Combined effects of intravenous perfluorocarbon emulsion and oxygen breathing on decompression-induced spinal cord injury in rats.

The spinal cord is one of the most commonly affected sites in decompression sickness (DCS). Alternative methods have long been sought to protect against DCS spinal cord dysfunction, especially when hyperbaric treatment is unavailable. Use of perfluorocarbon (PFC) emulsion with or without oxygen breathing has shown survival benefits in DCS animal models. The effectiveness of intravenous PFC emulsion with oxygen breathing on spinal cord function was studied. Somatosensory-evoked potentials (SSEPs) and histologic examination were chosen to serve as measures. After fast decompression (203 kPa/minute) from 709 kPa (for 60 minutes), male Sprague-Dawley rats randomly received: 1) air and saline; 2) oxygen (O2) and saline; 3) O2 and PFC emulsion. The incidence and average number of abnormal SSEP waves in survival animals that received O2 and PFC emulsion were significantly reduced (P < 0.05). Foci of demyelination, necrosis and round non-staining defects in white matter regions of the spinal cord could be found in severe DCS rats. We concluded that administration of PFC emulsion combined with oxygen breathing was beneficial for DCS spinal conductive dysfunction in rats.

Bidirectional influences of acetazolamide on central nervous system oxygen toxicity of rats.

Central nervous system oxygen toxicity, which occurs during diving and hyperbaric oxygen treatment, can lead to very dangerous situations, and it is of great importance to explore its mechanisms. We have speculated that cerebral blood flow plays a pivotal role in its occurrence. Except for acting as an anticonvulsant in clinical applications, acetazolamide is also a vasodilator used in both clinical and laboratory settings. In this study, when acetazolamide from 5 to 500 ug/kg body weight was administered by intracerebroventricular injection, the latency of central nervous system oxygen toxicity detected by electroencephalogram recording in rats subjected to hyperbaric oxygen at 6 atmospheres absolute was prolonged significantly. On the contrary, when the dose of intracerebroventricular injection achieved 5,000 ug/kg body weight, acetazolamide shortened the latency significantly. Intraperitoneal injection of acetazolamide more than 7.5 mg/kg body weight also shortened the latency significantly. Results also showed both intracerebroventricular injection of acetazolamide at a dose of 5,000 ug/kg body weight and intraperitoneal injection at dose of 7.5 mg/kg body weight inhibited the activity of carbonic anhydrase and increased the cerebral blood flow significantly, which helped aggravate oxidation damage and resulted in increased MDA and impaired glutathione peroxidase in brain tissue. But intracerebroventricular injection of acetazolamide at 5 ug/kg body weight had no effect on MDA and glutathione peroxidase, though it inhibited the activity of carbonic anhydrase. These observations indicated acetazolamide covers bidirectional influences on central nervous system oxygen toxicity. Within local brain tissue, especially neurons, it could exert its anticonvulsive effect on the central nervous system at low doses. On the other hand, under high doses, it would display its convulsive-hastening effect through increasing cerebral blood flow to aggravate the oxidation state of brain tissues and exacerbate central nervous system oxygen toxicity when subjected to hyperbaric oxygen. Blood flow of brain plays a pivotal role in central nervous system oxygen toxicity.

[Influence of acetazolamide given intraperitoneally on the latency to hyperbaric oxygen-induced convulsion of rats.].

The purpose of the present study was to explore the relation between the modulation of cerebral blood flow and the latency of hyperbaric oxygen-induced convulsion. There were two parts in this study. First, the effect of acetazolamide or (and) indomethacin on the latency of hyperbaric oxygen-induced convulsion was observed. Seventy Sprague-Dawley (SD) rats were randomly divided into 7 groups: the acetazolamide 200, 20, 10, 7.5, 5, 2.5 mg/kg body weight and normal saline (NS) group. Forty rats were divided into 5 groups: indomethacin 20, 10, 5, 2.5 mg/kg body weight and NS groups. Another 40 rats were divided into 5 groups which were administered with indomethacin in the dose of 0 mg/kg (NS), 0 mg/kg (NS), 5, 10 and 20 mg/kg body weight. Thirty min later the first group was given NS, and all the other four groups were given acetazolamide with a dose of 7.5 mg/kg body weight. The animals were given acetazolamide or (and) indomethacin intraperitoneally, and 20 min later they were exposed to the pressure of 6 ATA (absolute atmosphere) of pure oxygen. The time from exposure to the onset of seizure (clonic-tonic convulsion) was recorded for each animal according to behavioral observation. Second, the change of maleic dialdehyde (MDA) was measured after acetazolamide and (or) indomethacin treatment. Seventy-two SD rats were randomly divided into 9 groups: Control, 6 and 16 min respectively with NS, acetazolamide, indomethacin, and both acetazolamide and indomethacin group. The dose of acetazolamide was 7.5 mg/kg body weight and the dose of indomethacin was 20 mg/kg body weight. After injection of drugs, the animals were subjected to the pressure of 6 ATA of pure oxygen in respect to its time course group. Then the rats were decapitated and the cerebral cortex was dissected and homogenized. The content of MDA was determined. We found that (1) when the dose of acetazolamide is higher than 7.5 mg/kg, it shortened the latency to hyperbaric oxygen-induced convulsion significantly (P<0.05, P<0.01). There was no significant difference in the latency between every to hyperbaric oxygen-induced convulsion significantly (P<0.05, P<0.01). There was no significant difference in the latency between every two groups of rats treated with different doses of indomethacin. But when the rats were administered acetazolamide of 7.5 mg/kg body weight after being pretreated with indomethacin of 20 mg/kg body weight, the outbreak of convulsion was put off remarkably (P<0.05). (2) In comparison with the control, the content of MDA in the group treated with acetazolamide increased significantly (P<0.01), but when the rats were treated with both acetazolamide and indomethacin, the content of MDA was reduced significantly both in 6 and 16 min exposure time projects (P<0.05, P<0.01). These results suggest that acetazolamide which dilates the brain arterioles can obviously shorten the latency of hyperbaric oxygen-induced convulsion and aggravate the oxidation of the brain. Indomethacin can resist acetazolamideos effect on the latency and oxidation level when the animals were exposed to the hyperbaric oxygen. The activity of carbonic anhydrase correlates closely with the oxidation injury.

[Effect of acetazolamide on the latency of hyperbaric oxygen-induced convulsion].

The purpose of the present study was to explore the relation between the modulation of cerebral blood flow and the latency of hyperbaric oxygen-induced convulsion. There were two parts in this study. First, the effect of acetazolamide on the latency of hyperbaric oxygen-induced convulsion was observed. 32 Sprague-Dawley (SD) rats were randomly divided into four groups: the acetazolamide 200, 20, 2 mg/kg body weight and normal saline (NS) group. The animals were given intraperitoneally acetazolamide or NS, respectively, before being exposed to the pressure of 6 ATA (absolute atmosphere) of pure oxygen. The time from exposure to the onset of seizure (clonic-tonic convulsion) was recorded for each animal according to behavioral observation. Second, the changes in maleic dialdehyde (MDA) and the activity of glutathione peroxidase (GSH-PX) were measured after acetazolamide treatment. 40 SD rats were randomly divided into five groups: NS group, 6 min with NS group, 6 min with acetazolamide group, 16 min with NS group, and 16 min with acetazolamide group. The dose of acetazolamide was 20 mg/kg body weight. After injection of NS or acetazolamide, the animals were subjected to the pressure of 6 ATA of pure oxygen in respect to its time course group. The rats were decapitated and the cortex, hippocampus, and striatum of brains were dissected and homogenized. The content of MDA and the activity of GSH-PX in these tissues were determined. We found that (1) there was a significant difference in the latency of hyperbaric oxygen-induced convulsion between the acetazolamide 200 mg/kg group and the NS control group, as well as between the acetazolamide 20 mg/kg group and the NS control group (P<0.01), whereas there was no significant difference between the NS group and the acetazolamide 2 mg/kg weight group (P>0.05). The latency of these groups were listed as follows: 9.78+/-1.94 min for 200 mg/kg body weight group, 10.92+/-1.68 min for 20 mg/kg body weight group, 24.32+/-4.33 min for 2 mg/kg body weight group and 22.02+/-4.32 min for NS control group. (2) there was no significant difference between all groups in the activity of GSH-PX, though it varied with the oxidation levels. In the cortex and hippocampus, the activity of GSH-PX boosted up at first, but with the progress of the oxidation it was impaired. In the striatum, the activity of GSH-PX increased stepwise with the aggravation of the oxidation. The MDA content in the cortex increased significantly in the group of 6 min with acetazolamide (P<0.01), as well as the group of 16 min with acetazolamide group both in cortex and hippocampus (P<0.01, P<0.05). The MDA content of all groups is correlated with the dose of acetazolamide and the exposure time. These results suggest that acetazolamide which dilates the brain arteriolar obviously shortens the latency of hyperbaric oxygen-induced convulsion, and that acetazolamide dilates the vessels and increases the supply of the oxygen breaking into the brain tissues and aggravates the oxidation. The hyperbaric oxygen-induced convulsion correlates closely with the oxidation injury.

Natural gas and indoor air pollution: a comparison with coal gas and liquefied petroleum gas / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>The study was designed to compare the combustion products of coal gas, liquefied petroleum gas and natural gas in relation to indoor air pollution.</p><p><b>METHODS</b>Regular pollutants including B(a)P were monitored and 1-hydroxy pyrene were tested in urine of the enrolled subjects. Radon concentrations and their changes in four seasons were also monitored in the city natural gas from its source plant and transfer stations to final users. To analyze organic components of coal gas, liquefied petroleum gas and natural gas, a high-flow sampling device specially designed was used to collect their combustion products, and semi-volatile organic compounds contained in the particles were detected by gas chromatograph-mass spectrograph (GC/MS).</p><p><b>RESULTS</b>Findings in the study showed that the regular indoor air pollutants particles and CO were all above the standard in winter when heating facilities were operated in the city, but they were lowest in kitchens using natural gas; furthermore, although NO2 and CO2 were slightly higher in natural gas, B(a)P concentration was lower in this group and 1-hydroxy pyrene was lowest in urine of the subjects exposed to natural gas. Organic compounds were more complicated in coal gas and liquefied petroleum gas than in natural gas. The concentration of radon in natural gas accounted for less than 1% of its effective dose contributing to indoor air pollution in Beijing households.</p><p><b>CONCLUSION</b>Compared to traditional fuels, gases are deemed as clean ones, and natural gas is shown to be cleaner than the other two gases.</p>