Prostaglandin E-1 produces spasmolytic effects on histamine-induced bronchoconstriction in dogs

Citation
Y. Hashimoto et al., Prostaglandin E-1 produces spasmolytic effects on histamine-induced bronchoconstriction in dogs, CRIT CARE M, 27(12), 1999, pp. 2755-2759
Citations number
27
Categorie Soggetti
Aneshtesia & Intensive Care
Journal title
CRITICAL CARE MEDICINE
ISSN journal
00903493 → ACNP
Volume
27
Issue
12
Year of publication
1999
Pages
2755 - 2759
Database
ISI
SICI code
0090-3493(199912)27:12<2755:PEPSEO>2.0.ZU;2-W
Abstract
Objective: In this study, we evaluated the spasmolytic effect of intravenou s prostaglandin (PG) E-1 on histamine-induced bronchoconstriction with a di rect visualization method using a superfine fiberoptic bronchoscope, Setting: A university research laboratory. Subjects: Mongrel dogs. Interventions: The bronchial cross-sectional area (BCA) of mongrel dogs was measured by a direct visualization method using a superfine fiberoptic bro nchoscope. Bronchoconstriction was elicited with histamine (H) infusion: 10 mu g/kg iv bolus + 500 mu g/kg/h continuous iv. The first protocol (n = 7) was designed to determine the effects of intravenous bolus of PGE(1): 0 (s aline), 0.01, 0.1, 1.0 and 10 mu g/kg on H-induced bronchoconstriction, BCA was assessed before and 30 min after starting the H infusion and 5 min aft er each dose of intravenous PGE(1), The second protocol was designed to det ermine whether continuous intravenous infusion of PGE(1) reverses H-induced bronchoconstriction, In the PG group (n = 6), PGE(1) was continuously infu sed at 0.1 mu g/kg/min (20 mL/hr), In the control group (0 = 6), saline was administered at a rate of 20 mL/hr iv. BCA was assessed before and 30 min after starting the H-infusion and at 5, 10, 30 and 60 min after commencing the PGE(1) or saline infusion. Arterial blood was obtained simultaneously f or measurement of plasma concentrations of epinephrine and norepinephrine b y gas chromatography mass spectrometry. Measurements and Main Results: In the first protocol, PGE(1) produced a dos e-dependent increase in the percentage of BCA and 10 mu g/kg of PGE(1) almo st fully reversed the H-induced bronchoconstriction. Plasma catecholamines did not change significantly. In the second protocol, continuous infusion o f PGE(1) produced a time-dependent reversal of H-induced bronchoconstrictio n (percentage of BCA increased to 80.0 +/- 9.0% 60 min after the start of P GE(1) infusion), whereas saline infusion did not reverse the bronchoconstri ction. Plasma catecholamines did not change significantly in either group. Conclusions: Both intravenous bolus and continuous intravenous infusion of PGE(1) reversed the H-induced bronchoconstriction, PGE(1) may be used safel y for patients with the hyperreactive airway and might be useful as a thera peutic agent for these patients.