Prevention of High-Altitude Pulmonary Edema by Nifedipine

Bärtsch, Peter; Maggiorine, M.; Ritter, Manfred; Noti, C; Vock, Peter; Oelz, O

doi:10.1097/00132586-199208000-00065

Cited by 54 publications

(74 citation statements)

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“…K + channels have recently been suggested to participate in vascular remodeling by regulating cell proliferation and apoptosis [18] . Global hypoxia, as it occurs at high altitude, causes pulmonary vasoconstriction or vascular remodeling and increases pulmonary vascular resistance [27] . Impaired K + channels (K ATP , K Ca , K V , and K IR ) in vascular smooth muscle cells are also related to the development of hypertension [22,28] .…”

Section: Discussionmentioning

confidence: 99%

Echinacoside induces rat pulmonary artery vasorelaxation by opening the NO-cGMP-PKG-BKCa channels and reducing intracellular Ca2+ levels

et al. 2015

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altitude diseases that are associated with significant morbidity and mortality, such as high-altitude pulmonary edema and heart diseases [3] . Echinacoside (ECH) (Figure 1) is a phenylethanoid glycoside found in a variety of Chinese herbs such as the Tibetan herb Lagotis brevituba Maxim and Cistanche tubulosa [4,5] . Lagotis brevituba Maxim is a species of Lagotis spp belonging to the Scrophulariaceae and grows widely at an altitude over 3000 meter in the Qinghai-Tibet Plateau. ECH has various desirable pharmacological characteristics, such as antioxidative, anti-inflammatory, neuroprotective, hepatoprotective, and nitric oxide (NO) radical-scavenging properties [6] . It can also elicit endothelium-dependent relaxation in rat thoracic aortic rings and cure cardiovascular diseases [7] . HowEchinacoside induces rat pulmonary artery vasorelaxation by opening the NO-cGMP-PKG-BK Ca channels and reducing intracellular Ca 2+ levels Aim: Sustained pulmonary vasoconstriction as experienced at high altitude can lead to pulmonary hypertension (PH). The main purpose of this study is to investigate the vasorelaxant effect of echinacoside (ECH), a phenylethanoid glycoside from the Tibetan herb Lagotis brevituba Maxim and Cistanche tubulosa, on the pulmonary artery and its potential mechanism. Methods: Pulmonary arterial rings obtained from male Wistar rats were suspended in organ chambers filled with Krebs-Henseleit solution, and isometric tension was measured using a force transducer. Intracellular Ca 2+ levels were measured in cultured rat pulmonary arterial smooth muscle cells (PASMCs) using Fluo 4-AM. Results: ECH (30-300 μmol/L) relaxed rat pulmonary arteries precontracted by noradrenaline (NE) in a concentration-dependent manner, and this effect could be observed in both intact endothelium and endothelium-denuded rings, but with a significantly lower maximum response and a higher EC 50 in endothelium-denuded rings. This effect was significantly blocked by L-NAME, TEA, and BaCl 2 . However, IMT, 4-AP, and Gli did not inhibit ECH-induced relaxation. Under extracellular Ca 2+ -free conditions, the maximum contraction was reduced to 24.54%±2.97% and 10.60%±2.07% in rings treated with 100 and 300 μmol/L of ECH, respectively. Under extracellular calcium influx conditions, the maximum contraction was reduced to 112.42%±7.30%, 100.29%±8.66%, and 74.74%±4.95% in rings treated with 30, 100, and 300 μmol/L of ECH, respectively. After cells were loaded with Fluo 4-AM, the mean fluorescence intensity was lower in cells treated with ECH (100 μmol/L) than with NE. Conclusion: ECH suppresses NE-induced contraction of rat pulmonary artery via reducing intracellular Ca 2+ levels, and induces its relaxation through the NO-cGMP pathway and opening of K + channels (BK Ca and K IR ).

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Section: Discussionmentioning

confidence: 99%

Echinacoside induces rat pulmonary artery vasorelaxation by opening the NO-cGMP-PKG-BKCa channels and reducing intracellular Ca2+ levels

et al. 2015

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“…These pioneering studies put to rest the idea that HAPE was acute left heart failure at high altitude. Excessive pulmonary artery pressures precede the development of HAPE and are not a consequence of the disease [63]. The critical role of high pulmonary artery pressure is further confirmed by the fact that descent, oxygen or drugs that lower pulmonary artery pressure are effective for prevention and treatment as discussed below.…”

Section: Haemodynamicsmentioning

confidence: 92%

Acute high-altitude sickness

2017

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At any point 1-5 days following ascent to altitudes ⩾2500 m, individuals are at risk of developing one of three forms of acute altitude illness: acute mountain sickness, a syndrome of nonspecific symptoms including headache, lassitude, dizziness and nausea; high-altitude cerebral oedema, a potentially fatal illness characterised by ataxia, decreased consciousness and characteristic changes on magnetic resonance imaging; and high-altitude pulmonary oedema, a noncardiogenic form of pulmonary oedema resulting from excessive hypoxic pulmonary vasoconstriction which can be fatal if not recognised and treated promptly. This review provides detailed information about each of these important clinical entities. After reviewing the clinical features, epidemiology and current understanding of the pathophysiology of each disorder, we describe the current pharmacological and nonpharmacological approaches to the prevention and treatment of these diseases.

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“…Although it is well known that HAPE can be avoided by slow ascent and resolved in the early stages by rapid descent, these two protective strategies are not always feasible (due to urgent situations or the condition going unrecognized). Thus, the rates of morbidity and mortality remain relatively high (Bärtsch et al 1990(Bärtsch et al , 1991. Epidemiologic studies have revealed that individuals under identical ascent conditions show different levels of susceptibility to HAPE (Maloney and Broeckel 2005).…”

Section: Introductionmentioning

confidence: 99%

Polymorphisms of Angiotensin Converting Enzyme and Nitric Oxide Synthase 3 Genes as Risk Factors of High-Altitude Pulmonary Edema: A Case-Control Study and Meta-Analysis

Wang

Huang

et al. 2013

Tohoku J. Exp. Med.

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High-altitude pulmonary edema (HAPE) is a non-cardiogenic type of pulmonary edema developing altitudes >2,500 m. Angiotensin converting enzyme (ACE) and nitric oxide synthase 3 (NOS3) play important roles in regulating pulmonary vascular tone. To assess associations between genetic variants in the ACE and NOS3 genes and HAPE risk, 27 HAPE patients and 108 matched controls were genotyped and analyzed. The indicated HAPE association of the NOS3 G894T (Glu298Asp) single nucleotide polymorphism (SNP), which may change NO production, was further evaluated by a meta-analysis of six studies involving 399 HAPE patients and 495 controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were determined with fixed-effects models. Stratification analyses of ethnicity and geographic location were performed. Significant associations were observed for the dominant model in two ACE tag SNPs influencing serum ACE concentrations (rs8066114 polymorphism: GG+CG vs. CC; rs4461142 polymorphism: TT+CT vs. CC). Furthermore, Single-locus analysis indicated significantly different distributions of G allele frequency between the cases (29.63%) and controls (17.13%) for the ACE rs8066114 polymorphism. The casecontrol distributions of genotype frequencies and T allele frequency of NOS3 G894T (Glu298Asp) polymorphism were significantly higher in the cases than controls, and the NOS3 G894T (Glu298Asp) SNP showed elevated HAPE risk under the dominant model (TT+GT vs. GG). Meta-analysis showed overall association of NOS3 G894T SNP with HAPE risk under the allele contrast and dominant genetic models, which remained significant for Asians. In conclusion, ACE rs8066114 and rs4461142 and NOS3 rs1799983 (G894T) polymorphisms may be associated with increased HAPE risk in Asians.

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Prevention of High-Altitude Pulmonary Edema by Nifedipine

Cited by 54 publications

References 0 publications

Echinacoside induces rat pulmonary artery vasorelaxation by opening the NO-cGMP-PKG-BKCa channels and reducing intracellular Ca2+ levels

Echinacoside induces rat pulmonary artery vasorelaxation by opening the NO-cGMP-PKG-BKCa channels and reducing intracellular Ca2+ levels

Acute high-altitude sickness

Polymorphisms of Angiotensin Converting Enzyme and Nitric Oxide Synthase 3 Genes as Risk Factors of High-Altitude Pulmonary Edema: A Case-Control Study and Meta-Analysis

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