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Dose‐dependence of hydrogen sulfide on vascular endothelial function following ischemia‐reperfusion in perfused rat lung
Author(s) -
Patel Prayash,
Russell Michael James
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.775.24
Subject(s) - ischemia , myograph , edema , lung , chemistry , pulmonary edema , pulmonary artery , vasodilation , medicine , anesthesia , reperfusion injury , endocrinology
Hydrogen sulfide (H 2 S) modulates vascular tone dose‐dependently in vessels from every vertebrate class, and H 2 S may protect against ischemia‐reperfusion injury in rat hearts and isolated rat lungs. We have shown that inhibition of H 2 S reduced acute edema formation following ischemia‐reperfusion while exogenous (200 μM) H 2 S did not affect edema formation or pulmonary artery (PA) endothelial function in a constant flow, in‐situ rat lung model. In the present study we examined edema formation and endothelial function in isolated rat lungs exposed to high‐dose (10 mM) H 2 S and 90 min of warm (37°) ischemia. Lungs were ventilated at 3 cm H 2 O positive end expiratory pressure (PEEP) and perfused at 5.9 ml/min in‐situ for 30 min, exposed to 90 min warm ischemia while inflated to 10 PEEP, then reperfused and ventilated for 30 min at 3 PEEP. Left PA were hung in a myograph. The right lung was dried and weighed for wet/dry ratio. Endothelial function was assessed by acetylcholine (ACh) relaxation of a norepinephrine (NE) contraction. Wet/dry ratio in high‐dose H 2 S (2.19 ± 0.07; n=5) was not different than either control (2.35 ± 0.12; n=4) or low‐dose H 2 S (2.26 ± 0.12; n=5) lungs, whereas ACh relaxation of NE was nearly abolished in PA exposed to high‐dose H 2 S (6.73±6.85%). H 2 S effects on rat lung following ischemia‐reperfusion are dose‐ and protocol‐dependent. Supported by a Mercer University seed grant.