scholarly journals Central nervous system oxygen toxicity during 100% oxygen breathing at normobaric pressure

2020 ◽  
Vol 50 (3) ◽  
pp. 306-306
Author(s):  
Richard E Moon ◽  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Oxygen Toxicity ◽  
Oxygen Breathing

Prediction of central nervous system oxygen toxicity in rats

1994 ◽  
Vol 77 (4) ◽  
pp. 1903-1906 ◽  
Author(s):  
R. Arieli ◽  
G. Hershko
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Exposure Time ◽  
Electrical Discharge ◽  
Oxygen Toxicity ◽  
Threshold Value ◽  
Power Equation ◽  
The Mean

Cumulative O2 toxicity (K) can be calculated using the expression K = t2 x PO2c, where t is exposure time and the power c is to be determined; the phenomenon is liable to occur when K reaches Kc, the threshold value of K at which a symptom is manifested. Six rats were each exposed six times to 6 ATA O2 at 2-day intervals until the first electrical discharge (FED) was noted in an electroencephalogram. There was no difference in latency to FED in the series of six exposures. Thirteen rats were exposed to O2 until FED was noted in an electroencephalogram. They were exposed to four constant PO2's of 5, 6, 7, and 8 ATA and to two combined profiles of 1) 5 min at 7 ATA followed by 5 ATA and 2) 15 min at 5 ATA followed by 7 ATA. The solution of the equation for each rat was used to predict its latency to FED on the combined profile. The correlation of predicted to measured latency was significant (P < 0.0001), and the slope was not different from 1. Solving for these parameters using the combination of all the data, we obtained Kc = 5.71 x 10(6) and c = 5.39, which correctly predicted the mean latency but failed to predict individual latency. It is preferable to use each rat as its own control. The significance of the correlation supports the validity of the power equation for calculating K.

Effect of Interaction between Adenosine and Nitric Oxide on Central Nervous System Oxygen Toxicity

2019 ◽  
Vol 36 (1) ◽  
pp. 193-203 ◽  
Author(s):  
Cheng-wei Xie ◽  
Zhong-zhuang Wang ◽  
Ya-nan Zhang ◽  
Yu-liang Chen ◽  
Run-ping Li ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Central Nervous System ◽  
Nervous System ◽  
Oxygen Toxicity

scholarly journals Female rats are more susceptible to central nervous system oxygen toxicity than male rats

2014 ◽  
Vol 2 (4) ◽  
pp. e00282 ◽  
Author(s):  
Heather E. Held ◽  
Raffaele Pilla ◽  
Geoffrey E. Ciarlone ◽  
Carol S. Landon ◽  
Jay B. Dean
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Oxygen Toxicity ◽  
Female Rats ◽  
Male Rats

The effect of vigabatrin on central nervous system oxygen toxicity in rats

1991 ◽  
Vol 202 (2) ◽  
pp. 171-175 ◽  
Author(s):  
Tzahala Tzuk-Shina ◽  
Noemi Bitterman ◽  
Dan Harel
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Oxygen Toxicity

scholarly journals Common Uses and Adverse Effects of Hyperbaric Oxygen Therapy in a Cohort of Small Animal Patients: A Retrospective Analysis of 2,792 Treatment Sessions

2021 ◽  
Vol 8 ◽  
Author(s):  
Christina Montalbano ◽  
Caroline Kiorpes ◽  
Lindsay Elam ◽  
Erin Miscioscia ◽  
Justin Shmalberg
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adverse Event ◽  
Adverse Effects ◽  
Adverse Events ◽  
Hyperbaric Oxygen Therapy ◽  
Medical Records ◽  
Oxygen Therapy ◽  
Oxygen Toxicity ◽  
Small Animals

Hyperbaric oxygen therapy (HBOT) is commonly utilized for various human conditions with a low incidence of major adverse effects (0.002–0.035%). Despite growing use in veterinary patients, there remains a paucity of literature describing its use and associated complications. The purpose of this study was to report clinical use of HBOT in small animals and identify the rate of major adverse events at a university teaching hospital. Electronic medical records were searched for small animals receiving HBOT between November 2012 and February 2020. Data extracted from the medical records included signalment, treatment indication, and adverse events. Treatment sessions totaled 2,792 in 542 dogs, 24 cats, and 10 pocket pets and exotics. Common indications included neurologic injuries (50.4%), tissue healing (31.4%), control of oomycete infection (5.5%), neoplasia or post-radiation injury (5.4%), and various miscellaneous conditions (7.4%). Observed minor adverse events included agitation in two dogs and vomiting in three dogs. The most common major adverse event was central nervous system (CNS) oxygen toxicity in 19 dogs. Central nervous system oxygen toxicity, manifesting as focal or generalized seizures, occurred in 0.7% of treatment sessions, with increasing age (p = 0.01) and female sex (p = 0.01) identified as risk factors. One dog developed pulmonary edema following HBOT which is a reported adverse event in humans or may have been a manifestation of progression of the dog's underlying disease. No adverse events were noted in cats or other species. In conclusion, HBOT appeared safe across various indications, although oxygen toxicity affecting the CNS was higher than reports in humans. Future prospective, randomized, controlled trials should evaluate specific clinical indications and outcomes.

Pco 2 threshold for CNS oxygen toxicity in rats in the low range of hyperbaric Po 2

2001 ◽  
Vol 91 (4) ◽  
pp. 1582-1587 ◽  
Author(s):  
R. Arieli ◽  
G. Rashkovan ◽  
Y. Moskovitz ◽  
O. Ertracht
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Electrical Discharge ◽  
Oxygen Toxicity ◽  
Entire Population ◽  
Closed Circuit ◽  
Loss Of Consciousness ◽  
Risk Zone ◽  
Increased Risk ◽  
Ph Reduction

Central nervous system (CNS) oxygen toxicity, as manifested by the first electrical discharge (FED) in the electroencephalogram, can occur as convulsions and loss of consciousness. CO2potentiates this risk by vasodilation and pH reduction. We suggest that CO2 can produce CNS oxygen toxicity at a Po 2 that does not on its own ultimately cause FED. We searched for the CO2 threshold that will result in the appearance of FED at a Po 2 between 507 and 253 kPa. Rats were exposed to a Po 2 and an inspired Pco 2 in 1-kPa steps to define the threshold for FED. The results confirmed our assumption that each rat has its own Pco 2 threshold, any Pco 2 above which will cause FED but below which no FED will occur. As Po 2 decreased from 507 to 456, 405, and 355 kPa, the percentage of rats that exhibited FED without the addition of CO2 (F0) dropped from 91 to 62, to 8 and 0%, respectively. The percentage of rats (F) having FED as a function of Pco 2 was sigmoid in shape and displaced toward high Pco 2 with the reduction in Po 2. The following formula is suggested to express risk as a function of Pco 2and Po 2 [Formula: see text] [Formula: see text] [Formula: see text]where P50 is the Pco 2 for the half response and N is power. A small increase in Pco 2 at a Po 2 that does not cause CNS oxygen toxicity may shift an entire population into the risk zone. Closed-circuit divers who are CO2 retainers or divers who have elevated inspired CO2 are at increased risk of CNS oxygen toxicity.

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