Comparison of the effects of drugs on nitrogen narcosis and oxygen toxicity in rats

Life Sciences ◽  
1962 ◽  
Vol 1 (12) ◽  
pp. 721-727 ◽  
Author(s):  
P.B. Bennett
Keyword(s):  
Oxygen Toxicity ◽  
Nitrogen Narcosis

scholarly journals Effects of nitrogen and helium on CNS oxygen toxicity in the rat

2005 ◽  
Vol 98 (1) ◽  
pp. 144-150 ◽  
Author(s):  
R. Arieli ◽  
O. Ertracht ◽  
I. Oster ◽  
A. Vitenstein ◽  
Y. Adir
Keyword(s):  
Oxygen Toxicity ◽  
Nitrogen Pressure ◽  
Repeated Measurements ◽  
Inert Gases ◽  
Helium Pressure ◽  
Mixed Gas ◽  
Nitrogen Narcosis ◽  
Individual Trait ◽  
The Difference ◽  
Different Levels

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 (Po2). We studied the effects of nitrogen and helium (0, 15, 25, 40, 50, and 60%) and different levels of Po2 (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 N2 against CNS oxygen toxicity in rat may lead to a personal O2 limit in mixed-gas diving based on the diver sensitivity to N2 narcosis.

scholarly journals Impaired consciousness when scuba diving associated with vasovagal syncope

2020 ◽  
Vol 50 (4) ◽  
pp. 421-423
Author(s):  
Peter Wilmshurst ◽  
◽  
Margaret Clamp ◽  
Keyword(s):  
Vasovagal Syncope ◽  
Oxygen Toxicity ◽  
Scuba Diving ◽  
Toxic Effects ◽  
Gas Embolism ◽  
Impaired Consciousness ◽  
Scuba Divers ◽  
Nitrogen Narcosis ◽  
Arterial Gas Embolism ◽  
Hyperbaric Medicine

(Wilmshurst P, Clamp M. Impaired consciousness when scuba diving associated with vasovagal syncope. Diving and Hyperbaric Medicine. 2020 December 20;50(4):421–423. doi: 10.28920/dhm50.4.421-423. PMID: 33325026.) Introduction: Drowning is likely to result from impairment of consciousness when scuba diving. Causes include toxic effects of breathing gas, including nitrogen narcosis and oxygen toxicity, and arterial gas embolism. Methods: Review of the medical records of scuba divers who had impaired consciousness underwater that could not be attributed to toxic effects of breathing gas or arterial gas embolism. Results: Four scuba divers had episodes of impaired consciousness when at shallow depths (8−18 m) underwater. The descriptions of the episodes were very similar. Three had histories of recurrent episodes of vasovagal syncope on land. Conclusions: Absence of other causes for their impaired consciousness underwater leads to the conclusion that the probable cause was vasovagal syncope.

Acute Pulmonary Oxygen Toxicity in Rats: Findings and Lung Density Changes in High Resolution Computed Tomography

2000 ◽  
Vol 42 (3) ◽  
pp. 473
Author(s):  
Dae Sik Ryu ◽  
Kun Sang Kim ◽  
Kil Hyen Kang ◽  
Haing Sup Chung ◽  
Bung Wok Lee ◽  
...  
Keyword(s):  
Computed Tomography ◽  
High Resolution ◽  
Oxygen Toxicity ◽  
High Resolution Computed Tomography ◽  
Lung Density

Puthology of Oxygen Toxicity

Pathology ◽  
1984 ◽  
Vol 16 (4) ◽  
pp. 486
Author(s):  
David Henderson-Smart
Keyword(s):  
Oxygen Toxicity

Hyperoxic myopia: a case series of four divers

2020 ◽  
pp. 261-265
Author(s):  
Jonathan W. Brügger ◽  
Glenn A. Rauscher ◽  
John P. Florian ◽  
Keyword(s):  
Hyperbaric Oxygen ◽  
Prolonged Exposure ◽  
Case Series ◽  
Oxygen Toxicity ◽  
Hyperbaric Oxygen Treatment ◽  
Subjective Data ◽  
Residual Symptoms ◽  
Oxygen Treatment ◽  
Blurry Vision ◽  
Record Review

Hyperoxic myopia is a phenomenon reported in individuals who have prolonged exposure to an increased partial pressure of oxygen (PO2) and subsequently have a myopic (nearsighted) change in their vision. To date, there are numerous accounts of hyperoxic myopia in dry hyperbaric oxygen treatment patients; however, there have been only three confirmed cases reported in wet divers. This case series adds four confirmed cases of hyperoxic myopia in wet divers using 1.35 atmospheres (ATM) PO2 at the Navy Experimental Diving Unit (NEDU). The four divers involved were the first author’s patients at NEDU. Conditions for two divers were confirmed via record review, whereas the other two divers were diagnosed by the first author. All subjects were interviewed to correlate subjective data with objective findings. Each subject completed five consecutive six-hour hyperoxic (PO2 of 1.35 ATM) dives with 18-hour surface intervals. Each individual was within the U. S. Navy Dive Manual’s standards for general health. Visual acuity was measured prior to diving. Within three to four days after diving, the individuals reported blurry vision with an associated myopic refraction shift. Each diver had spontaneous resolution of his myopia over the next two to three weeks, with no significant residual symptoms. The divers in this case series were exposed to an increased PO2 (1.35 ATM for 30 hours over five days), a lesser exposure than that in other reports of hyperoxic myopia in wet divers diagnosed with hyperoxic myopia (1.3-1.6 ATM for 45-85 hours in 12-18 days). Furthermore, this pulse of exposure was more concentrated than typically seen with traditional hyperbaric oxygen therapy. Hyperoxic myopia continues to be a risk for those conducting intensive diving with a PO2 between 1.3-1.6 ATM. Additional investigation is warranted to better define risk factors and PO2 limits regarding ocular oxygen toxicity.

Effect of prenatal isoxsuprine on pulmonary oxygen toxicity in the newborn rat

1980 ◽  
Vol 48 (3) ◽  
pp. 505-510 ◽  
Author(s):  
L. Frank ◽  
J. Summerville ◽  
D. Massaro
Keyword(s):  
Enzyme Activities ◽  
Oxygen Toxicity ◽  
Fetal Lung ◽  
Antioxidant Enzyme Activities ◽  
Newborn Rats ◽  
Lung Maturation ◽  
Lung Weight ◽  
Pregnant Rats ◽  
Rat Pups ◽  
Hyperoxic Exposure

Isoxsuprine, a beta-sympathomimetic agent used clinically to delay premature parturition and to possibly accelerate fetal lung maturation, was administered to pregnant rats at 48 and 24 h prior to delivery. Newborn rats were placed in 96-98% O2 (or room air) to determine if the prenatal isoxsuprine treatment compromised their tolerance to prolonged hyperoxic exposure. (Exogenous catecholamines are known to exacerbate O2 toxicity in adult animals). Survival of the isoxsuprine-treated pups in O2 (52%) was no different than for control neonates exposed to hyperoxia for 7 days (57%) (P = 0.22). Body weight, lung weight, lung protein, and DNA content of the newborns were also not altered by the prenatal isoxsuprine treatment. Lung antioxidant enzyme activities for superoxide dismutase, catalase, and glutathione peroxidase were the same at birth in the isoxsuprine-treated and control rat pups, and the enzyme activities increased in response to hyperoxic exposure in each group to an equivalent degree. Thus, in utero treatment with isoxsuprine had no apparent adverse effect on newborn rats exposed to a prolonged O2 challenge.

OXYGEN TOXICITY IN MAN

1972 ◽  
Vol 16 (2) ◽  
pp. 113???114
Author(s):  
R. E. Barber ◽  
J. Lee ◽  
W. K. Hamilton
Keyword(s):  
Oxygen Toxicity

scholarly journals The genetics of catalase in Drosophila melanogaster: isolation and characterization of acatalasemic mutants.

Genetics ◽  
1989 ◽  
Vol 122 (3) ◽  
pp. 643-652 ◽  
Author(s):  
W J Mackay ◽  
G C Bewley
Keyword(s):  
Drosophila Melanogaster ◽  
Free Radical ◽  
Catalase Activity ◽  
Oxygen Toxicity ◽  
Threshold Effect ◽  
Culture Conditions ◽  
Free Radical Damage ◽  
Isolation And Characterization ◽  
Standard Culture ◽  
Hypomorphic Alleles

Abstract Activated oxygen species have been demonstrated to be the important agents in oxygen toxicity by disrupting the structural and functional integrity of cells through lipid peroxidation events, DNA damage and protein inactivation. The biological consequences of free radical damage have long been hypothesized to be a causal agent in many aging-related diseases. Catalase (H2O2:H2O2 oxidoreductase; EC 1.15.1.1) is one of several enzymes involved in the scavenging of oxygen free radicals and free radical derivatives. The structural gene for catalase in Drosophila melanogaster has been localized to region 75D1-76A on chromosome 3L by dosage responses to segmental aneuploidy. This study reports the isolation of a stable deficiency, Df(3L)CatDH104(75C1-2;75F1), that uncovers the catalase locus and the subsequent isolation of six acatalasemic mutants. All catalase mutants are viable under standard culture conditions and recessive lethal mutations within the 75Cl-F1 interval have been shown not to affect catalase activity. Two catalase mutations are amorphic while four are hypomorphic alleles of the Cat+ locus. The lack of intergenic complementation between the six catalase mutations strongly suggests that there is only one functional gene in Drosophila. One acatalesemic mutation was mapped to position 3-47.0 which resides within the catalase dosage sensitive region. While complete loss of catalase activity confers a severe viability effect, residual levels are sufficient to restore viability to wild type levels. These results suggest a threshold effect for viability and offer an explanation for the general lack of phenotypic effects associated with the known mammalian acatalasemics.

Sign in / Sign up

Export Citation Format

Share Document