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.

scholarly journals Humidity does not affect central nervous system oxygen toxicity

2001 ◽  
Vol 91 (3) ◽  
pp. 1327-1333 ◽  
Author(s):  
R. Arieli ◽  
Y. Moskovitz
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Water Vapor ◽  
Metabolic Rate ◽  
Hyperbaric Oxygen ◽  
Medical Therapy ◽  
Electrical Discharge ◽  
Oxygen Toxicity ◽  
Loss Of Consciousness ◽  
Hyperbaric Therapy

Central nervous system (CNS) oxygen toxicity can occur as convulsions and loss of consciousness when hyperbaric oxygen is breathed in diving and hyperbaric medical therapy. Lin and Jamieson ( J Appl Physiol 75: 1980–1983, 1993) reported that humidity in the inspired gas enhances CNS oxygen toxicity. Because alveolar gas is fully saturated with water vapor, we could not see a cause and effect and surmised that other factors, such as metabolic rate, might be involved. Rats were exposed to 507- and 608-kPa O2 in dry (31 or 14%) or humid (99%) atmosphere until the appearance of the first electrical discharge preceding the clinical convulsions. Each rat served as its own control. A thermoneutral temperature (28 ± 0.4°C) yielded resting CO2 production of 0.81 ± 0.06 ml · g−1 · h−1. Latency to the first electrical discharge was not affected by humidity. At 507-kPa O2, latency was 23 ± 0.4 and 22 ± 0.7 min in dry and humid conditions, respectively, and, at 608-kPa O2, latency was 15 ± 4 and 14 ± 3 min in dry and humid conditions, respectively. When no effects of CO2 and metabolic rate are present, humidity does not affect CNS oxygen toxicity. Relevance of the findings to diving and hyperbaric therapy is discussed.

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.

Response to CO2 in novice closed-circuit apparatus divers and after 1 year of active oxygen diving at shallow depths

2005 ◽  
Vol 98 (5) ◽  
pp. 1653-1659 ◽  
Author(s):  
Mirit Eynan ◽  
Ran Arieli ◽  
Yochai Adir
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Oxygen Toxicity ◽  
Major Effect ◽  
Active Oxygen ◽  
Closed Circuit ◽  
Two Phases ◽  
One Year ◽  
End Tidal

Elevated arterial Pco2 (hypercapnia) has a major effect on central nervous system oxygen toxicity in diving with a closed-circuit breathing apparatus. The purpose of the present study was to follow up the ability of divers to detect CO2 and to determine the CO2 retention trait after 1 year of active oxygen diving with closed-circuit apparatus. Ventilatory and perceptual responses to variations in inspired CO2 (range: 0–5.6 kPa, 0–42 Torr) during moderate exercise were assessed in Israeli Navy combat divers on active duty. Tests were carried out on 40 divers during the novice oxygen diving phase (ND) and the experienced oxygen diving phase. No significant changes were found between the two phases for the minimal mean inspired Pco2 that could be detected. The mean (with SD in parentheses) end-tidal Pco2 during exposure to an inspired Pco2 of 5.6 kPa (42 Torr) was significantly higher in the novice diving phase than in the experienced diving phase [8.1 kPa (SD 0.7), 62 Torr (SD 5) and 7.8 kPa (SD 0.6), 59 Torr (SD 4), respectively; P ≤ 0.001]. One year of shallow oxygen diving activity with a closed-circuit apparatus does not affect the ability to detect CO2 nor does it lead to increased CO2 retention; rather, it may even bring about a decrease in this trait. This finding suggests that acquiring experience in oxygen diving with a closed-circuit apparatus at shallow depths does not place the diver at a greater risk of central nervous system oxygen toxicity due to CO2 retention.

scholarly journals Severe haemophilia A in a preterm girl with Turner syndrome: case report – a diagnostic and therapeutic challenge for a paediatrician (Part 2)

2021 ◽  
Vol 47 (1) ◽  
Author(s):  
Berendt Agnieszka ◽  
Wójtowicz-Marzec Monika ◽  
Wysokińska Barbara ◽  
Kwaśniewska Anna
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Family History ◽  
Factor Viii ◽  
Turner Syndrome ◽  
Factor Viii Inhibitor ◽  
Haemophilia A ◽  
Severe Haemophilia ◽  
Prolonged Bleeding ◽  
Increased Risk

Abstract Background Haemophilia A is an X-linked genetic condition which manifests itself mainly in male children in the first 2 years of life, during gross motor skill development. This disorder is rare in females. The clinical manifestation of severe haemophilia in preterm infants poses a great challenge to the therapeutic team. As extreme prematurity is linked to an increased risk of central nervous system or gastrointestinal bleeding, a well-informed and balanced treatment from the first days of life is crucial to prevent long-term damage. Haemophilia is most commonly caused by inheriting defective genes, and can also be linked to skewed X inactivation and Turner syndrome. The coincidental occurrence of haemophilia A and Turner syndrome is extremely rare, with only isolated cases described to date. Hence, a multidisciplinary approach is needed. Case presentation The authors report on a preterm girl (gestational age 28 weeks) diagnosed with haemophilia and Turner syndrome. The first manifestation of haemophilia was prolonged bleeding from injection sites on the second day of life. Indeterminate aPTT and factor VIII level < 1% confirmed the diagnosis of haemophilia A. Dysmorphic features which did not match the typical clinical picture of haemophilia, the female sex, and a negative paternal family history led to the diagnosis of Turner syndrome. While in hospital, the girl received multiple doses of recombinant factor VIII in response to prolonged bleedings from the injection sites and from a nodule on the girl’s head, and before and after retinal laser photocoagulation. No central nervous system or abdominal cavity bleeding was observed. The substitutive therapy was complicated by the development of factor VIII inhibitor (anti-factor VIII (FVIII) antibodies). Treatment was continued with recombinant factor VIIa. This article aims at demonstrating the complexity of the diagnostics and treatment of a preterm child with two genetic disorders. Conclusions Haemophilia should always be considered in the differential diagnosis of prolonged bleeding, even in patients with a negative family history. In the case of coinciding atypical phenotypic features, further diagnostics for another genetic disease are recommended. Infant care should follow current care standards, while considering certain individual features.

scholarly journals Maternal Overnutrition Induces Long-Term Cognitive Deficits across Several Generations

Nutrients ◽  
2018 ◽  
Vol 11 (1) ◽  
pp. 7 ◽  
Author(s):  
Gitalee Sarker ◽  
Daria Peleg-Raibstein
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cognitive Deficits ◽  
Maternal Obesity ◽  
Cognitive Impairments ◽  
Long Term Effects ◽  
Ample Evidence ◽  
Increased Risk ◽  
Maternal Overnutrition

Ample evidence from epidemiological studies has linked maternal obesity with metabolic disorders such as obesity, cardiovascular disease, and diabetes in the next generation. Recently, it was also shown that maternal obesity has long-term effects on the progeny’s central nervous system. However, very little is known regarding how maternal overnutrition may affect, in particular, the cognitive abilities of the offspring. We reported that first-generation offspring exposed to a maternal high-fat diet (MHFD) displayed age-dependent cognitive deficits. These deficits were associated with attenuations of amino acid levels in the medial prefrontal cortex and the hippocampus regions of MHFD offspring. Here, we tested the hypothesis that MHFD in mice may induce long-term cognitive impairments and neurochemical dysfunctions in the second and third generations. We found that MHFD led to cognitive disabilities and an altered response to a noncompetitive receptor antagonist of the N-Methyl-D-aspartic acid (NMDA) receptor in adult MHFD offspring in both second and third generations in a sex-specific manner. Our results suggest that maternal overnutrition leads to an increased risk of developing obesity in subsequent generations as well as to cognitive impairments, affecting learning and memory processes in adulthood. Furthermore, MHFD exposure may facilitate pathological brain aging which is not a consequence of obesity. Our findings shed light on the long-term effects of maternal overnutrition on the development of the central nervous system and the underlying mechanisms which these traits relate to disease predisposition.

scholarly journals Systemic inflammatory response syndrome and multiple-organ damage / dysfunction in complicated canine babesiosis

2001 ◽  
Vol 72 (3) ◽  
Author(s):  
C. Welzl ◽  
A.L. Leisewitz ◽  
L.S. Jacobson ◽  
T. Vaughan-Scott ◽  
E. Myburgh
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Renal Involvement ◽  
Organ Damage ◽  
Multiple Organ ◽  
Systemic Inflammatory Response ◽  
The Body ◽  
Increased Risk

This study was designed to document the systemic inflammatory response syndrome (SIRS) and multiple-organ dysfunction syndrome (MODS) in dogs with complicated babesiosis, and to assess their impact on outcome. Ninety-one cases were evaluated retro-spectively for SIRS and 56 for MODS. The liver, kidneys, lungs, central nervous system and musculature were assessed. Eighty-seven percent of cases were SIRS-positive. Fifty-two percent of the cases assessed for organ damage had single-organ damage and 48 % had MODS. Outcome was not significantly affected by either SIRS or MODS, but involvement of specific organs had a profound effect. Central nervous system involvement resulted in a 57 times greater chance of death and renal involvement in a 5-fold increased risk compared to all other complications. Lung involvement could not be statistically evaluated owing to co-linearity with other organs, but was associated with high mortality. Liver and muscle damage were common, but did not significantly affect outcome. There are manysimilarities between the observations in this study and previous human and animal studies in related fields, lending additional support to the body of evidence for shared underlying pathophysiological mechanisms in systemic inflammatory states.

scholarly journals The Impact of Diabetes on Hippocampus

2021 ◽  
Author(s):  
Saeed Vafaei-Nezhad ◽  
Masood Vafaei-Nezhad ◽  
Mehri Shadi ◽  
Samira Ezi
Keyword(s):  
Central Nervous System ◽  
Developing Countries ◽  
Nervous System ◽  
Child Mortality ◽  
Maternal Diabetes ◽  
Mortality And Morbidity ◽  
Increased Risk ◽  
The Impact ◽  
Diabetic Mothers ◽  
Lines Of Evidence

Maternal Diabetes is one of the most common metabolic disorders resulting an increased risk of abnormalities in the developing fetus and offspring. It is estimated that the prevalence of diabetes during pregnancy among women in developing countries is approximately 4.5 percent and this range varies between 1 to 14 percent in different societies. According to earlier studies, diabetes during pregnancy is associated with an increased risk of maternal and child mortality and morbidity as well as major congenital anomalies including central nervous system (CNS) in their offspring. Multiple lines of evidence have suggested that infants of diabetic women are at risk of having neurodevelopmental sequelae. Previous studies reveal that the offspring of diabetic mothers exhibit disturbances in behavioral and intellectual functioning. In the examination of cognitive functioning, a poorer performance was observed in the children born to diabetic mothers when compared with the children of non-diabetic mothers. Therefore, it is important to study the possible effects of maternal diabetes on the hippocampus of these infants.

scholarly journals Catastrophizing Interferes with Cognitive Modulation of Pain in Women with Fibromyalgia

Pain Medicine ◽  
2018 ◽  
Vol 19 (12) ◽  
pp. 2408-2422 ◽  
Author(s):  
Laura D Ellingson ◽  
Aaron J Stegner ◽  
Isaac J Schwabacher ◽  
Jacob B Lindheimer ◽  
Dane B Cook
Keyword(s):  
Central Nervous System ◽  
Chronic Pain ◽  
Nervous System ◽  
Pain Catastrophizing ◽  
Pain Modulation ◽  
Critical Function ◽  
Sensory Stimuli ◽  
Brain Responses ◽  
Increased Risk ◽  
Pain Ratings

Abstract Background Pain modulation is a critical function of the nociceptive system that includes the ability to engage descending pain control systems to maintain a functional balance between facilitation and inhibition of incoming sensory stimuli. Dysfunctional pain modulation is associated with increased risk for chronic pain and is characteristic of fibromyalgia (FM). Catastrophizing is also common in FM. However, its influence on pain modulation is poorly understood. Objective To determine the role of catastrophizing on central nervous system processing during pain modulation in FM via examining brain responses and pain sensitivity during an attention-distraction paradigm. Methods Twenty FM patients and 18 healthy controls (CO) underwent functional magnetic resonance imaging while receiving pain stimuli, administered alone and during distracting cognitive tasks. Pain ratings were assessed after each stimulus. Catastrophizing was assessed with the Pain Catastrophizing Scale (PCS). Results The ability to modulate pain during distraction varied among FM patients and was associated with catastrophizing. This was demonstrated by significant positive relationships between PCS scores and pain ratings (P < 0.05) and brain responses in the dorsolateral prefrontal cortex (P < 0.01). Relationships between catastrophizing and pain modulation did not differ between FM and CO (P > 0.05). Conclusions FM patients with higher levels of catastrophizing were less able to distract themselves from pain, indicative of catastrophizing-related impairments in pain modulation. These results suggest that the tendency to catastrophize interacts with attention-resource allocation and may represent a mechanism of chronic pain exacerbation and/or maintenance. Reducing catastrophizing may improve FM symptoms via improving central nervous system regulation of pain.

Conclusion

2020 ◽  
pp. 237-238
Author(s):  
John F. Peppin ◽  
Joseph V. Pergolizzi ◽  
Robert B. Raffa ◽  
Steven L. Wright
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Side Effects ◽  
Mechanism Of Action ◽  
Term Treatment ◽  
Risk Of Death ◽  
Increased Risk ◽  
Treatment Plans ◽  
The Central Nervous System ◽  
System Data

The authors summarize the harmful and understudied aspects of the overuse of benzodiazepines. Increased and longer-term use of benzodiazepines has been observed to lead to side effects such as sedation, cognitive issues, abuse, and dependence, as well as many other unanticipated side effects that do not fit their known mechanism of action in the central nervous system. Data also shows a correlation between concomitant use of benzodiazepines and opioids and increased risk of death from overdose. The authors advocate for stricter guidelines for prescribing benzodiazepines, as well as close clinical monitor and shorter-term treatment plans.

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