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In vivo spasmolytic effect of ketamine and adrenaline on histamine‐induced airway constriction
Author(s) -
Hirota K.,
Hashimoto Y.,
Sakai T.,
Sato T.,
Ishihara H.,
Matsuki A.
Publication year - 1998
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1998.tb05106.x
Subject(s) - medicine , bronchoconstriction , in vivo , anesthesia , ketamine , histamine , bronchodilation , airway , bronchus , pentobarbital , constriction , lung , asthma , bronchodilator , pharmacology , respiratory disease , biology , microbiology and biotechnology
Background : Ketamine (K) has been reported to produce bronchodilation in patients suffering from asthma. Although most researchers have used indirect measurements to study the effect of K in vivo , the reliability of these indirect methods are controversial. We have developed a new technique to measure the bronchial cross‐sectional area (BCA) in vivo with a superfine fibreoptic bronchoscope (SFB). Employing this method, we evaluated in vivo spasmolytic effect of K and adrenaline (A). Methods : Twenty‐one mongrel dogs were anaesthetized with pentobarbitone (30 mg . kg ‐1 ) and paralyzed with pancuronium (200μg . kg ‐1 . h ‐1 ). The trachea was intubated with an endotracheal tube that has a second lumen for insertion of a SFB (OD: 2.2 mm) to measure the BCA continuously. The tip of the SFB was placed between the 2nd and 3rd bronchial bifurcation of the right lung. A videoprinter printed the BCA, which was then measured with NIH Image. Bronchoconstriction was produced with histamine (H: 10μg . kg ‐1 +500μg . kg ‐1 . h ‐1 ) which was administered until the end of the experiment. The BCA was assessed before and 30 min after the start of H infusion. The dogs were randomly allocated to 3 groups of 7 dogs each. In group K, K (0–10 mg . kg ‐1 ) was given i.v., and the BCA was measured 5 min after each K dose. In group A, A (0‐0.4μg . kg ‐1 ) was given i.v., and the BCA was measured 1 min after each A dose. In group A+K, K (1 mg . kg ‐1 i.v. +1 mg . kg ‐1 . h ‐1 i.v.) was given followed, 30 min after, by A i.v. in the same doses as in group A. The BCA was assessed 30 min after the start of K and again 1 min after each A dose. Results : K 10 mg . kg ‐1 reversed H‐induced bronchoconstriction. A subthreshold dose of K significantly potentiated the effect of A, reversing the decrease in BCA by H. Conclusion : We have found that K could reverse the H‐induced bronchoconstriction and potentiate the A‐induced bronchial relaxation.