A 27-yr-old postgraduate student was found lying at the floor of an unsealed underground dry area, where a valve-opened empty cylinder of liquid nitrogen (150 L) was connected to a cap-removed empty Dewar-flask (10 L) via a copper infusion tube. No injury was found externally or internally. There were petechiae in the bilateral conjunctivae and periorbital skin. The dry area, measuring 300X130X260 cm, had a communication to the basement of the research building by a window measuring 90X60 cm in size at 130 cm above the floor. The scene reconstruction and atmosphere gas analysis revealed that the O2 concentration at 60 cm above the base dropped to 12.0% in 3 min and 10 sec, 10.0% in 8 min and 53 sec, 6.0% in 18 min and 40 sec, and 4.2% in 20 min and 28 sec. The primary cause of death was asphyxia by evaporated liquid nitrogen..
*Accidents, Occupational ; Adult ; Asphyxia/*chemically induced ; Cause of Death ; Humans ; Male ; Nitrogen/*poisoning

OBJECTIVETo Evaluate the effects of different oxygen therapies on the rats with acute nitrogen asphyxia and to study the best oxygen therapic protocol for patients with acute nitrogen asphyxia on the spot.

METHODSSixty healthy male Wistar rats were divided into 5 groups: control, exposure to nitrogen, 33% oxygen treatment, 50% oxygen treatment and hyperbaric oxygen treatment groups. The behavioral performance, arterial oxygen pressure (PO2), carbon dioxide partial pressure (PCO2) and oxygen saturation (SPO2), biochemical changes in liver and kidney function and myocardial enzymes in 5 groups were measured.

RESULTSThe rats exposed to nitrogen firstly were excited then inactive symptoms, but consciousness was recovered after oxygen therapy. The PO2 and SPO2 in nitrogen exposure group were (79.67 +/- 9.12) and (94.92 +/- 2.78) mm Hg, respectively, which were significantly lower than those in control group (P<0.01). The PO2 and SPO2 of 3 oxygen treatment groups were (94.75 +/- 7.24), (94.92 +/- 8.98), (104.58 +/- 7.12)mm Hg and (97.17 +/- 0.83), (96.92 +/- 1.16), (97.42 +/- 0.67)mm Hg, respectively, which were significantly higher than those in nitrogen exposure group (P<0.05). The PO2 in hyperbaric oxygen treatment group was significantly higher than those in other 2 oxygen treatment groups (P<0.05). The SPO2 in hyperbaric oxygen treatment group was (51.42 +/- 6.60) mm Hg which was significantly higher than that [(44.58 +/- 3.42)mm Hg] in 50% oxygen treatment groups (P< 0.05). AST [(270.50 +/- 49.05 )U/L], ALT [(122.67 +/- 55.44 )U/L], BUN [(7.31 +/- 0.93 )mmol/L], Cr[(28.32 +/- 4.35) micromol/L], CK [(1808.42 +/- 582.05)U/L] and CtnI [(22.52 +/- 14.29 )ng/ml] in nitrogen exposure group were significantly higher than those in control group (P<0.05). AST [(165.25 +/- 30.87) U/L], HBDH [(350.83 +/- 103.00)U/L] and CtnI [(11.23 +/- 5.38) ng/ml] in hyperbaric oxygen treatment group were significantly lower than those in other 2 oxygen treatment groups (P<0.05).

CONCLUSIONTimely and effective oxygen therapy can significantly increase arterial pressure of oxygen and oxygen saturation in the rats with acute nitrogen asphyxia, and can improve liver function and cardiac damage. The hyperbaric oxygen chamber can significantly increase the therapeutic effects on rats with acute nitrogen asphyxiation.

Animals ; Asphyxia ; blood ; chemically induced ; Blood Gas Analysis ; Hyperbaric Oxygenation ; Male ; Nitrogen ; toxicity ; Oxygen Inhalation Therapy ; Rats ; Rats, Wistar