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The formation of the swim-bladder gases of some sea and fresh water fishes were investigated and the results may be summarized as follows : 1. As a rule, oxygen content in the swim-bladder is higher in a fish living at greater depth than at shallow, and sea water fishes, than fresh water ones. 2. Oxygen content in the swim-bladder of the fish living at great depth decreases after 1-2 days stay in the aquarium. 3. Carbon dioxide content in the swim-bladder of all fishes examined is very small. 4. Through the poisoning of carbon monoxide, the swim-bladder gas decreases in its oxygen content and increases slightly in its carbon dioxide. 5. Corresponding to the artificial increase or decrease of the external pressures influencing the body surface of the fish, oxygen content of the swim-bladder gases increases or decreases respectively. 6. After the evacuation of the swim-bladder gases, newly formed gases always contain high oxygen percentage. 7. When oxygen or carbon dioxide of high concentration are injected in the swim-bladder, these gases diffuse out easily through the wall of the swim-bladder during 1-2 days. 8. Oxygen dissociation curve of carp blood is remarkably steep compared with the human blood, and influenced very much with the presence of carbon dioxide so as to decrease the affinity of the blood to oxygen. 9. Histological examination of the swim-bladder of Sebastiscus marmoratus and Carassius auratus indicate characteristic structure of the blood capillaries which distributed in the internal layer of membranes and sinus-like dilated. 10. From the above experimental results, some considerations on the gas formation in the swim-bladder were offered.

Some mechanisms to reduce methemoglobin (metHb) formation for the maintenance of normal oxygen transport have been proposed. To study the role of catalase (EC 1.11.1.6), metHb formation in the hemolysate of normal and Japanese acatalasemic human subjects were examined spectrophotometrically. Significantly increased level of metHb was induced by potassium ferrocyanide in the hemolysate of acatalasemic subject. The addition of catalase reduced the metHb formation, while 3-amino-1,2,4-triazole (AT), a specific inhibitor of catalase-H2O2 compound I, increased it. These results obtained from human subjects were well consistent with those from mice and suggested that catalase plays a role in protecting erythrocytes against metHb formation.

Effects of antioxidants, such as superoxide dismutase, vitamin C, vitamin E, 4-(0-benzylphenoxy)-N-methylbutylamine hydrochloride (bifemelane), and selenite on survival of adult rat hepatocytes were examined under normoxic and hyperoxic conditions in serum-free primary culture. The tested antioxidants, except for vitamin C, significantly increased the survival rate of hepatocytes under the normoxic condition (under air). Thus, even the normoxic culture condition is hyperoxic for hepatocytes. Elevation of oxygen tension (40% O2) caused severe morphologic degeneration of hepatocytes and remarkable decrease in the survival rate of the cells. Addition of the antioxidants effectively protected hepatocytes from the morphologic degeneration, and significantly improved the survival of the cells under the hyperoxic condition. These findings indicate that the antioxidants can maintain the long-term survival of hepatocytes in serum-free primary culture.

<p>Iron plays a critical role in the production of activated oxygen species and the activity of chelated iron in the biological system depends on the chemical forms of the chelators. In the present study, we used ferric nitrolotriacetate (Fe-NTA, molar ratio of iron to chelators = 1:3), ferric ethylenediaminetetraacetate (Fe-EDTA, 1:3 complex) and ferric Desferal (Fe-Des, 1:1.1 complex) to see their "free" iron content in aqueous solutions in vitro and in the serum obtained after a single intraperitoneal injection of the chelates to rats (7.5 mg of iron/kg). "Free" iron was measured by the bleomycin-assay system. When Fe-NTA was dissolved in water, "free" iron increased linearly with total iron concentration up to 10 microM, whereas Fe-EDTA and Fe-Des showed no "free" iron with corresponding iron concentrations. When these three ferric chelates were dissolved in normal rat serum, "free" iron in Fe-NTA increased abruptly between 40 microM and 60 microM iron concentrations, then increased slowly up to 100 microM. Fe-Des did not show any "free" iron at comparable iron concentrations. Fe-EDTA had an intermediate "free" iron level in the serum. Among the ferric chelate complexes, Fe-NTA showed a much faster increase of and a higher content of "free" iron in the serum than the other two complexes after a single injection of the chelates into rats.(ABSTRACT TRUNCATED AT 250 WORDS)</p>

Head injury or hemorrhagic cortical infarction results in extravasation of blood and breakdown of red blood cells and hemoglobin. Iron liberated from hemoglobin, and hemoglobin itself, are associated with the generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS). ROS and RNS have been demonstrated to be involved in the mechanism of seizures induced by iron ions in the rat brain, an experimental animal model for posttraumatic epilepsy (PTE). ROS are responsible for the induction for peroxidation of neural lipids, i.e., an injury of neuronal membranes, and also could induce disorders in the excitatory and inhibitory neurotransmitters. Antioxidants, such as a phosphate diester of vitamin E and C (EPC-K1) and antiepileptic zonisamide, have been known to prevent the epileptogenic focus formation, or to attenuate seizure activities in the iron-injected rat brain. Natural antioxidants, such as alpha-tocopherol, and condensed tannins, including (-)-epigallocatechin and (-)-epigallocatechin-3-O-gallate, adenosine and its derivative, melatonin, uyaku (Lindera Strychnifolia), fermented papaya preparations, Gastrodia elata BI., and Guilingji, have been demonstrated to scavenge ROS and/or RNS and to be prophylactic for the occurrence of epileptic discharge in the iron-injected rat brain.

To elucidate the mechanism by which hyperbaric oxygen (HBO2) induces electrical discharge, changes in the extracellular concentrations of GABA and glutamate were measured every 5 min using a microdialysis technique in rats during a period of exposure to HBO2 (5 atm abs). Electrical discharge was observed at 28 +/- 4 min after the onset of exposure. Though the extracellular concentrations of glutamate remained unchanged, the extracellular GABA concentrations (pre-exposure level, 0.026 +/- 0.005 microM in dialysate) began to decrease 15 min after the onset of exposure and reached their lowest level (74 +/- 14%, 0.019 +/- 0.004 microM) at the time of appearance of the discharge. There was a close logistic relationship between extracellular GABA concentrations and the discharge incidence, and the extracellular concentrations of GABA causing electrical discharge in 50% of the animals were estimated to be 80% of the pre-exposure level. These results suggest a possible mechanism that HBO2 exposure-induced discharge is caused by the decrease in extracellular concentration of GABA.

The mechanisms of arterial hypotension following intravenous anesthetic induction agents are multifactorial. The purpose of this study was to evaluate and compare the effects of thiopental, propofol and etomidate on hemodynamics, sympathetic outflow and arterial baroreflex sensitivity using not only neuraxis-intact but also totally baro-denervated rabbits. A total of 60 rabbits was anesthetized with urethane, tracheotomized, and mechanically ventilated with oxygen in nitrogen (FiO2 0.5). The left renal sympathetic nerve was isolated and placed on a bipolar electrode to record renal sympathetic nerve activity (RSNA). Thirty animals underwent a surgical preparation of total baroreceptor denervation. Bolus injections of an anesthesia induction dose of thiopental 4 mg/kg and twice the induction dose of propofol 4 mg/kg significantly decreased RSNA to the same extent (19.4+/-6.7 and 19.7+/-5.2% reduction, mean +/- SEM) and mean arterial pressure (MAP) also to the same extent (19.5+/-4.6 and 22.1+/-3.1% reduction) in the neuraxis-intact animals. RSNA was increased (34.5+/-6%) without reduction of MAP by an induction dose of etomidate, 0.3 mg/kg. Sympathetic barosensitivity was attenuated even 10 min after thiopental at 4 mg/kg or propofol at 4 mg/kg (68% and 54% of control, respectively). Propofol at 2 mg/kg (induction dose) and etomidate at 0.6 mg/kg decreased RSNA and MAP only in the baro-denervated animals. It was found from the barosensitivity study that patients can be hemodynamically unstable even though blood pressure has returned to normal after thiopental and propofol administration. Data suggest that etomidate can even stimulate the sympathetic nervous system and increase sympathetic outflow. It was also clearly found from the baro-denervated animal study that thiopental was stronger than propofol in directly suppressing sympathetic outflow at the induction dose.

Ferric nitrilotriacetate (Fe3+-NTA) solution showed maximum absorbance at pH 7.5. The iron was in ferric high-spin state and coordinated octahedrally with a relatively symmetric structure and also probably pentagonally. A spin trapping technique employing 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) yielded a DMPO spin adduct of unknown radical with three doublets (DMPO-Z) and a simple nitroxide radical (Y-NO.) in serum from rats injected intraperitoneally with Fe3+-NTA. When the Fe3+-NTA solution was diluted 500-fold with 50 mM NTA solution, DMPO-Z, Y-NO. and an additional signal, DMPO-OH were observed. The DMPO-Z signal was suppressed by a decrease in oxygen tension, alpha-tocopherol and 3-tert-butyl-4-hydroxy-anisole (BHA). The DMPO-OH signal was suppressed in the presence of ethanol and catalase. Fe2+-NTA solution hardly produced DMPO spin adducts. The Fe3+-NTA solution produced a strong DMPO-OH signal in the presence of H2O2. Rose Bengal solution, a singlet oxygen generating system, produced the same DMPO adducts. Fe3+-NTA reacted with oxygen in solution. The oxygen was activated and might be similar to singlet molecular oxygen. In the presence of H2O2, the Fe3+-NTA solution generated a hydroxyl radical. Fe3+-NTA itself generated free radicals, but Fe2+-NTA did not.

This study evaluated the effects of chronic hypoxia from birth on the resistance of rat hearts to global ischemia, with special emphasis on the duration of hypoxia. Male Wistar rats were housed from birth for 4 weeks or 8 weeks either in a hypoxic environment (FiO20.12) or in ambient air (8 animals for each group). Isolated rat hearts were perfused for 40 min with oxygenated Krebs-Henseleit buffer, subjected to 20 min global no-flow ischemia at 37, and then underwent 40 min of reperfusion. A non-elastic balloon was inserted into the left ventricle and inflated until the pre-ischemic LVEDP rose to 8mmHg. Cardiac function was measured before and after ischemia. The post-ischemic percent recovery of LVDP in hypoxic hearts was worse than in normoxic hearts (4 weeks:55+/-7 vs. 96+/-3%, p0.01;8 weeks:40+/-5 vs. 92+/-4%, p0.01), and was worst in the 8-week-hypoxic hearts. Similarly, the percent recovery of dP/dt in the hypoxic hearts was lower than in the normoxic hearts (4 weeks:51+/-5 vs. 96+/-7%, p0.01;8 weeks:31+/-6 vs. 92+/-7%, p0.01), and was lowest in the 8-week-hypoxic hearts. In conclusion, cyanotic myocardium revealed an age-dependent vulnerability to ischemia-reperfusion injury in a chronic hypoxic rat model.

We encountered a rare case of suffocation by an advertising balloon filled with pure helium gas. Suffocation caused by inhalation of atmosphere lacking in oxygen is not exceptional, but reports of death by suffocation due to a pure inert gas such as helium are very rare. In this case, the balloon mooring on the ground was enclosed, warning signs were displayed, and it was clear that entering the balloon filled with an atmosphere lacking in oxygen was extremely dangerous and should not be done; the accident did, however, occur. Accidents of this kind may occur in the future unless appropriate education and countermeasures are taken.

We previously reported that anthracyclines, which could generate reactive oxygen species (ROS), could induce the urokinase-type plasminogen activator (uPA) gene expression in human RC-K8 malignant lymphoma cells and in H69 small cell lung cancer (SCLC) cells. In screening other uPA-inducible anti-cancer agents, we found that camptothecin (CPT) and its derivative, SN38, could induce uPA in RC-K8 and H69 cells. CPT and SN38, which are also used for the treatment of lymphoma and SCLC, significantly increased the uPA accumulation in the conditioned media of both cells in a dose-dependent manner. The maximum induction of uPA mRNA levels was observed 24 h after stimulation. Pretreatment with pyrrolidine dithiocarbamate (PDTC), an anti-oxidant, inhibited the CPT-induced uPA mRNA expression. Thus, CPT induces uPA through gene expression, and, therefore, CPT may influence the tumor-cell biology by up-regulating the uPA/plasmin system.

Leukotrienes, one of the mediators of inflammation in asthma, have a strong bronchoconstrictive effect. L-carnitine has been reported to influence respiratory functions. It has also been reported that L-carnitine inhibits leukotriene synthesis. To evaluate the effects of L-carnitine on oxygen saturation, urine leukotriene E4 levels and lung histopathology in a murine model of asthma, high IgE responder BALB/c mice (n = 24) were systemically sensitized to ovalbumin and chronically challenged with low particle mass concentrations of aerosolized ovalbumin, and then they were divided into 3 groups (study groups A, B, and C) each including eight mice. After methacholine-induced bronchoconstriction, the mice in groups A and B were given intraperitoneal L-carnitine (250 and 125 mg/kg, respectively), while the mice in group C were given placebo. Oxygen saturation of the mice was measured by pulse oxymeter before and after methacholine and after L-carnitine/ placebo application. In addition, urine leukotriene E4 levels were measured before asthma development, and 24-h after L-carnitine injection in asthmatic mice. Inflammation in the lung tissues of the sacrificed animals was scored histopathologically to determine the effect of L-carnitine on tissue level. A control group of non-sensitized mice (n = 8) treated with placebo only was used for comparison of urine leukotriene E4 levels and of histopathological parameters. Oxygen saturation of the mice in the study groups tended to decrease after methacholine and to improve after L-carnitine injection, although these changes were not significant at all time points. Urine leukotriene E4 levels of all 3 study groups increased significantly after asthma development. The rate of increment was smallest in the group given the highest L-carnitine dose (group A). Inflammation at the tissue level was also mildest in group A, and severest in the group that was not given carnitine (group C). All of the study groups and the control group differed significantly with respect to inflammation scores. In conclusion, L-carnitine improved oxygen saturation, and decreased urine leukotriene E4 levels and inflammation in lung tissues in the present murine model of asthma.

The ferric nitrilotriacetate-induced carcinogenesis model is unique in that reactive oxygen species-free radicals are involved in the carcinogenic process. But the effects of iron-withdrawal in the progression of renal cell carcinoma are not well understood. We performed repeated phlebotomies on animals that had been administered ferric nitrilotriacetate in the initiation stage of renal cell carcinoma (phlebotomy group), and compared the development of renal tumors with those not receiving repeated phlebotomies (non-phlebotomy group). Ferric nitrilotriacetate-treated male Wistar rats were randomly divided into 2 groups: a phlebotomy group (21 rats) and a non-phlebotomy group (17 rats). Ten age-adjusted normal rats were also observed as a normal group. Hematocrit was maintained under 25% in the phlebotomy group. Hematocrit levels in the normal group and in the non-phlebotomy group were not significantly different. As a result, the incidence of renal cell carcinoma was not significantly different between phlebotomy and non-phlebotomy animals. However, the total weight of the renal cell carcinoma was significantly heavier in the animals from non-phlebotomy group than in those from the phlebotomy group (23.64 g +/- 18.54 vs. 54.40 g +/- 42.40, P < 0.05). The present study demonstrated that phlebotomy after the administration of ferric nitrilotriacetate did not reduce the incidence of renal cell carcinoma. In addition, we showed that iron withdrawal at the promotion stage of carcinogenesis will retard tumor growth.

In recent years it has been reported that free oxygen radicals play an important role in the pathogenesis of degenerative diseases and that antioxidant vitamins such as vitamins E or C prevent their harmful effects. In this study, we evaluated the following: Erythrocyte susceptibility to lipid peroxidation; the role of erythrocyte glutathione (GSH) as an antioxidant; plasma lipid fractions; and the relationship between plasma lipid peroxides and antioxidant vitamin levels. Thiobarbituric acid-reactive substance (TBARS) levels were measured to determine the levels of plasma lipid peroxides and the susceptibility to lipid peroxidation when erythrocytes were stressed by hydrogen peroxide for 2 h in vitro. Erythrocyte TBARS production was significantly higher in patients with coronary atherosclerosis than in the controls. On the other hand, the levels of plasma high-density lipoproteins, vitamin C, vitamin E and erythrocyte GSH were significantly lower, and the levels of plasma total cholesterol, triglycerides, low-density lipoproteins and TBARS were significantly higher in the patients with coronary atherosclerosis than in the controls. In conclusion, our results indicate that erythrocytes from patients with coronary atherosclerosis are more susceptible to oxidation than those of controls and that these patients have lowered antioxidant capacity as revealed by decreased plasma levels of vitamins C and E.

Nipradilol (3,4-dihydro-8-(2-hydroxy-3-isopropylamino) propoxy-3-nitroxy-2H-1-benzopyran) is a newly synthesized chemical agent designed to possess beta-adrenoceptor blocking and vasodilating actions. Nipradilol decreased left ventricular contractility index (Emax, slope of the ventricular end-systolic pressure-volume relation), systolic pressure-volume area (PVA, a measure of ventricular total mechanical energy) and oxygen consumption in cross-circulated excised dog hearts. However, nipradilol did not decrease total coronary resistance. These results indicate that nipradilol, like propranolol, depresses myocardial mechanoenergetics and that the vasodilating action of nipradilol could not be detected in the present study.

We evaluated the viability of the cadaver lung and the effect of lung inflation with 100% oxygen using a canine allotransplantation model. Donor animals were killed by potassium chloride (KCl) injection and were kept at room temperature until lung extraction. The animals were divided into the following 3 groups: group 1 (n = 6) in which the donor lungs were retrieved 2h after sacrifice, group 2 (n = 6) in which the donor lungs were retrieved 3h after sacrifice, and group 3 (n = 6) in which the donor lungs were retrieved 3h after sacrifice as in group 2 except that they were kept inflated for 3h with 100% oxygen using a double lumen endotracheal tube. Heparin was not given and lungs were not flushed with preservation solution. After left lung transplantation, the transplanted lung function including gas exchange and pulmonary hemodynamics was assessed for 6h by ligating the right pulmonary artery of the recipient animals. All 6 animals in groups 1 and 3 survived for 6 h with excellent lung function. Only 2 of 6 animals in group 2 survived for 6h with poor lung function. These results led us to conclude the following: a) the cadaver lung kept at room temperature for 2h might be available for lung transplantation, and b) when the cadaver lung is inflated with 100% oxygen, the length of safe ischemic time could be prolonged up to 3h.

Experiments were undertaken to determine the relationship between evoked spinal cord potential (ESP) and the partial pressure of oxygen in tissue in the epidural space (E-pO2) during aortic clamping. Eighteen adult mongrel dogs were studied as follows. In group I (n = 6), the descending thoracic aorta was clamped partially at the proximal site for 15 min to maintain the distal arterial pressure at 60, 40, and 20 mmHg consecutively at 15 min intervals. In group II (n = 6), the descending thoracic aorta was clamped proximally for 30 min. In group III (n = 6), the descending thoracic aorta was cross-clamped at proximal and distal sites for 30 min. Postoperative complete paraplegia was observed in 4 of 6 dogs in group III, but none in group II. The change in ESP with aorta cross-clamping was very mild in groups I and II. Transient increases and decreases in the ESP amplitude were observed in group III. The decrease of E-pO2 correlated well with the distal arterial pressure, and a rapid return to baseline of the E-pO2 was observed after declamping. The E-pO2 changed in response to spinal ischemia more rapidly than did ESP in all groups. The critical level of E-pO2 was 50 mmHg or a 40% decrease from baseline. Because the ESP reflects spinal function and the E-pO2 reflects spinal blood pressure, we propose that combined recording of ESP and E-pO2 would improve spinal monitoring during thoracic aortic surgery.

With the purpose to see if GABOB is in any way concerned with the mechanism of the epileptic attack observations were carried on the oxygen consumption of the brain homogenates of rabbits, normal and CLA, and of human, epileptic and non-epileptic. The experiment proved that the oxygen consumption is increased in the epileptic brain and in the brain of CLA rabbit. It was raised by adding ATP-Na salt or DPN, but GABOB itself showed only a slight effect. The results suggested that the oxygen consumption of brain is not so closely correlated with GABOB, but there is a possibility that the decrease in GABOB contents in epileptic brain by the accelerated decomposition with its elevated oxygen consumption may be correlated to the epileptic attack, though the final conclusion requires further observations.

In connection with the cloudy swelling of the liver cell seen in the CCl4 intoxication the author observed the oxygen consumption rate of the liver slices at frequent intervals within 20 hours of CCl4 intoxication in rats. Unexpectedly, the oxygen consumption did not decrease by CCl4, intoxication in the stage where the cloudy swelling can be seen, especially in the media added with succinate. This finding suggests that the energy produced by respiration is not concerned with the swelling phenomenon in the case of CCl4 intoxication, differing from the supposition on the experiment of protozoa by using cyanide and others.