Effect of hyperbaric oxygen treatment on patients with heatstroke complicated by multiple organ dysfunction:A retrospective study.

Background: The benefits of hyperbaric oxygen (HBO) in treating animals with heat stroke (HS) have been established. This study aims to retrospectively analyze the effect of HBO on multiple organ dysfunction following HS in humans. Methods: Retrospective data were collected from patients with HS admitted to our hospital in the past 7 years. Patients were categorized into groups based on whether they received HBO therapy. The study compared various factors, including sequential organ failure assessment (SOFA) and acute physiology and chronic health evaluation-Ⅱ (APACHE-Ⅱ) scores, mortality rates, neurological function scores, serum myocardial enzyme levels, liver, kidney, and coagulation function indicators, blood routine results, electrolyte levels, and modified Barthel index (MBI) score for standard daily living ability before treatment and after 2 and 4 weeks of treatment. Results: The mortality rates in the HBO and control group were 0% and 8.49%, respectively. Upon admission, the HBO group had higher SOFA and APACHE-Ⅱ scores and lower neurological, coagulation, and liver functions than those of the control group. HBO treatment significantly improved SOFA, APACHE-Ⅱ, and neurological scores while relieving levels of alanine aminotransferase, aspartate aminotransferase, creatinine, and myocardial enzymes. Additionally, it mitigating lymphocyte and platelet count decline caused by HS. The MBI score was significantly enhanced after treatment in the HBO group. Conclusions: Clinical practice advocates administering HBO therapy to patients with severe illness, organ damage, and nerve impairment. Compared with conventional treatment, combined HBO therapy demonstrated superior efficacy in alleviating multiple organ dysfunction and improving daily living ability in patients with HS.

Analysis of Clinical Symptoms of Guillain-Barré Syndrome Induced by Heat Stroke: Three Case Reports and Literature Review.

Background: Heat stroke is a potentially fatal condition that is caused by elevated core temperature. Guillain-Barré syndrome (GBS) induced by heat stroke is extremely rare and has only been reported in few case reports. The purpose of this case study was to evaluate the clinical symptoms, neuroelectrophysiological and imageological features of GBS after heat stroke. Methods: We reviewed our hospital records and previously published reports to find the cases of GBS after heat stroke. The clinical, imageological, and electrophysiological profiles, treatment and prognosis were presented and analyzed. Results: We retrieved three cases of GBS induced by heat stroke from our hospital, which presented as lesions on multiple cranial and peripheral nerves and albuminocytologic dissociation in the cerebrospinal fluid. All of these patients had disorders of consciousness at the early stage of heat stroke and a "pseudo-recovery period" after they recovered from coma after heat stroke. After immunoglobulin administration and immunoregulation therapy, these patients' neurological deficiencies were relieved significantly. But there are still disabilities and almost totally reliant on others. Conclusions: The number of the cases of GBS induced by HS reported in this study has been the most in the recent 5 years. Clinicians should pay attention to patients with heat stroke with sustained coma and the sudden quadriplegia. Early, exact and timely diagnosis and treatment of GBS need to be performed, to accelerate recovery and improve prognosis.

Protective Effects of Hyperbaric Oxygen Therapy on Brain Injury by Regulating the Phosphorylation of Drp1 Through ROS/PKC Pathway in Heatstroke Rats.

This study aimed to elucidate the neurotherapeutic effect of hyperbaric oxygen (HBO) on brain injury and the potential role of dynamin-related protein 1 (Drp1) and its regulatory pathway in heatstroke (HS) rats. In in vivo experiments, rats were exposed to HBO after the onset of HS, or the same pressure but normal air as a control. The results indicated that HBO decreased the mortality and thermoregulatory dysfunction and prolonged the survival time of HS rats. Neurological dysfunction induced by HS was attenuated by HBO through assessment of modified neurological severity score and Morris water maze. HBO also alleviated histopathologic changes and oxidative injury (malondialdehyde and 8-hydroxyguanine), increased activities of superoxide dismutase (SOD) and glutathione/oxidized glutathione and ameliorated apoptotic parameters (caspase-3/6 activities and the number of apoptotic cells) of the hippocampus, hypothalamus and brain stem in rats compared to the HS group. Phosphorylation of DrpSer616 was increased by HS but decreased by HBO in the brains of rats determined by Western blot and immunohistochemical staining. In experiments in vitro, rat hippocampal neurons were used as a heat stress (HS) cellular model to examine the effects of HBO. As the results, HBO attenuated HS-induced cytotoxicity, oxidative injury (malondialdehyde), reactive oxygen species (ROS) generation, decreasing SOD activity and apoptosis. Drp1 inhibitor (Mdivi-1) treatment produced the same effects and had a trend to decrease oxidative injury. But the difference is not statistically significant. HBO and Mdivi-1decreased the phosphorylation of DrpSer616 induced by HS and HBO decreased the phosphorylation of protein kinase C (PKC) induced by HS. Moreover, both PKC inhibitor and ROS scavenger inhibited HS-induced p-DrpSer616. In conclusion, HBO may alleviate the brain injury caused by HS by decreasing ROS/PKC-regulated p-DrpSer616.

[Factors affecting recovery of consciousness in patients with disorders of consciousness following brain trauma: a logistic regression analysis].

OBJECTIVE: To explore the factors that affect the recovery of consciousness in patients with disorders of consciousness following brain trauma. METHODS: We analyzed the data of 114 patients with disorders of consciousness following brain trauma admitted for rehabilitation. Bilateral logistic regression analysis was used to explore the factors that affected the recovery of the patients' consciousness. A logistic regression model was established and the ROC curve was drawn to obtain the optimal threshold of the prognostic model. RESULTS: Univariate analysis showed that vegetative state duration (P<0.001), CRS-R scores (P<0.001), hydrocephalus (P=0.037), hypertonia (P=0.034), central fever (P=0.035), paroxysmal sympathetic hyperactivity (PSH) (P=0.004), and epilepsy seizures were correlated with the recovery of consciousness. Logistic multivariate analysis showed that central fever (OR=3.493, P=0.044), vegetative state duration (OR=1.016, P=0.008), PSH (OR=4.223, P=0.034) and CRS-R scores (OR=0.640, P=0.002) all significantly affected the recovery of consciousness. The χ2 value of the Hosmer-Lemeshow test was 10.214 (P=0.250), and the goodness of fit of this model indicated an outstanding fitting (c=0.91). CONCLUSIONS: The presence of PSH is the one of the most important factor followed by centric fever to affect the outcome of patients with disorders of consciousness. A lower CRS-R score and a longer duration of vegetative state also predict a poor recovery of consciousness in these patients.

Heat-shock protein 70 is involved in hyperbaric oxygen preconditioning on decompression sickness in rats.

Decompression sickness (DCS) is a major concern in diving and space walk. Hyperbaric oxygen (HBO) preconditioning has been proved to enhance tolerance to DCS via nitric oxide. Heat-shock protein (HSP) 70 was also found to have protective effects against DCS. We hypothesized that the beneficial effects of HBO preconditioning on DCS was related to levels of elevated HSP70. HSPs (70, 27 and 90) expressed in tissues of spinal cord and lung in rats was detected at different time points following HBO exposure by Western blot. HSP27 and HSP90 showed a slight but not significant increase after HBO. HSP70 increased and reached highest at 18 h following exposure before decreasing. Then rats were exposed to HBO and subjected to simulated air dive and rapid decompression to induce DCS 18 h after HBO. The severity of DCS, along with levels of HSP70 expression, as well as the extent of oxidative and apoptotic parameters in the lung and spinal cord were compared among different groups of rats pretreated with HBO, HBO plus NG-nitro-l-arginine-methyl ester (l-NAME), HBO plus quercetin or normobaric air. HBO preconditioning significantly reduced the morbidity of DCS (from 66.7% to 36.7%), reduced levels of oxidation (malondialdehyde, 8-hydroxyguanine and hydrogen peroxide) and apoptosis (caspase-3 and -9 activities and the number of apoptotic cells). l-NAME or quercetin eliminated most of the beneficial effects of HBO on DCS, and counteracted the stimulation of HSP70 by HBO. Bubbles in pulmonary artery were detected using ultrasound imaging to observe the possible effect of HBO preconditioning on DCS bubble formation. The amounts of bubbles in rats pretreated with HBO or air showed no difference. These results suggest that HSP70 was involved in the beneficial effects of HBO on DCS in rats, suspected be by the antioxidation and antiapoptosis effects.

Combined effects of intravenous perfluorocarbon emulsion and oxygen breathing on decompression-induced spinal cord injury in rats.

The spinal cord is one of the most commonly affected sites in decompression sickness (DCS). Alternative methods have long been sought to protect against DCS spinal cord dysfunction, especially when hyperbaric treatment is unavailable. Use of perfluorocarbon (PFC) emulsion with or without oxygen breathing has shown survival benefits in DCS animal models. The effectiveness of intravenous PFC emulsion with oxygen breathing on spinal cord function was studied. Somatosensory-evoked potentials (SSEPs) and histologic examination were chosen to serve as measures. After fast decompression (203 kPa/minute) from 709 kPa (for 60 minutes), male Sprague-Dawley rats randomly received: 1) air and saline; 2) oxygen (O2) and saline; 3) O2 and PFC emulsion. The incidence and average number of abnormal SSEP waves in survival animals that received O2 and PFC emulsion were significantly reduced (P < 0.05). Foci of demyelination, necrosis and round non-staining defects in white matter regions of the spinal cord could be found in severe DCS rats. We concluded that administration of PFC emulsion combined with oxygen breathing was beneficial for DCS spinal conductive dysfunction in rats.

Protective effect of hydrogen-rich saline on decompression sickness in rats.

INTRODUCTION: Hydrogen (H2) has been reported to be effective in the treatment of oxidative injury, which plays an important role in the process of decompression sickness (DCS). This study was designed to test whether H2-rich saline (saline saturated with molecular hydrogen) protected rats against DCS. METHODS: Models of DCS were induced in male Sprague-Dawley rats weighing 300-310 g. H2-rich (0.86 mmol x L(-1)) saline was administered intraperitoneally (10 ml x kg(-1)) at 24 h, 12 h, immediately before compression, and right after fast decompression. RESULTS: H2-rich saline significantly decreased the incidence of DCS from 67.57 to 35.14% and partially counteracted the increases in the total concentration of protein in the bronchoalveolar lavage from 0.33 +/- 0.05 to 0.14 +/- 0.01 mg x ml(-1) (mean +/- SD; P < 0.05), myeloperoxidase activity from 0.86 +/- 0.16 to 0.44 +/- 0.13 U/g, levels of malondialdehyde (MDA) from 0.80 +/- 0.10 to 0.48 +/- 0.05 nmol x mg(-1), 8-hydroxydeoxyguanosine from 253.7 +/- 9.3 to 191.2 +/- 4.8 pg x mg(-1) in the lungs, and MDA level from 1.77 +/- 0.20 to 0.87 +/- 0.23 nmol x mg(-1) in the spinal cord in rat DCS models. The histopathology results also showed that H2-rich saline ameliorated DCS injuries. DISCUSSION: It is concluded that H2-rich saline may have a protective effect against DCS, possibly due to its antioxidant action.