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Biomedical subjects

H Tsubone

Publications and source records attributed to H Tsubone.

85 records · Page 5Linked to original sources
PubMed1982

Biochemical studies on strain differences of mice in the susceptibility to nitrogen dioxide.

Strain differences of mice in their susceptibility to nitrogen dioxide (NO2) were examined by measuring the activities of antioxidative protective enzymes, and the amounts of antioxidants and lipid peroxides in lungs. Four strains of mice: ICR, BALB/c, ddy and C57BL/6 were used in this study and their LC50 values after exposure to NO2 for 16 hr were: 38, 49, 51 and 64 ppm, respectively (1). Genetic strain differences were observed in the enzyme activities, the antioxidant contents and lipid peroxide contents among these four different strains. The activities of glutathione peroxidase (GPX), glutathione S-transferase, and superoxide dismutase (SOD), and the contents of non-protein sulfhydryls (NPSH), alpha-tocopherol (alpha-Toc) and total lipids in lungs of the four strains were related to their LC50, while TBA reactants in lungs of the four strains were inversely related to their LC50. After exposure to 20 ppm NO2 for 16 hr, the activities of the protective enzymes and the contents of NPSH decreased, while the level of alpha-Toc increased markedly. The activities of GPX, 6-phosphogluconate dehydrogenase, SOD and disulfide reductase, and the contents of NPSH, alpha-Toc and total lipids were also related to their LC50. On the other hand, TBA reactants increased higher than those of the control groups and were inversely related to their LC50. These results suggest that the protective enzymes and the antioxidants are important factors at defence mechanism in lungs to NO2 and that the intensity of the protective systems in pigmented strains is generally greater than that in albino strains.

Animals↗
PubMed1982

Changes of gaseous exchange in the lungs of mice exposed to nitrogen dioxide and their recovery process.

To elucidate the accurate effects of NO2 on gaseous exchange in the lungs of mice during and after NO2 exposure, O2 and CO2 concentrations in the respiratory gas and respiratory rate (RR) were measured using the head-enclosed method, and arterial blood pHa, Paco2 and Pao2, lung wet weight, and lung water content were also examined. The results of the present study indicate that the gaseous exchange in the lungs of mice exposed to 20 ppm NO2 was acutely inhibited during NO2 exposure from the 3rd to 24th h, but it recovered functionally to the control level on the 3rd day after NO2 exposure.

Animals↗
PubMed1982

Electrocardiographic abnormalities in rats by acute exposure to nitrogen dioxide.

Changes in cardiac function of rats acutely exposed to nitrogen dioxide (NO2) were examined by electrocardiographic (ECG) records. Bradycardia and arrhythmia which were observed by exposure to 20 ppm NO2 or more for 3 h were abolished by injection of atropine sulfate. ECGs were recorded following experimental formation of nitrite (NO-2) and nitrate (NO-3) in blood of normal rats by administration of NaNO2 solution, but no remarkable changes were observed on ECG. These results suggest that abnormal cardiac function observed during acute exposure to NO2 is attributable to changes in parasympathetic nervous activity and not to elevated NO2- and NO3- concentration in blood.

Animals↗
PubMed1982

Changes of gaseous exchange in the lung of mice acutely exposed to nitrogen dioxide.

To clarify the acute effects of NO2 on gaseous exchange in the lung of mice, O2 and CO2 concentrations in respiratory gas, respiratory rate (RR), arterial blood pH, PaCO2, PaO2, lung wet weight and lung water content were examined using the head-enclosed method. The results of the present study indicate that in mice exposed to 5 ppm NO2 for 24 h the gaseous exchange in the lung and metabolic rate of O2 and CO2 in the body are accelerated, whereas in mice exposed to 10 ppm and 20 ppm NO2 the gaseous exchange in the lung is inhibited to change the gaseous metabolism.

Animals↗
PubMed1982

Effects of acute nitrogen dioxide exposure on swimming performance of mice.

To evaluate the acute effects of NO2 on the physical performance of experimental animals, male mice 15-16 wk old were exposed to 5, 10, 20, or 40 ppm NO2 for 24 h, and forced swimming endurance time (FSET), the changes in FSET during the postexposure days, lung wet weight, lung water content, and blood lactate level were examined. FSET of mice exposed to NO2 at 10, 20, and 40 ppm decreased immediately after exposure, FSET of mice exposed to 5 ppm NO2 did not change immediately after exposure, but a significant decrease was observed from d 1 to d 4 after exposure. FSET recovered to the initial control level after 5-6 d, 7-8 d, and over 9 d in mice exposed to NO2 at 5, 10, and 20 ppm, respectively. Lung wet weight of mice exposed to 20 and 40 ppm NO2 and lung water content of mice exposed to 10, 20, and 40 ppm NO2 increased with dose. A negative relation was demonstrated between FSET and lung wet weight and between FSET and lung water content. Without forced swimming exercise, the blood lactate level of mice exposed to 5 ppm NO2 was almost equivalent to that of control mice, but the blood lactate level of the exposed mice significantly increased immediately and 24 h after forced swimming exercise for 4 min.

Animals↗
PubMedDate not supplied

Respiratory reflexes in response to upper-airway administration of sevoflurane and isoflurane in anesthetized, spontaneously breathing dogs.

OBJECTIVE: To evaluate the respiratory effects occurring during administration of sevoflurane or isoflurane to the upper airway in dogs. STUDY DESIGN: A prospective, randomized study. ANIMALS: Twelve healthy adult beagles (6 males, 6 females). METHODS: At least 2 weeks after undergoing permanent tracheostomy, dogs were premedicated with acepromazine-buprenorphine, and anesthesia was induced with thiopental and maintained with alpha-chloralose. The upper airway was functionally isolated so that the inhalant could be administered to the upper airway while dogs were breathing 100% O2 via the tracheostomy. Respiratory reflexes in response to the administration of sevoflurane or isoflurane at concentrations of 1.2, 1.8, and 2.4 times the minimal alveolar concentration (MAC) (administered in 100% O2 at a flow rate of 5 L/min) were recorded. Reflexes in response to administration of each anesthetic were also recorded following upper-airway administration of lidocaine. RESULTS: Respiratory reflexes elicited by upper-airway administration of each anesthetic were characterized by a dose-dependent increase in expiration time, with a resultant decrease in respiratory minute ventilation and increase in end-tidal PCO2. The magnitude of these responses was greater with isoflurane than with sevoflurane at 1.8 and 2.4 MAC. These reflexes were abolished after lidocaine nebulization into the upper airway. CONCLUSION: Isoflurane induces greater reflex inhibition of breathing than does sevoflurane when the anesthetic is inhaled into the upper airway at concentrations used for mask induction.

Anesthetics, Inhalation↗
PubMedDate not supplied

Effect of ozone toxicity in the drinking behavior of rats.

To clarify the effects of ozone on behavior, drinking activity was observed continuously in animals exposed to ozone at concentrations of 0.2, 0.4, and 0.8 ppm for 1 wk. Drinking decreased considerably on the first day after onset of exposure. On the first day the suppression rate was calculated to be 28.1%, 69.5%, and 93.1%, for the 0.2 ppm, 0.4 ppm, and 0.8 ppm group, respectively. The suppression of drinking and recovery were dependent on the concentration of ozone.

Animals↗