ArticleThe Journal of clinical investigation1999
Pressure is proinflammatory in lung venular capillaries.
Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
57 citing papers in PubMed, 2 syntheses or guidelines pooled it, 152 citations in OpenAlex.
- European Society of Intensive Care Medicine (ESICM) 2025 clinical practice guideline on fluid therapy in adult critically ill patients: part 2-the volume of resuscitation fluids.Intensive care medicine · 2025Guideline
- A Barrier to Defend - Models of Pulmonary Barrier to Study Acute Inflammatory Diseases.Frontiers in immunology · 2022Pooled it
- Plasma angiopoietin-2 in clinical acute lung injury: prognostic and pathogenetic significance.Critical care medicine · 2012Trial
- Acute Respiratory Distress Syndrome: Pathophysiological Insights, Subphenotypes, and Clinical Implications-A Comprehensive Review.Journal of clinical medicine · 2025Review
- Lung endothelial cell heterogeneity in health and pulmonary vascular disease.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- Yes-associated Protein Induces Age-dependent Inflammatory Signaling in the Pulmonary Endothelium.bioRxiv : the preprint server for biology · 2025Article
- Fluid responsiveness in acute respiratory distress syndrome patients: a post hoc analysis of the HEMOPRED study.Intensive care medicine · 2024Article
- Fluid Overload in Pediatric Acute Respiratory Distress Syndrome after Allogeneic Hematopoietic Cell Transplantation.Journal of pediatric intensive care · 2024Article
- Mitochondria of lung venular capillaries mediate lung-liver cross talk in pneumonia.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Endothelial dysfunction triggers acute respiratory distress syndrome in patients with sepsis: a narrative review.Frontiers in medicine · 2023Review
- Systemic mapping of organ plasma extravasation at multiple stages of chronic heart failure.Frontiers in physiology · 2023Article
- Repeated endo-tracheal tube disconnection generates pulmonary edema in a model of volume overload: an experimental study.Critical care (London, England) · 2022Article
- Care of the critically ill neonate with hypoxemic respiratory failure and acute pulmonary hypertension: framework for practice based on consensus opinion of neonatal hemodynamics working group.Journal of perinatology : official journal of the California Perinatal Association · 2022Review
- Biological impact of restrictive and liberal fluid strategies at low and high PEEP levels on lung and distal organs in experimental acute respiratory distress syndrome.Frontiers in physiology · 2022Article
- Biotrauma during ultra-low tidal volume ventilation and venoarterial extracorporeal membrane oxygenation in cardiogenic shock: a randomized crossover clinical trial.Annals of intensive care · 2021Article
- The impact of fluid status and decremental PEEP strategy on cardiac function and lung and kidney damage in mild-moderate experimental acute respiratory distress syndrome.Respiratory research · 2021Article
- Fluid administration and monitoring in ARDS: which management?Intensive care medicine · 2020Review
- Live Imaging of the Lung.Current protocols in cytometry · 2020Article
- A Perspective: Division of Lung Diseases at Fifty.American journal of respiratory and critical care medicine · 2019Article
- Smooth Muscle Cells: A Novel Site of P-Selectin Expression with Pathophysiological and Therapeutic Relevance in Pulmonary Hypertension.American journal of respiratory and critical care medicine · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Endothelial responses may contribute importantly to the pathology of high vascular pressure. In lung venular capillaries, we determined endothelial [Ca(2+)](i) by the fura-2 ratioing method and fusion pore formation by quantifying the fluorescence of FM1-43. Pressure elevation increased endothelial [Ca(2+)](i). Concomitantly evoked exocytotic events were evident in a novel spatial-temporal pattern of fusion pore formation. Fusion pores formed predominantly at vascular branch points and colocalized with the expression of P-selectin. Blockade of mechanogated Ca(2+) channels inhibited these responses, identifying entry of external Ca(2+) as the critical triggering mechanism. These endothelial responses point to a proinflammatory effect of high vascular pressure that may be relevant in the pathogenesis of pressure-induced lung disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.