The plasma level changes of VEGF and soluble VEGF receptor-1 are associated with high-altitude pulmonary edema (original) (raw)
Related papers
Greater free plasma VEGF and lower soluble VEGF receptor-1 in acute mountain sickness
Journal of Applied Physiology, 2005
Vascular endothelial growth factor (VEGF) is a hypoxia-induced protein that produces vascular permeability, and limited evidence suggests a possible role for VEGF in the pathophysiology of acute mountain sickness (AMS) and/or high-altitude cerebral edema (HACE). Previous studies demonstrated that plasma VEGF alone does not correlate with AMS; however, soluble VEGF receptor (sFlt-1), not accounted for in previous studies, can bind VEGF in the circulation, reducing VEGF activity. In the present study, we hypothesized that free VEGF is greater and sFlt-1 less in subjects with AMS compared with well individuals at high altitude. Subjects were exposed to 4,300 m for 19–20 h (baseline 1,600 m). The incidence of AMS was determined by using a modified Lake Louise symptom score and the Environmental Symptoms Questionnaire for cerebral effects. Plasma was collected at low altitude and after 24 h at high altitude, or at time of illness, and then analyzed by ELISA for VEGF and for soluble VEGF ...
Acute hypoxia decreases plasma VEGF concentration in healthy humans
AJP: Endocrinology and Metabolism, 2005
Vascular endothelial growth factor (VEGF) is known to be upregulated by hypoxia in vitro. However, in vivo data about VEGF regulation in chronic hypoxic diseases are conflicting. We investigated the effects of hypoxia on plasma VEGF concentration in healthy subjects. To control known confounders such as insulin, glucose concentrations or exercise, hypoxic effects on VEGF were studied during experimentally clamping glucose concentrations at rest. In a double-blind cross-over study design, we induced hypoxia for 30 minutes by decreasing oxygen saturation to 75% (versus normoxic control) in 14 healthy men.
Respiratory Medicine, 2007
There is an increasing body of evidence suggesting that altered vascular permeability may be an important component of the pathogenesis of acute mountain sickness (AMS). Vascular endothelial growth factor (VEGF) is a potent permeability factor subject to hypoxic regulation but its role in the pathogenesis of AMS is yet to be defined. We examined the relationship between plasma VEGF and AMS on ascent to high altitude and subsequent acclimatisation. Thirty-eight healthy lowlanders (median age 21, range 18-31) flew to La Paz, Bolivia (3650 m) on the Apex 2 research expedition. After 4-5 days acclimatisation, they ascended by vehicle over 90 min to the Chacaltaya laboratory (5200 m). We measured plasma VEGF in venous blood at sea level and at 6 h and 3 and 7 days at 5200 m. AMS was scored using the Lake Louise consensus system. Using serial measurement of plasma VEGF at 5200 m, following partial acclimatisation at 3650 m, we demonstrated a highly significant change in VEGF levels (Po0.0005) with a rise in VEGF in approximately 80% of subjects by day 7 at 5200 m. We found no evidence of an association between AMS and change in VEGF levels on ascent to either 3650 or 5200 m. We provide novel data of change in plasma VEGF levels during acclimatisation to high altitude, but our results do not support the hypothesis that circulating unbound VEGF is an important component of the pathogenesis of AMS.
High Altitude Pulmonary Edema: An Update on Omics Data
High altitude pulmonary edema (HAPE) is a serious pathological condition associated with rapid ascent to high altitude occurring in non-acclimatized but otherwise healthy individuals. Decades of scientific studies on HAPE have unraveled the disease pathology, diagnosis and therapeutic interventions yet, the etiology is still unknown. A vast scientific literature is available on HAPE for a quick reference of clinicians, researchers and academicians. Perhaps, the view of mountain travelers is different and their anticipation of HAPE susceptibility comprises of personal experience. Ever-increasing number of visitors to high altitude demands the possibility of HAPE susceptibility screening, however, scientific community is yet to find a staunch solution. This review is an update of recent information on HAPE susceptibility indicators from genomics, proteomics and metabolomics as well as information pertaining to treatment/prognosis of HAPE.
Raised HIF1α during normoxia in high altitude pulmonary edema susceptible non-mountaineers
Scientific reports, 2016
High altitude pulmonary edema (HAPE) susceptibility is associated with EGLN1 polymorphisms, we hypothesized that HAPE-susceptible (HAPE-S, had HAPE episode in past) subjects may exhibit abnormal HIF1α levels in normoxic conditions. We measured HIF1α levels in HAPE-S and HAPE resistant (HAPE-R, no HAPE episode) individuals with similar pulmonary functions. Hemodynamic responses were also measured before and after normobaric hypoxia (Fi02 = 0.12 for 30 min duration at sea level) in both groups. . HIF1α was higher in HAPE-S (320.3 ± 267.5 vs 58.75 ± 33.88 pg/ml, P < 0.05) than HAPE-R, at baseline, despite no significant difference in baseline oxygen saturations (97.7 ± 1.7% and 98.8 ± 0.7). As expected, HAPE-S showed an exaggerated increase in pulmonary artery pressure (27.9 ± 6 vs 19.3 ± 3.7 mm Hg, P < 0.05) and a fall in peripheral oxygen saturation (66.9 ± 11.7 vs 78.7 ± 3.8%, P < 0.05), when exposed to hypoxia. HIF1α levels at baseline could accurately classify members of ...
Respiratory research, 2018
Dysregulation of VEGF-A bioavailability has been implicated in the development of lung injury/fibrosis, exemplified by Idiopathic Pulmonary Fibrosis (IPF). VEGF-A is a target of the hypoxic response via its translational regulation by HIF-1α. The role of hypoxia and hyperoxia in the development and progression of IPF has not been explored. In normal lung (NF) and IPF-derived fibroblasts (FF) VEGF-Aa protein expression was upregulated by hypoxia, mediated through activation of VEGF-Aa gene transcription. VEGF-A receptors and co-receptors were differentially expressed by hypoxia and hyperoxia. Our data supports a potential role for hypoxia, hyperoxia and VEGF-Aa isoforms as drivers of fibrogenesis.
Advances in Virology, 2012
Hantavirus pulmonary syndrome is characterized by vascular permeability, hypoxia, and acute pulmonary edema. Vascular endothelial growth factor (VEGF) is induced by hypoxia, potently induces vascular permeability, and is associated with high-altitude-induced pulmonary edema. Hantaviruses alter the normal regulation ofβ3 integrins that restrict VEGF-directed permeability and hantavirus infected endothelial cells are hyperresponsive to the permeabilizing effects of VEGF. However, the role of VEGF in acute pulmonary edema observed in HPS patients remains unclear. Here we retrospectively evaluate VEGF levels in pulmonary edema fluid (PEF), plasma, sera, and PBMCs from 31 HPS patients. VEGF was elevated in HPS patients PEF compared to controls with the highest levels observed in PEF samples from a fatal HPS case. VEGF levels were highest in PBMC samples during the first five days of hospitalization and diminished during recovery. Significantly increased PEF and PBMC VEGF levels are consi...