Spasmolytic effects of prostaglandin E-1 on serotonin-induced bronchoconstriction and pulmonary hypertension in dogs

Citation
Y. Hashimoto et al., Spasmolytic effects of prostaglandin E-1 on serotonin-induced bronchoconstriction and pulmonary hypertension in dogs, BR J ANAEST, 85(3), 2000, pp. 460-462
Citations number
10
Categorie Soggetti
Aneshtesia & Intensive Care","Medical Research Diagnosis & Treatment
Journal title
BRITISH JOURNAL OF ANAESTHESIA
ISSN journal
00070912 → ACNP
Volume
85
Issue
3
Year of publication
2000
Pages
460 - 462
Database
ISI
SICI code
0007-0912(200009)85:3<460:SEOPEO>2.0.ZU;2-P
Abstract
In this study, we simultaneously evaluated the spasmolytic effects of prost aglandin E-1 (PGE(1)) on serotonin-induced bronchoconstriction and pulmonar y hypertension. Eleven mongrel dogs (8 - 12 kg) anaesthetized with pentobar bital were assigned to two groups: saline (n = 4) and PGE(1) (n = 7). Bronc hoconstriction and pulmonary hypertension were elicited with serotonin 10 m u g kg(-1) + 1 mg kg(-1) h(-1) and assessed as the percentage change in bro nchial cross-sectional area (BCA) measured by bronchoscopy and pulmonary va scular resistance (PVR), respectively. Thirty minutes after starting the se rotonin infusion, saline or PGE(1) 0 (saline), 0.01, 0.1, 1.0 or 10 mu g kg (-1) i.v. was given. %BCA and %PVR (basal = 100%) were assessed before and 30 min after serotonin, and 30 and 60 min after saline (saline group) or 5 min after each dose of PGE(1) (PGE(1) group). In the saline group, pulmonar y hypertension and bronchoconstriction were stable. In the PGE(1) group, PG E(1) at greater than or equal to 0.1 mu g kg(-1) significantly decreased %B CA and 10 mu g kg(-1) almost fully reversed the constriction (from mean (SE M) 56.2% (4.9%) to 94.4% (3.7%)). %PVR was significantly decreased at 10 mu g kg(-1) (from 230% (24%) to 176% (11%)) only. We suggest that PGE(1) may produce bronchodilation rather than pulmonary vasodilation.