent high-intensity running or lifting performance.     

Human skeletal muscle function and metabolism during intense exercise at high O2 and N2 pressures

The maximal contractile force (peak torque) of the quadriceps femoris was studied during 60 repeated unilateral dynamic knee extensions in nine subjects under three different conditions, viz., during air breathing at normal (1 ATA) and raised (6 ATA) ambient pressures and during O2 breathing at 1.3 ATA. In six subjects the electromyographic (EMG) activity of the working muscle was recorded. Muscle biopsies were obtained from the vastus lateralis before, immediately after, and 1 min after exercise. Tissue specimens were subsequently assayed for various muscle metabolites. Peak torque, as an average of the 60 knee extensions, was higher (P less than 0.05) at 1.3 ATA than at 6 or 1 ATA. Peak torque of the exercising muscle declined more rapidly at 1 ATA than at 1.3 ATA, differing in the final 24 contractions by 14%. At 6 ATA peak torque of the initial 12 contractions was 6% lower (P less than 0.05) than at 1 ATA but equaled 1-ATA values in the latter third of the exercise bout. Although the EMG activity at 1 ATA increased relative to that at 6 ATA as exercise proceeded, the rate of force decline was greater at 1 ATA. Despite greater total work produced at 1.3 ATA than at 1 ATA, the metabolic response to exercise was not substantially altered at increased O2 pressure. However, the restitution rate of energy-rich phosphagens and the elimination of lactate during recovery were greater (P less than 0.05) at 1.3 ATA. These results suggest that hyperoxia may enhance the rate of energy release, whereas high N2 pressure and/or high hydrostatic pressure seem to interfere with neuromuscular activity.     

Human respiration at rest in rapid compression and at high pressures and gas densities

Ventilation (V), end-tidal PCO2 (PACO2), and CO2 elimination rate were measured in men at rest breathing CO2-free gas over the pressure range 1-50 ATA and the gas density range 0.4-25 g/l, during slow and rapid compressions, at stable elevated ambient pressures and during slow decompressions in several phases of Predictive Studies III-1971 and Predictive Studies IV-1975. Inspired O2 was at or near natural O2 levels during compressions and at stable high pressures; it was 0.5 ATA during decompressions. Rapid compressions to high pressures did not impair respiratory homeostasis. Progressive increase in pulmonary gas flow resistance due to elevation of ambient pressure and inspired gas density to the He-O2 equivalent of 5,000 feet of seawater was not observed to progressively decrease resting V, or to progressively increase resting PACO2. Rather, a complex pattern of change in PACO2 was seen. As both ambient pressure and pulmonary gas flow resistance were progressively raised, PACO2 at first increased, went through a maximum, and then declined towards values near the 1 ATA level. It is suggested that this pattern of PACO2 change results from interaction on ventilation of 1) increase in pulmonary resistance due to elevation of gas density with 2) increase in respiratory drive postulated as due to generalized CNS excitation associated with exposure to high hydrostatic pressure. There may be a similar interaction between increased gas flow resistance and increase in respiratory drive related to nitrogen partial pressure and the narcosis resulting therefrom.     

Why can the eel, unlike the trout, migrate under pressure

In order to elucidate the difference between pressure resistance in trout (Onchorhyncus mykiss) and eel (Anguilla anguilla), oxygen consumption of red muscle permeabilised cells and mitochondria were measured at 101 ATA hydrostatic pressure per se. Such an experiment involved the setting up of a special system allowing measurements under high pressure. The results show that hydrostatic pressure strongly alters the oxidative phosphorylation in trout but not in eel, which exhibits mitochondrial pressure resistance. It is hypothesised that the eel has a supranormal mitochondria functioning at atmospheric pressure in order to cope with the high pressure environment encountered during its migration.     

Effect of pressure on [3H]GABA release by synaptosomes isolated from cerebral cortex

High hydrostatic pressure has been shown to produce neurological changes in humans which manifest, in part, as tremor, myoclonic jerks, electroencephalographic changes, and convulsions. This clinical pattern has been termed high-pressure nervous syndrome (HPNS). These symptoms may represent an alteration in synaptic transmission in the central nervous system with the inhibitory neural pathways being affected in particular. Since gamma-aminobutyric acid (GABA) transmission has been implicated in other seizure disorders, it was of interest to study GABAergic function at high pressure. Isolated synaptosomes were used to follow GABA release at 67.7 ATA of pressure. The major observation was a 33% depression in total [3H]GABA efflux from depolarized cerebrocortical synaptosomes at 67.7 ATA. The Ca2+-dependent component of release was found to be completely blocked during the 1st min of [3H]GABA efflux with a slow rise over the subsequent 3 min. These findings lead us to conclude that high pressure interferes with the intraterminal cascade for Ca2+-dependent release of GABA.