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Hypersensitivity of pulmonary C fiber induced by arterial hypotension in anesthetized rat
Author(s) -
Lin RueiLung,
Lin YuJung,
Lee LuYuan
Publication year - 2013
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.27.1_supplement.930.20
Subject(s) - medicine , anesthesia , hypoxia (environmental) , blood pressure , arterial blood , acidosis , chemistry , oxygen , organic chemistry
This study was carried out to investigate whether arterial hypotension altered the sensitivity of pulmonary C‐fibers. Rats were anesthetized, ventilated, and their femoral arteries connected to a height‐adjustable reservoir for lowering the arterial blood pressure (ABP). Arterial hypotension (decreasing ABP to ~50 % of its control baseline) generated by lowering the level of blood reservoir induced a striking elevation of the base‐line activity of pulmonary C fibers and their responses to intravenous (iv) injection of capsaicin (0.25–1.00 μg/kg). The hypersensitivity developed shortly after the onset of hypotension (control, 2.18 ± 0.56 imp/sec; hypotension, 10.82 ± 1.72 imp/sec; n = 11, P < 0.05), sustained for the entire 20‐min duration of hypotension, and recovered slowly after ABP was returned to control. Furthermore, pulmonary C‐fiber sensitivity to lung hyperinflation (30 cmH 2 O), iv injections of phynylbiguanide (1.0–8.0 μg/kg), lactic acid (5–10 mg/kg) and adenosine (0.1–0.3 mg/kg) were all markedly potentiated by hypotension in a similar pattern. Infusion of sodium bicarbonate (70 μM/kg/min for 30 min) and ventilation with 100% O 2 prevented systemic ischemic acidosis and tissue hypoxia, respectively, but they failed to attenuate the hypotension‐induced hypersensitivity. The mechanism(s) underlying the C‐fiber hypersensitivity remains to be determined. (Supported by NIH and DoD grants)