| 상호 작용 | Central nervous system (CNS) oxygen toxicity of mixtures of oxygen with inert gas was studied in rats. Male Charles-River-rats with surgically implanted electroencephalograph (EEG) electrodes were exposed to binary mixtures of oxygen with nitrogen or helium having total pressures of 5 to 10 atmospheres absolute (ATA) in a hyperbaric chamber. The oxygen partial pressure in each mixture was 5ATA. CNS toxicity was evaluated by measuring the length of time between obtaining the desired pressure in the chamber until the appearance of electrical discharges in the EEG (latency period). The animals were observed for signs of intoxication. The results for both nitrogen and helium mixtures were the same. The duration of the latency period decreased with increasing inert gas partial pressure, the minimum latency occurring with mixtures containing 3ATA nitrogen or helium. Several rats exposed to mixtures containing 4 or 5ATA nitrogen appeared drowsy, although when the electrical discharges began these rats showed the characteristic signs of epileptic seizures. Duration of the latent period was not correlated with severity of the epileptic seizures. The authors suggest that the risk of CNS oxygen toxicity does not depend just on the partial pressure of oxygen, and that when calculating the oxygen partial pressure in breathing gas mixtures for divers, the partial pressures of the other (inert) gases should be considered.The contribution of inert gases to the risk of central nervous system (CNS) oxygen toxicity is a matter of controversy. Therefore, diving regulations apply strict rules regarding permissible oxygen pressures (Po(2)). We studied the effects of nitrogen and helium (0, 15, 25, 40, 50, and 60%) and different levels of Po(2) (507, 557, 608, and 658 kPa) on the latency to the first electrical discharge (FED) in the EEG in rats, with repeated measurements in each animal. Latency as a function of the nitrogen pressure was not homogeneous for each rat. The prolongation of latency observed in some rats at certain nitrogen pressures, mostly in the range 100 to 500 kPa, was superimposed on the general trend for a reduction in latency as nitrogen pressure increased. This pattern was an individual trait. In contrast with nitrogen, no prolongation of latency to CNS oxygen toxicity was observed with helium, where an increase in helium pressure caused a reduction in latency. This bimodal response and the variation in the response between rats, together with a possible effect of ambient temperature on metabolic rate, may explain the conflicting findings reported in the literature. The difference between the two inert gases may be related to the difference in the narcotic effect of nitrogen. Proof through further research of a correlation between individual sensitivity to nitrogen narcosis and protection by N(2) against CNS oxygen toxicity in rat may lead to a personal O(2) limit in mixed-gas diving based on the diver sensitivity to N(2) narcosis.The effects of adenosine-5'-diphosphate (ADP), epinephrine, nd 5-hydroxytryptamine (5HT) on nitrogen microbubble induced platelet aggregation were studied in-vitro. Platelet rich plasma (PRP) obtained from healthy human blood donors was stirred for 30 minutes in the presence of nitrogen microbubbles, 0.5 to 5 micromolar (microM) ADP, 0.1 to 1microM epinephrine, or 0.5 to 10microM 5HT, alone or in combination. The experiments with epinephrine were also performed in the presence or absence of 25microM indomethacin, 10microM acetylsalicylic-acid (ASA), or 1microM (146485). Some of the experiments with 5HT had 12.5microM ketanserin present. The extent of platelet aggregation was determined by measuring changes in platelet density in a cellcounter. A similar experiment was performed in which the PRP was pretreated with nitrogen microbubbles for 5 minutes before the ADP, epinephrine, or 5HT was added. Nitrogen microbubbles alone caused a progressive, irreversible aggregation of platelets. ADP alone caused an immediate platelet aggregation. Microbubbles plus ADP showed an additive, irreversible effect. Epinephrine alone caused a progressive, irreversible decrease in platelet density. Nitrogen microbubbles plus epinephrine showed a strong synergistic effect on platelet aggregation. Indomethacin and ASA partially countered the synergistic effect. 5HT caused a slight decrease in platelet density. 5HT plus nitrogen microbubbles inhibited platelet aggregation. The effect of 5HT was abolished by ketanserin. Microbubble stimulation of PRP before adding ADP, 5HT, and epinephrine made the platelets more responsive to epinephrine only. The authors conclude that epinephrine has a clear synergistic effect on nitrogen microbubble induced platelet aggregation. ...The effect of oxygen on nitrogen elimination was studied for six healthy nonsmoking males, 22 to 35 years old. Subjects breathed oxygen/argon mixtures having oxygen partial pressures (PO2s) of 0.12, 0.2, 1.0, 2.0, or 2.5 atmospheres (atm) for 125 minutes in a closed circuit system. Respiratory elimination of nitrogen by the subjects was measured using a gas tight rebreathing apparatus. Heart rate, cardiac output, calf blood flow, skin perfusion, blood pressure, and mean arterial pressure were monitored. Breathing 0.12atm oxygen caused a 9.4% increase in nitrogen elimination compared to the normoxic condition, PO2 0.2atm. Breathing pure oxygen, PO2 1.0atm, caused a 3.5% decrease in nitrogen elimination. Breathing mixtures containing 2.0 and 2.5atm oxygen caused 8.9 and 16.9% decreases in nitrogen elimination, respectively. Increasing the PO2 in the breathing mixture caused decreases in heart rate, cardiac output, skin perfusion, and calf blood flow. Systolic blood pressure was not affected. Diastolic blood pressure was decreased by the hypoxic gas mixture, but increased with increasing PO2 in the other mixtures. Mean arterial pressure increased with increasing PO2. The authors conclude that increasing PO2 in breathing mixtures causes a decrease in perfusion dependent nitrogen elimination that is secondary to a vasoconstrictive effect. These results suggest that oxygen breathing during post dive decompression treatment should be done at the lowest possible PO2 that does not induce decompression sickness.The physiological consequences of anoxia caused by exposure to carbon-monoxide and nitrogen were studied in isolated hearts of rats. Male Sprague-Dawley-rats were anesthetized, and hearts were removed, suspended in saline, cannulated, and perfused in a mixture of 95 percent oxygen/5 percent carbon-dioxide, 95 percent carbon-monoxide/5 percent carbon-dioxide, or 95 percent nitrogen/5 percent carbon-dioxide. All hearts were perfused with oxygen for 30 minutes before switching to test perfusate. Heart function was constantly monitored under the different conditions. The lactic-acid content of perfusate was measured. The glycogen contents of the hearts were determined by a spectrophotometric method. The water content was determined by measuring the difference in wet and dry weights of the heart. Data was analyzed for statistical significance. Heart rate declined rapidly when hearts were subjected to stress in the presence of nitrogen or carbon-monoxidethe decline in heart rate was 64 and 44 percent of control values in the presence of carbon-monoxide and nitrogen, respectively. Lactic-acid concentrations increased significantly after nitrogen and carbon-monoxide exposure. Heart tissue water content did not differ between carbon-monoxide and nitrogen exposed hearts. Heart tissue glycogen content decreased significantly in nitrogen or carbon-monoxide exposed hearts. The authors conclude that nitrogen and carbon-monoxide exert differential effects in physiological and biochemical events in the myocardia. |
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