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March 1, 1996AJP Cell Physiology

Role of nitric oxide and phosphodiesterase isoenzyme II for reduction of endothelial hyperpermeability

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Population

H2O2-exposed porcine pulmonary artery endothelial cell monolayers

Comparison

Pretreatment with nitric oxide donors, atrial… vs Untreated cells or cells treated with NO…

Design

Preclinical

Authors

NSNorbert SuttorpHumboldt-Universität zu BerlinSHStefan HippenstielHumboldt-Universität zu BerlinMFMartin FuhrmannGerman Center for Neurodegenerative Diseases

Discussion

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Implication

Hypothesis-generating for PDE II inhibition in endothelial protection; leaves open in vivo translation and clinical relevance.

Structured PICO

P
Population
H2O2-exposed porcine pulmonary artery endothelial cell monolayers
I
Intervention
Pretreatment with nitric oxide (NO) donors, atrial natriuretic peptide (ANP), or phosphodiesterase (PDE) II inhibitors
C
Comparator
Untreated cells or cells treated with NO synthase inhibitor
O
Outcome
Endothelial permeability and cGMP contentsurrogate

Simultaneous guanylate cyclase activation and/or PDE II inhibition may be a valuable approach to treat endothelial hyperpermeability based on in vitro findings.

Cite This Study

Suttorp et al. (1996) studied this question.

synapsesocial.com/papers/6a6ffb928031ec7bb1dc0c2fhttps://doi.org/10.1152/ajpcell.1996.270.3.c778
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  3. 3Inhibition of nitric oxide production. Mechanisms of vascular albumin leakage.1993 · 344 citations
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  5. 5Potent leukocidal action of Escherichia coli hemolysin mediated by permeabilization of target cell membranes.1989 · 135 citations