In critically ill patients requiring intensive care, increased oxidative stress plays an important role in pathogenesis. Sedatives are widely used for sedation in many of these patients. Some sedatives are known antioxidants. However, no studies have evaluated the direct scavenging activity of various sedative agents on different free radicals. This study aimed to determine whether common sedatives (propofol, thiopental, and dexmedetomidine (DEX)) have direct free radical scavenging activity against various free radicals using in vitro electron spin resonance. Superoxide, hydroxyl radical, singlet oxygen, and nitric oxide (NO) direct scavenging activities were measured. All sedatives scavenged different types of free radicals. DEX, a new sedative, also scavenged hydroxyl radicals. Thiopental scavenged all types of free radicals, including NO, whereas propofol did not scavenge superoxide radicals. In this retrospective analysis, we observed changes in oxidative antioxidant markers following the administration of thiopental in patients with severe head trauma. We identified the direct radical-scavenging activity of various sedatives used in clinical settings. Furthermore, we reported a representative case of traumatic brain injury wherein thiopental administration dramatically affected oxidative-stress-related biomarkers. This study suggests that, in the future, sedatives containing thiopental may be redeveloped as an antioxidant therapy through further clinical research.

Heat stroke is a life-threatening illness caused by exposure to high ambient temperatures and relative humidity. The incidence of heat stroke is expected to increase due to climate change. Although pituitary adenylate cyclase-activating polypeptide (PACAP) has been implicated in thermoregulation, the role of PACAP on heat stress remains unclear. PACAP knockout (KO) and wild-type ICR mice were subjected to heat exposure at an ambient temperature of 36 °C and relative humidity of 99% for 30–150 min. After heat exposure, the PACAP KO mice had a greater survival rate and maintained a lower body temperature than the wild-type mice. Moreover, the gene expression and immunoreaction of c-Fos in the ventromedially preoptic area of the hypothalamus, which is known to harbor temperature-sensitive neurons, were significantly lower in PACAP KO mice than those in wild-type mice. In addition, differences were observed in the brown adipose tissue, the primary site of heat production, between PACAP KO and wild-type mice. These results suggest that PACAP KO mice are resistant to heat exposure. The heat production mechanism differs between PACAP KO and wild-type mice.

Background: Patients under cardiopulmonary resuscitation (CPR) are at high risk of aspirating gastric contents. Nasogastric tube insertion (NGTI) after tracheal intubation is usually performed blindly. This sometimes causes laryngopharyngeal mucosal injury (LPMI), leading to severe bleeding. This study clarified the incidence of LPMI due to blind NGTI during CPR. Methods: We retrospectively analyzed 84 patients presenting with cardiopulmonary arrest on arrival, categorized them into a Smooth group (Smooth; blind NGTI was possible within 2 min), and Difficult group (blind NGTI was not possible), and consequently performed video laryngoscope-assisted NGTI. The laryngopharyngeal mucosal condition was recorded using video laryngoscope. Success rates and insertion time for the Smooth group were calculated. Insertion number and LPMI scores were compared between the groups. Each regression line of outcome measurements was obtained using simple regression analysis. We also analyzed the causes of the Difficult group, using recorded video laryngoscope-assisted videos. Results: The success rate was 78.6% (66/84). NGTI time was 48.8 ± 4.0 s in the Smooth group. Insertion number and injury scores in the Smooth group were significantly lower than those in the Difficult group. The severity of LPMI increased with NGT insertion time and insertion number. Conclusions: Whenever blind NGTI is difficult, switching to other methods is essential to prevent unnecessary persistence.

Background: Aconitum poisoning can cause severe arrhythmias. We report, for the first time, the detailed blood and urine concentrations of four aconitine alkaloids in a male patient in his 20s who ingested aconite roots with suicidal intent. Case Presentation: The patient developed refractory torsade de pointes (TdP) and required veno‐arterial extracorporeal membrane oxygenation. His TdP resolved 7 h after arrival, with sinus rhythm returning within 12 h. The patient was discharged 6 days later. Subsequent measurements of the four alkaloids over time showed that jesaconitine had the highest serum concentration, with the patient's sinus rhythm returning when the jesaconitine concentration was less than 1 ng/mL. Conclusion: This report provides valuable insights into the disposition of aconitine alkaloids during severe intoxication. The changes in jesaconitine concentrations over time correlate with clinical symptoms, suggesting that these levels could guide treatment decisions in patients with severe Aconitum poisoning.

Heat stroke may cause multi-organ dysfunction and death. Some patients with neurological abnormalities in the acute phase have neurological sequelae, particularly cerebellar ataxia, in the recovery phase. However, there is no method to predict the neurological prognosis, and the usefulness of imaging has not yet been established. We report the case of an 86-year-old woman with dementia brought to our emergency department in a coma and hyperthermia. The patient was diagnosed with heat stroke and promptly treated in the ICU but remained unconscious. The patient gained consciousness on day 19, but difficulty with stillness associated with cerebellar ataxia in her right upper extremity became apparent. On day 1, head magnetic resonance imaging (MRI) showed no obvious abnormality. However, on day 6, high-signal areas, suggestive of edema, were seen in the bilateral cerebellar hemispheres. Single-photon emission computed tomography (SPECT) on day 9 revealed significant hypoperfusion in the right cerebellum. These changes improved at the time of hospital discharge. This was a case of persistent cerebellar ataxia due to heat stroke, in which imaging findings improved over time. In most cases, MRI findings do not match clinical symptoms. However, the low cerebral blood flow in the early SPECT images was consistent with the clinical symptoms. MRI may not be a prognostic indicator; however, SPECT images may be useful for predicting sequelae.

Heatstroke induces fluid loss and electrolyte abnormalities owing to high ambient temperature (AT) and relative humidity (RH). Aquaporin 1 (AQP1) is a key protein for water homeostasis; however, its role in heatstroke remains unclear. This study examines endothelial AQP1 in Tie2-Cre/LNL-AQP1 double transgenic (dTG) mice with upregulated Aqp1 in endothelial cells. For experimental heatstroke, mice were exposed to 41 °C AT and >99% RH. Blood, brain, kidney, and liver samples were collected 24 h later. Blood was analyzed for electrolytes and tissue damage markers, and organs were examined using morphological and immunohistological staining for 3-nitrotyrosine (3-NT), AQP1, and Iba-1. No difference in Aqp1 expression was observed in the whole brain; however, it was detected in dTG mice after capillary deprivation. AQP1 immunostaining revealed immunoreaction in blood vessels. After heat exposure, wild-type and dTG mice showed electrolyte abnormalities compared with non-heatstroke wild-type mice. Hepatic damage markers were significantly higher in dTG mice than in wild-type mice. Hematoxylin–eosin staining and 3-NT immunoreactivity in the liver indicated hepatic damage. The number of Iba-1-positive cells adherent to hepatic vasculature was significantly higher in dTG mice than in wild-type mice. This study is the first to suggest that endothelial AQP1 contributes to hepatic damage after heatstroke.