Metabonomic potential plasma biomarkers in abnormal fast buoyancy ascent escape-induced decompression sickness model and the protective effects of pyrrolidine dithiocarbamic acid

2017 ◽  
Vol 44 (2) ◽  
pp. 109-119 ◽  
Author(s):  
Fang Yiqun ◽  
◽  
You Pu ◽  
Wang Haitao ◽  
Bai Xiaochen ◽  
...  
Keyword(s):  
Decompression Sickness ◽  
Protective Effects ◽  
Plasma Biomarkers ◽  
Dithiocarbamic Acid

Effects of hyperbaric oxygen pretreatment on brain antioxidant capacity in rats with decompression sickness

2021 ◽  
pp. 287-295
Author(s):  
Ya Li ◽  
◽  
Xiaona Xu ◽  
Junxiang Bao Bao ◽  
Wenlan Wang ◽  
...  
Keyword(s):  
Hyperbaric Oxygen ◽  
Decompression Sickness ◽  
Neuroprotective Effect ◽  
Male Rats ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Rat Models ◽  
Metal Elements ◽  
Flame Atomic Absorption ◽  
Brain Tissues

Objective: Decompression sickness (DCS) causes serious brain hypoxic-ischemic injury. This experiment was designed to observe whether hyperbaric oxygen (HBO2) pretreatment played a neuroprotective effect in decompression sickness rat models and to explore the mechanism of protective effects. Methods: Sprague-Dawley (SD) male rats were pretreated with HBO2 and then underwent decompression to establish the DCS rat model. Antioxidant capacities were evaluated by detecting peroxides (GPx), superoxide dismutase (SOD), catalase (CAT) activity and malondialdehyde (MDA) content in brains. The levels of metal elements manganese (Mn), zinc (Zn), iron (Fe) and magnesium (Mg) in brain tissues were assessed by flame atomic absorption spectrometry. Necrosis and apoptosis of neurons were assessed by H-E staining and immunohistochemical staining. Results: HBO2 pretreatment reduced the degree of necrosis and apoptosis in brain tissues of decompression sickness rat models. In addition, HBO2 pretreatment increased GPx, SOD and CAT activities and reduced MDA accumulation. It also increased the content of Mn, Zn, Fe and Mg in brain tissue, which are all related to free radical metabolism. Conclusion: These results suggested that HBO2 pretreatment has protective effects on brain injury of rats with decompression sickness. The mechanism of the protective effects may be related to reducing oxidative damage by affecting metal elements in vivo.

The protective effects of 1,3-butanediol acetoacetate diester on decompression sickness in rats

2021 ◽  
Author(s):  
Kun Zhang ◽  
Haidong Zhang ◽  
Hongjie Yi ◽  
Guoyang Huang ◽  
Xupeng Zhao ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Decompression Sickness ◽  
Bubble Formation ◽  
Antioxidant Properties ◽  
Oxygen Toxicity ◽  
Causative Factor ◽  
Male Rats ◽  
Drug Candidate ◽  
Pharmacokinetic Analysis ◽  
Protective Effects

Inert gas bubbles are widely accepted as the causative factor of decompression sickness (DCS), resulting in gas embolism and systemic inflammatory responses. The anticonvulsive ketone ester 1,3-butanediol acetoacetate diester (BD-AcAc2) was reported to have the characteristics of increasing blood oxygen partial pressure and anti-inflammation, and was thought to have the potential to reduce bubble formation and alleviate the pathological process of DCS. This study aims to investigate the potential protection of BD-AcAc2 against DCS in a rat model. A single dose of BD-AcAc2 was administered orally to adult male rats (5 g/kg body weight), followed by pharmacokinetic analysis or simulated air dives. After decompression, signs of DCS were monitored, and blood was sampled for biochemical measurements. Blood ketosis peaked at 2 h and lasted for more than 4 h.The incidence of DCS was decreased and postponed significantly in rats treated with BD-AcAc2 compared with those treated with saline (P<0.05). Though BD-AcAc2 failed to reduce bubble load (P>0.05), it showed an obvious decreasing trend. BD-AcAc2 significantly increased blood ppO2 and ameliorated oxidative and inflammatory responses, representing by increased plasma MDA, IL-1, IL-6 and TNF-α and decreased glutathione thiol (P<0.05), while blood pH remained unchanged (P>0.05). These results suggest that BD-AcAc2 exerted beneficial effects on DCS rats mainly related to increasing ppO2, anti-inflammatory and antioxidant properties. Together with its capacity for delaying CNS oxygen toxicity seizures, BD-AcAc2 might be an ideal drug candidate for DCS prevention and treatment.

Effect of nitric oxide on spinal evoked potentials and survival rate in rats with decompression sickness

2015 ◽  
Vol 118 (1) ◽  
pp. 20-28
Author(s):  
T. Randsoe ◽  
C. F. Meehan ◽  
H. Broholm ◽  
O. Hyldegaard
Keyword(s):  
Nitric Oxide ◽  
Spinal Cord ◽  
Survival Rate ◽  
Evoked Potentials ◽  
Decompression Sickness ◽  
Bubble Formation ◽  
Control Group ◽  
Protective Effects ◽  
No Donor ◽  
Long Acting

Nitric oxide (NO) releasing agents have, in experimental settings, been shown to decrease intravascular nitrogen bubble formation and to increase the survival rate during decompression sickness (DCS) from diving. The effect has been ascribed to a possible removal of preexisting micronuclei or an increased nitrogen washout on decompression through augmented blood flow rate. The present experiments were conducted to investigate whether a short- or long-acting NO donor [glycerol trinitrate (GTN) or isosorbide-5-mononitrate (ISMN), respectively] would offer the same protection against spinal cord DCS evaluated by means of spinal evoked potentials (SEPs). Anesthetized rats were decompressed from a 1-h hyperbaric air dive at 506.6 kPa (40 m of seawater) for 3 min and 17 s, and spinal cord conduction was studied by measurements of SEPs. Histological samples of the spinal cord were analyzed for lesions of DCS. In total, 58 rats were divided into 6 different treatment groups. The first three received either saline ( group 1), 300 mg/kg iv ISMN ( group 2), or 10 mg/kg ip GTN ( group 3) before compression. The last three received either 300 mg/kg iv ISMN ( group 4), 1 mg/kg iv GTN ( group 5), or 75 μg/kg iv GTN ( group 6) during the dive, before decompression. In all groups, decompression caused considerable intravascular bubble formation. The ISMN groups showed no difference compared with the control group, whereas the GTN groups showed a tendency toward faster SEP disappearance and shorter survival times. In conclusion, neither a short- nor long-acting NO donor had any protective effect against fatal DCS by intravenous bubble formation. This effect is most likely due to a fast ascent rate overriding the protective effects of NO, rather than the total inert tissue gas load.

scholarly journals Protective Effects of Fluoxetine on Decompression Sickness in Mice

PLoS ONE ◽  
2012 ◽  
Vol 7 (11) ◽  
pp. e49069 ◽  
Author(s):  
Jean-Eric Blatteau ◽  
Sandrine Barre ◽  
Aurelie Pascual ◽  
Olivier Castagna ◽  
Jacques H. Abraini ◽  
...  
Keyword(s):  
Decompression Sickness ◽  
Protective Effects

Protective effects of pulmonary surfactant on decompression sickness in rats

2020 ◽  
Author(s):  
Xuhua Yu ◽  
Jiajun Xu ◽  
Wenwu Liu ◽  
Ze Zhang ◽  
Chunyang He ◽  
...  
Keyword(s):  
Pulmonary Surfactant ◽  
Decompression Sickness ◽  
Total Phospholipid ◽  
Protein A ◽  
Harmful Effect ◽  
Serum Levels ◽  
Lavage Fluid ◽  
Exogenous Surfactant ◽  
Protective Effects ◽  
Lung Dysfunction

Decompression sickness (DCS) is a systemic pathophysiological process featured by bubble load . Lung dysfunction plays a harmful effect on off-gassing, which contributes to bubble load and subsequent DCS occurrence. This study aimed to investigate the effects of pulmonary surfactant on DCS as it possessed multiple advantages on the lung. Rats were divided into three groups: the normal (n = 10), the surfactant (n = 36) and the saline (n = 36) group. Animals in surfactant or saline group were administered aerosol surfactant or saline 12 h before a stimulated diving, respectively. Signs of DCS were recorded and bubble load was detected. The contents of phospholipid and surfactant protein A (SPA), protein, IL-1 and IL-6 in bronchoalveolar lavage fluid (BALF) and lung wet/dry (W/D) ratio were determined. Serum levels of IL-6, ICAM-1, E-selectin, GSH and GSSG were detected. In surfactant treated rats, the morbidity and mortality of DCS markedly decreased (**P < 0.01, *P < 0.05, respectively). Survival time prolonged and the latency to DCS dramatically delayed (**P < 0.01). More importantly, bubble load markedly decreased (**P < 0.01). The increases of protein, IL-1 and IL-6 in BALF and lung W/D ratio were alleviated. Restoration of total phospholipid and SPA in BALF and ICAM-1 and E-selectin in serum were observed. The inflammation and oxidation were attenuated (# P < 0.01). In conclusion, pre-diving administrating exogenous surfactant by aerosolization is an efficient, simple and safe method for DCS prevention in rats.

Metabonomic studies on potential plasma biomarkers in rats exposed to ionizing radiation and the protective effects of Hong Shan Capsule

Metabolomics ◽  
2013 ◽  
Vol 9 (5) ◽  
pp. 1082-1095 ◽  
Author(s):  
Yue Liu ◽  
Ze-Bin Lin ◽  
Guang-Guo Tan ◽  
Zhi-Yong Chu ◽  
Zi-Yang Lou ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Protective Effects ◽  
Plasma Biomarkers

THE AMELIORATIVE EFFECTS OF HEPARIN AND DEPOLYMERIZED HYALURONATE ON DECOMPRESSION SICKNESS IN RATS

1964 ◽  
Vol 42 (6) ◽  
pp. 819-829 ◽  
Author(s):  
R. B. Philp
Keyword(s):  
Whole Blood ◽  
Blood Clotting ◽  
Decompression Sickness ◽  
Significant Degree ◽  
Protective Effects ◽  
Clotting Time ◽  
Degree Of Protection ◽  
Actual Evaluation ◽  
Dose Levels ◽  
Blood Clotting Time

The protective effects in decompression sickness of heparin, partially depolymerized hyaluronate (PDHA, a substance reported to have antilipaemic properties), and bishydroxycoumarin have been studied by a standardized compression–decompression technique in rats. Bishydroxycoumarin did not afford any significant degree of protection even at dose levels which prolonged the prothrombin time as much as five times normal. Heparin, however, significantly reduced the incidence of "bends" in rats at a dose which only briefly prolonged the whole-blood clotting time, and significantly reduced both the incidence and the severity at higher dose levels. PDHA produced the most marked reduction in both incidence and severity at dose levels which did not significantly alter the whole-blood clotting time. These protective effects were absent when heavy, fat rats were used, and when the compounds were administered before the compression (i.e. more than 2 hours before the actual evaluation of signs of the bends). In view of these results it is postulated that anticoagulation per se has little beneficial effect in treating the bends; the protection afforded by these mucopolysaccharides may be related to their lipaemia-clearing activity.

Melatonin reduces high levels of lipid peroxidation induced by potassium iodate in porcine thyroid

2019 ◽  
pp. 1-7 ◽  
Author(s):  
Paulina Iwan ◽  
Jan Stepniak ◽  
Malgorzata Karbownik-Lewinska
Keyword(s):  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Membrane Lipids ◽  
Chemical Properties ◽  
Iodine Concentration ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Protective Effects ◽  
Potassium Iodate ◽  
Hormone Synthesis

Abstract. Iodine is essential for thyroid hormone synthesis. Under normal iodine supply, calculated physiological iodine concentration in the thyroid is approx. 9 mM. Either potassium iodide (KI) or potassium iodate (KIO3) are used in iodine prophylaxis. KI is confirmed as absolutely safe. KIO3 possesses chemical properties suggesting its potential toxicity. Melatonin (N-acetyl-5-methoxytryptamine) is an effective antioxidant and free radical scavenger. Study aims: to evaluate potential protective effects of melatonin against oxidative damage to membrane lipids (lipid peroxidation, LPO) induced by KI or KIO3 in porcine thyroid. Homogenates of twenty four (24) thyroids were incubated in presence of either KI or KIO3 without/with melatonin (5 mM). As melatonin was not effective against KI-induced LPO, in the next step only KIO3 was used. Homogenates were incubated in presence of KIO3 (200; 100; 50; 25; 20; 15; 10; 7.5; 5.0; 2.5; 1.25 mM) without/with melatonin or 17ß-estradiol. Five experiments were performed with different concentrations of melatonin (5.0; 2.5; 1.25; 1.0; 0.625 mM) and one with 17ß-estradiol (1.0 mM). Malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) concentration (LPO index) was measured spectrophotometrically. KIO3 increased LPO with the strongest damaging effect (MDA + 4-HDA level: ≈1.28 nmol/mg protein, p < 0.05) revealed at concentrations of around 15 mM, thus corresponding to physiological iodine concentrations in the thyroid. Melatonin reduced LPO (MDA + 4-HDA levels: from ≈0.97 to ≈0,76 and from ≈0,64 to ≈0,49 nmol/mg protein, p < 0.05) induced by KIO3 at concentrations of 10 mM or 7.5 mM. Conclusion: Melatonin can reduce very strong oxidative damage to membrane lipids caused by KIO3 used in doses resulting in physiological iodine concentrations in the thyroid.

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