Vascular endothelial growth factor in patients with  high-altitude pulmonary edema

Hanaoka, Masayuki; Droma, Yunden; Naramoto, Atsuhiko; Honda, Takayuki; Kobayashi, Toshio; Kubo, Keishi

doi:10.1152/japplphysiol.00575.2002

Cited by 40 publications

(50 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Findings of Hanaoka et al (2003) suggest that VEGF is probably destroyed in the lungs of HAPE patients, and it does not appear to play a critical part in the pathogenesis of HAPE but has rather an important role in the repair process for the impaired cell layer 74) . The most commonly studied VEGF polymorphism is C(936)T, and it has been reported that subjects carrying the VEGF 936T allele had significantly lower plasma VEGF levels as compared with subjects carrying the VEGF 936CC genotype 75) .…”

Section: Endothelinmentioning

confidence: 99%

High‐altitude Pulmonary Edema: Review

Bhagi

Srivastava

Singh

2014

Journal of Occupational Health

View full text Add to dashboard Cite

High‐altitude Pulmonary Edema: Review: Shuchi BHAGI, et al. Defence Institute of Physiology and Allied Sciences (DIPAS), Defence Research and Development Organization (DRDO), India— Objective At High altitude (HA) (elevation >2,500 m), hypobaric hypoxia may lead to the development of symptoms associated with low oxygen pressure in many sojourners. High‐altitude pulmonary edema (HAPE) is a potentially fatal condition, occurring at altitudes greater than 3,000 m and affecting rapidly ascending, non‐acclimatized healthy individuals. It is a multifactorial disease involving both environmental and genetic risk factors. Since thousands of lowlanders travel to high altitude areas for various reasons every year, we thought it would be interesting to review pathological aspects related to hypobaric hypoxia, particularly HAPE. Method Since the pathogenesis of HAPE is still a subject of study, we systematically identified and categorized a broad range of facets of HAPE such as its incidence, symptoms, physiological effects, pathophysiology including physiological and genetic factors, prevention and treatment. Results This review focuses on HA‐related health problems in general with special reference to HAPE, which is one of the primary causes of deaths at extreme altitudes. Hence, it is extremely important, as it summarizes the literature in this area and provides an overview of this severe HA malady for evaluation of physiological, biochemical and genetic responses during early induction and acclimatization to HA. This article could be of broad scientific interest for researchers working in the field of high altitude medicine.

show abstract

Section: Endothelinmentioning

confidence: 99%

High‐altitude Pulmonary Edema: Review

Bhagi

Srivastava

Singh

2014

Journal of Occupational Health

View full text Add to dashboard Cite

show abstract

“…However, in some pathological conditions like hypoxia, VEGF is known to play important roles in alveolar and bronchial vessels (8,17). It was shown that during high-altitude hypoxic stress, VEGF expression is upregulated (18,19). Acute exposure of hypoxia leads to an increase in lung water content and total protein and albumin leakage in lavage fluids.…”

Section: Discussionmentioning

confidence: 99%

“…The results of VEGF expression may vary according to experimental models, procedure or technique, cell line types and how hypoxia was inducted, and the origin of sample of cells. The results, compared with the controls, also might show variability (such as high, low, or stable) (5,9,19,24). Hanaoka et al (19) reported that the VEGF levels in edema fluid of the high-altitude pulmonary edema (HAPE) patients were significantly decreased at the beginning of the acute phase compared with the recovery phase.…”

Section: Vegf (Average Of Staining Scores)mentioning

confidence: 99%

“…The results, compared with the controls, also might show variability (such as high, low, or stable) (5,9,19,24). Hanaoka et al (19) reported that the VEGF levels in edema fluid of the high-altitude pulmonary edema (HAPE) patients were significantly decreased at the beginning of the acute phase compared with the recovery phase. Moreover, the concentration of VEGF in the bronchoalveolar lavage fluid in HAPE patients was markedly depleted compared with that of controls (19).…”

Section: Vegf (Average Of Staining Scores)mentioning

confidence: 99%

“…Hanaoka et al (19) reported that the VEGF levels in edema fluid of the high-altitude pulmonary edema (HAPE) patients were significantly decreased at the beginning of the acute phase compared with the recovery phase. Moreover, the concentration of VEGF in the bronchoalveolar lavage fluid in HAPE patients was markedly depleted compared with that of controls (19). However, it was documented in another study that in lungs exposed to 5 h of hypoxia, VEGF in bronchoalveolar fluids was 1.5-fold increased compared with the controls (21).…”

Section: Vegf (Average Of Staining Scores)mentioning

confidence: 99%

See 2 more Smart Citations

The effects of hypoxia on the expression of vascular endothelialgrowth factor in broiler lung fibroblasts

Özyiğit

Kahraman²,

Akkoç³

2015

Turk J Vet Anim Sci

View full text Add to dashboard Cite

IntroductionAscites (pulmonary hypertension), is a metabolic disorder that causes economic losses and is characterized by the accumulation of lymph fluid in the abdomen due to right heart failure in meat-type chickens. At necropsy, besides the lesions observed, other common findings such as generalized edema and expansion of the air capillaries are typically observed in the lung tissues of the chickens (1). Although environmental factors such as cold, high altitude, and diet play significant roles in the development of the syndrome (2), the main cause is hypoxia caused by increased oxygen demand, pulmonary hypertension, and extra workload on the heart (1-4).Vascular endothelial growth factor (VEGF), which is also known as edema factor, is a potent and key factor in the development of tumoral angiogenesis and edema formation by increasing vascular permeability (5,6). There are five VEGF products of alternative splicing, VEGF 121, VEGF 145, VEGF 165, VEGF 189, and VEGF 206 (7). VEGF 121 and VEGF 165 are secreted and both have mitogenic and permeability-inducing properties. VEGF has been synthesized in both animals and humans in endothelial cells, in mesenchymal cells, in alveolar macrophages of lung, in neurons, in renal epithelial cells, in connective tissue cells, and in tumor cells (8). Hypoxia has an important role in triggering VEGF (5,9). Investigations on people living at high altitudes showed that there might be a direct relationship between hypoxia and VEGF level due to the observed higher levels of serum VEGF, while in vitro studies on VEGF revealed that fibroblasts inflicted with mechanical damage and exposed to hypoxia showed an increase in VEGF levels compared with the control group (9).During the formation of pulmonary edema, matrix metalloproteinases (MMPs) and their relation with hypoxic stress were examined through both in vivo and in vitro studies for pulmonary hypertension syndrome (10,11). It was shown that MMPs have the potential for damaging the vascular basement membrane, but the mechanisms by which hypoxia causes ascites by increasing vascular permeability remains unclear. Thus, the aim of this study is to investigate the effects of hypoxic stress on VEGF, also known as edema factor, and its contribution to the pathogenesis of the disease in cultured lung fibroblasts of meat-type chickens. Materials and methods Cell cultureThis study was carried out after receiving written approval from the Scientific and Ethics Committee of Uludağ

show abstract

High-Altitude Pulmonary Edema (HAPE)

Schoene

Swenson

2013

High Altitude

View full text Add to dashboard Cite

Much of the clinical impact of acute altitude illnesses stems from fl uid accumulation in interstitial spaces and nowhere is this more apparent than in the lungs as the edema escapes into the alveoli to cause life-threatening hypoxemia. This chapter will update our knowledge of HAPE over the past decade about the vasculature, alveolar epithelium, innervation, immune response, and genetics of the lung in hypoxia, as well as prophylactic and therapeutic strategies to reduce the toll of this most common alpine life-threatening illness. 406extend to HPV, would predict greater HAPE susceptibility. Although HAPE can develop in sedentary persons, exercise [ 6 ] and its pulmonary hemodynamic consequences (discussed below) are important precipitating factors.Symptoms, signs, and physiologic changes in lung function typical of pulmonary edema [ 1 -3 , 7 ] evolve in 2-4 days after ascent, often preceded or accompanying AMS (see Chap. 20 ), but can occur later with further ascent. Arterial saturations can fall as low as 40 % and PaO 2 s in the low 20 mmHg range. HAPE in its severest stage with profound hypoxemia can lead to high-altitude cerebral edema [ 8 ]. Repeat occurrences of HAPE do not always involve infi ltrates in the same areas, which suggests that fi xed structural aspects of lung parenchyma or vessels do not account for the timing of edema or its locale [ 9 ]. A special exception is unilateral absence of a pulmonary artery, in which edema always occurs in the contralateral lung receiving the entire cardiac output [ 10 ].It has been suggested that many persons (50-75 %) may have subclinical HAPE that resolves spontaneously despite remaining at altitude [ 11 -13 ]. This incidence equals that of AMS, which itself can cause mild gas exchange impairment [ 14 ] by unknown mechanisms perhaps related to altered autonomic infl uences on the pulmonary circulation and/or airways leading to ventilation-perfusion mismatching. Subclinical HAPE may be considerably overestimated without radiography [ 15 ] because indirect measures of interstitial edema such as spirometry, closing volume, and/or transthoracic impedance can vary for other reasons related to mountaineering including intense exercise and increased cardiac output, cold/dry air-induced bronchoconstriction, and hypocapnia [ 16 ]. With radiographically mild HAPE, only modest abnormalities were detectable [ 15 ] suggesting many lung function parameters are not sensitive enough to detect small changes in interstitial fl uid and may require highresolution tissue density measurements by CT or MR imaging. Reentry HAPE occurs when longterm high-altitude residents return to high altitude following a brief low-altitude sojourn. It has a strong familial basis and affl icts children more than adults [ 17 ], perhaps due to a twofold greater magnitude of HPV in preteen children (age 6-9) compared to teenagers (age 14-16) when tested 40 h after ascent to high altitude [ 18 ]. PathophysiologyFrom its fi rst modern descriptions, pulmonary hypertension and HAPE have been inex...

show abstract

Vascular endothelial growth factor in patients with high-altitude pulmonary edema

Abstract: Kubo. Vascular endothelial growth factor in patients with high-altitude pulmonary edema.

Cited by 40 publications

References 33 publications

High‐altitude Pulmonary Edema: Review

High‐altitude Pulmonary Edema: Review

The effects of hypoxia on the expression of vascular endothelialgrowth factor in broiler lung fibroblasts

High-Altitude Pulmonary Edema (HAPE)

Contact Info

Product

Resources

About