Effect of PACAP on Heat Exposure.

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.

Benign noninfectious subcutaneous emphysema with minor injury: A case report.

Posttraumatic subcutaneous emphysema, which can be benign and noninfectious, is associated with necrotizing fasciitis. Rarely, extensive emphysema occurs after a minor traumatic injury. A 23-year-old man came to our hospital with extensive emphysema, ranging from the left hand to the axilla, after a minor injury. Necrotizing fasciitis was suspected. Based on the blood and imaging tests, necrotizing fasciitis was not actively suspected. He was admitted and observed for one day, and he was discharged the following day. The mechanism by which air can enter through a small injury is unclear, but the one-way ball-valve mechanism is the most commonly proposed explanation. The nontraumatic causes of non-infectious subcutaneous emphysema include insect bites, skin biopsies, and the use of shock absorbers. Since it developed from a minor wound, other mechanisms, aside from the one-way ball-valve, were possibly involved. Based on the imaging results of this case, the air was predominantly distributed in the subcutaneous tissue along the neurovascular bundle. The relatively sparse tissue likely caused the extensive subcutaneous emphysema. While evaluating post-traumatic subcutaneous emphysema, benign and noninfectious cases should be differentiated to prevent unnecessary therapeutic intervention.

Obstructive shock due to right ventricular compression by a massively expanded reconstructed gastric tube.

Obstructive shock is often associated with poor right ventricular (RV) output and requires rapid obstruction release. A 54-year-old man was brought to our emergency department, presenting with shock. He had previously undergone esophagectomy with gastric interposition through the retrosternal route, after which he could not eat solid foods. After eating a ball of rice, he became critically ill, with a significantly increased lactate level, an indicator of shock. Though initial examinations showed no abnormalities, he was hospitalized for observation. The following day, he experienced similar discomfort while in the supine position, an hour after breakfast. Cardiac sonography revealed that the RV was remarkably compressed by a massively expanded gastric tube, causing diastolic dysfunction. After propping him into a sitting position, he recovered from shock. Upon a second examination of CT images, we recognized the massively dilated gastric tube compressing the RV. Anatomically, the retrosternal route is located directly in front of the RV. Thus, it is thought that the massively dilated gastric tube externally compressed the RV, preventing adequate RV filling and causing the obstructive shock. In such cases, the patient's position should be changed immediately to release the RV compression.

Heatstroke-induced late-onset neurological deficits in mice caused by white matter demyelination, Purkinje cell degeneration, and synaptic impairment in the cerebellum.

Global warming increases heatstroke incidence. After heatstroke, patients exhibit neurological symptoms, suggesting cerebellar damage. However, the potential long-term adverse outcomes are poorly understood. We studied the cerebellum after heatstroke in mouse heatstroke models. In this study, motor coordination disorder significantly appeared 3 weeks after heatstroke and gradually improved to some extent. Although white matter demyelination was detected at 1 and 3 weeks after heatstroke in the cerebellum, it was not found in the corpus callosum. The Purkinje cell numbers significantly decreased at 1, 3, and 9 weeks after heatstroke. The intensity of synaptophysin and postsynaptic density-95 temporarily appeared to attenuate at 3 weeks after heatstroke; however, both appeared to intensify at 9 weeks after heatstroke. Motor coordination loss occurred a few weeks after heatstroke and recovered to some extent. Late-onset motor impairment was suggested to be caused by cerebellar dysfunctions morphologically assessed by myelin staining of cerebellar white matter and immunostaining of Purkinje cells with pre- and postsynaptic markers. Purkinje cell number did not recover for 9 weeks; other factors, including motor coordination, partially recovered, probably by synaptic reconstruction, residual Purkinje cells, and other cerebellar white matter remyelination. These phenomena were associated with late-onset neurological deficits and recovery after heatstroke.

Guillain-Barré syndrome diagnosed as central cervical spinal cord injury after hyperextension injury.

The clinical features of Guillain-Barré syndrome (GBS) are progressive, fairly symmetric muscle weakness, and patients present a few days to a week after onset of symptoms. A 63-y-old man strongly hit his forehead, and next day felt paresthesia in both upper limbs, with difficulty in walking. Spinal cord injury (SCI) was suspected; the cervical cord was severely compressed at the C4 level. He was diagnosed with central cervical SCI and transferred to a community hospital. Three days after the injury, oxygenation worsened, and the patient was transferred to our hospital for laminoplasty. After admission, we noticed bilateral ptosis-an atypical finding for SCI. Under analgesic sedation, he could only move his fingertips. Severe respiratory muscle weakness and absence of reflexes were observed. Moreover, albuminocytologic dissociation and decreased motor nerve conduction were observed, and GBS was suspected. Intravenous immunoglobulin was administered; thereby, the muscle weakness gradually improved, and the patient returned to work. Muscle weakness usually starts in the legs in GBS; however, in 10% of patients, it starts in the arms. In our patient, the symptoms started with paresthesia, followed by severe respiratory muscle weakness in a short period. Furthermore, intubation made history-taking and neurological examination difficult. The degree of inflammation in the acute GBS phase correlates with the severity of nerve injury. Therefore, early diagnosis and treatment of GBS is important. We should perform detailed history-taking and consider GBS as a differential diagnosis, especially when neurological examination cannot be performed at the emergency department.

Hypovolemic shock induced by a large chest wall hematoma caused by a single rib fracture in an elderly patient.

Displaced rib fractures can injure intercostal vessels leading to chest wall hematomas. As the bleeding occurs within the vessel, compression of the vessel wall helps in preventing further bleeding. Therefore, chest wall hematomas rarely result in shock. A thin 78-year-old man transferred to the emergency department with complaints of left dorsal pain due to an injury. He had a history of hypertension and aorta dissection. He arrived at the ED in a state of shock and presented with a large left dorsal wall mass. Subsequent imaging using computed tomography angiography revealed a large hyperdense hematoma at the left dorsal-flank wall along with rib fracture (11th intercostal artery). Moreover, a large fusiform aneurysm was detected from the abdominal aorta to the iliac arteries. Extravasation of the contrast agent was detected at the branch of the 11th intercostal artery, and hence, embolization was performed. The dermis, which comprises collagen and elastin fibers, plays an important role in vessel compression to prevent bleeding. The aortic media also comprises collagen and elastin fibers. Cell turnover, loss of collagen, and excessive elastolysis are associated with the formation of abdominal aortic aneurysms. The systemic degeneration of connecting tissue (collagen and elastin fiber) appears to be progress in patients with an aortic aneurysms and history of aortic dissection compared with other healthy older individuals. Physicians should be cognizant of the potential unexpected large hematoma complications if a risk of systemic connecting tissue degradation exists, as seen in patients with aortic aneurysm or aortic dissection.

A novel mouse model of heatstroke accounting for ambient temperature and relative humidity.

BACKGROUND: Heatstroke is associated with exposure to high ambient temperature (AT) and relative humidity (RH), and an increased risk of organ damage or death. Previously proposed animal models of heatstroke disregard the impact of RH. Therefore, we aimed to establish and validate an animal model of heatstroke considering RH. To validate our model, we also examined the effect of hydration and investigated gene expression of cotransporter proteins in the intestinal membranes after heat exposure. METHODS: Mildly dehydrated adult male C57/BL6J mice were subjected to three AT conditions (37 °C, 41 °C, or 43 °C) at RH > 99% and monitored with WetBulb globe temperature (WBGT) for 1 h. The survival rate, body weight, core body temperature, blood parameters, and histologically confirmed tissue damage were evaluated to establish a mouse heatstroke model. Then, the mice received no treatment, water, or oral rehydration solution (ORS) before and after heat exposure; subsequent organ damage was compared using our model. Thereafter, we investigated cotransporter protein gene expressions in the intestinal membranes of mice that received no treatment, water, or ORS. RESULTS: The survival rates of mice exposed to ATs of 37 °C, 41 °C, and 43 °C were 100%, 83.3%, and 0%, respectively. From this result, we excluded AT43. Mice in the AT 41 °C group appeared to be more dehydrated than those in the AT 37 °C group. WBGT in the AT 41 °C group was > 44 °C; core body temperature in this group reached 41.3 ± 0.08 °C during heat exposure and decreased to 34.0 ± 0.18 °C, returning to baseline after 8 h which showed a biphasic thermal dysregulation response. The AT 41 °C group presented with greater hepatic, renal, and musculoskeletal damage than did the other groups. The impact of ORS on recovery was greater than that of water or no treatment. The administration of ORS with heat exposure increased cotransporter gene expression in the intestines and reduced heatstroke-related damage. CONCLUSIONS: We developed a novel mouse heatstroke model that considered AT and RH. We found that ORS administration improved inadequate circulation and reduced tissue injury by increasing cotransporter gene expression in the intestines.