ArticlePulmonary circulation2013
Optimization of isolated perfused/ventilated mouse lung to study hypoxic pulmonary vasoconstriction.
Article in Pulmonary circulation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Vacuum-stabilized lung window enables real-time and simultaneous imaging of vascular and calcium responses to hypoxia in vivo.Respiratory research · 2026Article
- Lung Development in a Dish: Models to Interrogate the Cellular Niche and the Role of Mechanical Forces in Development.Advances in experimental medicine and biology · 2023Article
- TRPC6, a therapeutic target for pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Halofuginone, a promising drug for treatment of pulmonary hypertension.British journal of pharmacology · 2021Article
- Article
- Tetramethylpyrazine: A promising drug for the treatment of pulmonary hypertension.British journal of pharmacology · 2020Article
- Endothelial HIF-2α contributes to severe pulmonary hypertension due to endothelial-to-mesenchymal transition.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Chloroquine is a potent pulmonary vasodilator that attenuates hypoxia-induced pulmonary hypertension.British journal of pharmacology · 2017Article
- Pathogenic role of calcium-sensing receptors in the development and progression of pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Notch Activation of Ca(2+) Signaling in the Development of Hypoxic Pulmonary Vasoconstriction and Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2015Article
- Upregulated expression of STIM2, TRPC6, and Orai2 contributes to the transition of pulmonary arterial smooth muscle cells from a contractile to proliferative phenotype.American journal of physiology. Cell physiology · 2015Article
- Deficiency of Akt1, but not Akt2, attenuates the development of pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Integrative understanding of hypoxic pulmonary vasoconstriction usingIntegrative medicine research · 2014Review
- The effects of genetic deletion of Macrophage migration inhibitory factor on the chronically hypoxic pulmonary circulation.Pulmonary circulationArticle
- Mouse model of experimental pulmonary hypertension: Lung angiogram and right heart catheterization.Pulmonary circulationArticle
- Revisiting the mechanism of hypoxic pulmonary vasoconstriction using isolated perfused/ventilated mouse lung.Pulmonary circulationArticle
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Hypoxic pulmonary vasoconstriction (HPV) is a compensatory physiological mechanism in the lung that optimizes the matching of ventilation to perfusion and thereby maximizes gas exchange. Historically, HPV has been primarily studied in isolated perfused/ventilated lungs; however, the results of these studies have varied greatly due to different experimental conditions and species. Therefore, in the present study, we utilized the mouse isolated perfused/ventilated lung model for investigation of the role of extracellular Ca(2+) and caveolin-1 and endothelial nitric oxide synthase expression on HPV. We also compared HPV using different perfusate solutions: Physiological salt solution (PSS) with albumin, Ficoll, rat blood, fetal bovine serum (FBS), or Dulbecco's Modified Eagle Medium (DMEM). After stabilization of the pulmonary arterial pressure (PAP), hypoxic (1% O2) and normoxic (21% O2) gases were applied via a ventilator in five-minute intervals to measure HPV. The addition of albumin or Ficoll with PSS did not induce persistent and strong HPV with or without a pretone agent. DMEM with the inclusion of FBS in the perfusate induced strong HPV in the first hypoxic challenge, but the HPV was neither persistent nor repetitive. PSS with rat blood only induced a small increase in HPV amplitude. Persistent and repetitive HPV occurred with PSS with 20% FBS as perfusate. HPV was significantly decreased by the removal of extracellular Ca(2+) along with addition of 1 mM EGTA to chelate residual Ca(2+) and voltage-dependent Ca(2+) channel blocker (nifedipine 1 μM). PAP was also reactive to contractile stimulation by high K(+) depolarization and U46619 (a stable analogue of thromboxane A2). In summary, optimal conditions for measuring HPV were established in the isolated perfused/ventilated mouse lung. Using this method, we further confirmed that HPV is dependent on Ca(2+) influx.
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