A stable rat model of high altitude pulmonary edema established by hypobaric hypoxia combined diurnal temperature fluctuation and exercise.

Hypobaric hypoxia (HH) is regarded as the main cause of high-altitude pulmonary edema (HAPE), however, the effect of diurnal temperature fluctuation and exercise has been overlooked. The aim of current study was to elucidate the role of diurnal temperature fluctuation and exercise in the development of HAPE and establish a reliable experimental rat model. Male SPF Wistar rats were assigned to control group (1400 m, 25 °C) and five model groups: Model Ⅰ group (6000 m, 25 °C), Model Ⅱ group (6000 m, 2 °C), Model Ⅲ group (6000 m, 12 °C/2 °C light/dark cycle), Model IV group (6000 m, 2 °C, and exercise) and Model V group (6000 m, 12 °C/2 °C light/dark cycle, and exercise).

Characteristics of Climbers with High Altitude Pulmonary Edema on Mount Aconcagua.

Introduction—: Mount Aconcagua (6961 m) in Argentina is the highest peak in the Americas, and more than 3000 climbers attempt to summit annually. High altitude pulmonary edema (HAPE) is a leading cause of mortality and evacuation on Aconcagua.

Objective—: This study sought to describe the characteristics of climbers who developed HAPE on Aconcagua to aid in future prevention efforts.

1,25-(OH)D improves SD rats high-altitude pulmonary edema by inhibiting ferroptosis and ferritinophagy in alveolar epithelial cells.

Background: This study investigates the protective effects and potential mechanisms of 1,25-(OH)D against high-altitude pulmonary edema (HAPE).

Methods: Hypoxia-induced rats were administered 1,25-(OH)D for 24, 48, and 72 hours, and we observed lung tissue injury and pulmonary edema. Immunohistochemistry (IHC) and Western blot analyses were employed to analyze the expression of markers associated with ferroptosis and ferritinophagy in rat lungs.

Hypoxic Pulmonary Vasoconstriction: An Important Component of the Homeostatic Oxygen Sensing System.

Hypoxic pulmonary vasoconstriction (HPV) rapidly and reversibly matches lung ventilation (V) and perfusion (Q), optimizing oxygen uptake and systemic oxygen delivery. HPV occurs in small pulmonary arteries (PA), which uniquely constrict to hypoxia. Although HPV is modulated by the endothelium the core mechanism of HPV resides in PA smooth muscle cells (PASMC).

Elevated Perspectives: Unraveling Cardiovascular Dynamics in High-Altitude Realms.

High-altitude regions pose distinctive challenges for cardiovascular health because of decreased oxygen levels, reduced barometric pressure, and colder temperatures. Approximately 82 million people live above 2400 meters, while over 100 million people visit these heights annually. Individuals ascending rapidly or those with pre-existing cardiovascular conditions are particularly vulnerable to altitude-related illnesses, including Acute Mountain Sickness (AMS) and Chronic Mountain Sickness (CMS).

A forensic overview of deaths in mountainous terrain.

Deaths at high altitudes may arise from a range of quite disparate entities including trauma (e.g. falls), environmental factors (e.

Lung function and blood gas of rats after different protocols of hypobaric exposure.

High-altitude pulmonary edema (HAPE) is a common disease observed in climbers, skiers and soldiers who ascend to high altitudes without previous acclimatization. Thus, a reliable and reproducible animal model that can mimic the mechanisms of pathophysiologic response in humans is crucial for successful investigations. Our results showed that exposure to 4500 m for 2 days had little influence on lung function or blood gas, and exposure to 6000 m for 2 or 3 days could change lung function and blood gas, but most parameters returned to nearly normal levels within 48 hours.

Clinical characteristics and a diagnostic model for high-altitude pulmonary edema in habitual low altitude dwellers.

Background: The fatal risk of high-altitude pulmonary edema (HAPE) is attributed to the inaccurate diagnosis and delayed treatment. This study aimed to identify the clinical characteristics and to establish an effective diagnostic nomogram for HAPE in habitual low altitude dwellers.

Methods: A total of 1,255 individuals of Han Chinese were included in the study on the Qinghai-Tibet Plateau at altitudes exceeding 3,000 m.

Physiopathology of High-Altitude Pulmonary Edema.

The air-blood barrier is well designed to accomplish the matching of gas diffusion with blood flow. This function is achieved by maintaining its thickness at ∼0.5 µm, a feature implying to keep extravascular lung water to the minimum.

ORENITRAM's decadal journey: unveiling safety profiles and adverse event through a real-world pharmacovigilance study of FAERS events.

Background: ORENITRAM, an oral treprostinil formulation, was approved in 2013 for pulmonary arterial hypertension (PAH) treatment, necessitating ongoing safety monitoring.

Research Design And Methods: This retrospective analysis used FDA Adverse Event Reporting System data from Q4 2013 to Q4 2023, employing disproportionality analysis and the reporting odds ratio (ROR) to identify adverse events (AEs) linked with ORENITRAM.

Results: Out of 15,660,695 reports, ORENITRAM was the primary suspect in 10,125 cases.

Identification and Validation of STC1 Act as a Biomarker for High-Altitude Diseases and Its Pan-Cancer Analysis.

High-altitude diseases, including acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE), are closely related to an individual's ability to adapt to hypoxic environments. However, specific research in this field is relatively limited, and further biomarker research and clinical trials are needed to clarify the exact role and potential therapeutic applications of key genes in high-altitude diseases. This study focuses on the role of the STC1 gene in high-altitude diseases and explores its expression patterns in different types of cancer.

Corrigendum to: B2M is a Biomarker Associated With Immune Infiltration In High Altitude Pulmonary Edema.

The funding details have been incorporated upon author's request in the funding section of this article titled "B2M is a Biomarker Associated With Immune Infiltration In High Altitude Pulmonary Edema ," 2024, 27(1), 168-185 [1]. Details of the error and a correction are provided here. Original: This work was supported by grants from the Chongqing Natural Science Gene General Project (No.

High-altitude Cerebral Edema and High-altitude Pulmonary Edema Diagnosed in the Desert: A Case Report.

Introduction: Acute mountain sickness, high-altitude pulmonary edema (HAPE), and high-altitude cerebral edema (HACE) are a spectrum of high-altitude conditions, with HACE being the most life-threatening. Most cases develop at altitudes of greater than 4,000 meters (∼13,000 feet) above sea level and after one to five days.

Case Report: A previously healthy 46-year-old female presented to the emergency department with ataxia, altered mental status, and vomiting that developed after rapidly ascending to ∼2,400 meters (∼7,800 feet) above sea level.