Electroencephalographic Studies on Liquefied Petroleum Gas Poisoning in Rabbits

Kômura, Saburô; Ueda, Masao; Fujimura, Kazuaki

doi:10.1620/tjem.111.33

Cited by 6 publications

(3 citation statements)

References 9 publications

(6 reference statements)

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“…Such smokes are now known to contain hydrocarbons and other harmful substances such as nitrogen IV oxide and ultrafine particles [14]. Some hazardous effects of DCG in exposed animals have also been documented [15]. Effects of chronic exposure of laboratory mice to DCG were examined in this study.…”

Section: Discussionmentioning

confidence: 99%

Exposure of Laboratory Mice to Domestic Cooking Gas: - Implications for Toxicity

Odunola

2008

Int. J. Environ. Res. Public Health

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Abstract:The ability of domestic cooking gas to induce hepatotoxicity and clastogenicity in mice was studied. The mice were exposed to domestic gas for twenty-one days at doses of 100 mg/kg, 200 mg/kg and 300 mg/kg respectively. The positive control group of mice were given sodium arsenite intraperitoneously at a dose of 2.5mg/kg body weight. While the negative control group had only distilled water, sodium arsenite significantly (p < 0.05) induced the formation of micronucleated polychromatic erythrocytes (mPCEs), serum and liver gamma glutamyl transferase (γGT) and alkaline phosphatase (AP) activities respectively as compared with the observations made in the negative control group. Similarly, the domestic gas significantly (p<0.05) induced mPCEs formation, serum and liver, γGT and AP activities. The degree of induction was in the order of 100 mg/kg < 200 mg/kg < 300 mg/kg. However, when compared with the positive control group, the domestic cooking gas at the tested doses was not as potent as sodium arsenite in its ability to induce enzyme activity and mPCEs formation. Limited histopathological analysis of liver samples from treated and untreated mice showed distended blood vessels, necrosis and hepatocellular degeneration in the groups treated with high doses of domestic gas or sodium arsenite as compared with the untreated group. Our findings suggest that the domestic cooking gas has some degree of clastogenic and hepatotoxic activities in mice. Health risks may therefore be associated with long-term occupational and / or domestic exposure in humans.

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Section: Discussionmentioning

confidence: 99%

Exposure of Laboratory Mice to Domestic Cooking Gas: - Implications for Toxicity

Odunola

2008

Int. J. Environ. Res. Public Health

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“…One end of the canulae was left open for breathing and the other end was connected with a 500 ml water reservoir with a dripping infusion apparatus, through which the fresh water or sea water was infused into the trachea at a rate of 0.5 to 2.0 ml per min. Implantation of permanent electrodes was done by the method reported previously (Komura et al 1973), according to the atlas of Sawyer et al (1954) and Monnier and Gangloff (1961). The position of cortical and subcortical electrodes was as follows: Cortex sensitivo-motorius (Cm) at anterior (A) 4, lateral (L) 3; Cortex opticus (Co) at posterior (P) 10, L 9; Cortex sensitivus (Cse), P 3, L 9; Amygdala (Amg), A 3, L 6.5, Height (H), 17.5; Nucl.…”

Section: Methodsmentioning

confidence: 99%

Electrophysiological Studies on Slowly Induced Sea and Fresh Water Drowning in Rabbits

Fujimura

Kômura

Furuno

et al. 1979

Tohoku J. Exp. Med.

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-255 -Surface and deep electroencephalograms , electrocardiogram and behavior of 10 male rabbits were studied by infusing fresh water or sea water slowly at a speed of 0.5-2.0 ml/min, by means of a dripping apparatus, into the canulated trachea until the death of the animals.From the behavior of the animal and EEG and ECG findings, the course was divided into 4 stages. The 1st, alert stage; 2nd, adapted or calm stage; 3rd, dyspnea stage; and 4th, covering from the agonal spasm to ECG silence. The course of this drowning death was quite different from that due to a large amount of water aspirated within a short period. The volume of fresh water needed to kill the animals was 7 times larger than that of the sea water in this method, and the latter was less than half of the volume of sea water necessary for the death due to short period aspira tion. The mechanism of death seems to be slow and prolonged asphyxia and, among the terminal events in fresh water drowning, there might occur marked pulmonary hypertension that results in a high degree of lung edema.In the ECG at terminal stage, final bradycardia (84.4% of normal pulse rate) at around the time of surface EEG disappearance, and final tachycardia (142.7% of normal pulse rate) about 120 sec later than final bradycardia and 40 min later than deep EEG disappearance were observed consistently. After clinical signs of death ECG still continued to beat slowly for 1-2 hr.slowly induced sea and fresh water drowning; permanent electrode; EEG; ECG Since the first heart transplantation was performed in 1967 in our country, the donor-problem has been widely discussed all over Japan, not only from the medical but also from the ethical and moral aspects. One of the authors, as a surgeon, has experienced an operative death case in which continuous ECG tracing was taken for more than one hr after the clinical signs of death. But the courses of events around the time of death of living creatures were not clearly documented so as to be readily applied for the resuscitation and/or organ transplantation etc. by any physicians or surgeons.

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“…The degree of intoxication was measured by observing the behavior, by recording the drinking behavior on a pulse recorder, by calculating gaschromatographically the blood alcohol concentration (Ueda 1967) and by taking depth electroencephalogram readings (Komura et al 1973). …”

Section: Methodsmentioning

confidence: 99%