2024-03-28T15:31:21Z
https://tsukuba.repo.nii.ac.jp/oai
oai:tsukuba.repo.nii.ac.jp:00029427
2022-04-27T08:57:49Z
2780:1504
2780:1505
2871:2876:2620
3:62:5592:2557
Influence of Acidosis on Cardiotonic Effects of Colforsin and Epinephrine: A Dose-Response Study
高橋, 宏
猪股, 伸一
田中, 誠
Hagiya, Keiichi
Takahashi, Hiroshi
Isaka, Yumi
Inomata, Shinichi
Tanaka, Makoto
Objective
Acidosis produces a negative inotropic effect on cardiac muscle against which catecholamines and phosphodiesterase III inhibitors have limited therapeutic effects. This study evaluated the effects of colforsin, which directly activates adenylate cyclase without β-adrenergic receptor activation, in isolated Langendorff rat hearts in a pH- and concentration-dependent manner.
Design
Experimental animal study.
Setting
A university laboratory.
Participants
Sprague-Dawley rats.
Interventions
Hearts were isolated and perfused with 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid/Tyrode solution (pH 7.4) in the Langendorff preparation. The hearts were assigned randomly to the control (pH 7.4), mild acidosis (pH 7.0), or severe acidosis (pH 6.6) group (n = 8 per group) and were perfused continuously with colforsin 10−7, 10−6, and 10−5 mol/L.
Measurements and Main Results
Maximum dP/dt was determined, and the concentration-response relation was evaluated at each pH. Colforsin at 10−6 mol/L increased the maximum dP/dt from 2,592 ± 557 to 5,189 ± 721 mmHg/s (p < 0.001) and from 1,942 ± 325 to 3,399 ± 608 mmHg/s (p < 0.001) in the control and mild acidosis groups, respectively; whereas colforsin, 10−5 mol/L, significantly increased the maximum dP/dt even in the severe acidosis group. No significant difference was seen in maximum dP/dt among the 3 groups after infusion with colforsin 10−5 mol/L.
Conclusions
In contrast to catecholamines and other inodilators, colforsin at a high concentration restores decreased cardiac contractility against severe acidosis to an extent similar to physiologic pH.
journal article
Elsevier
2013-10
application/pdf
Journal of cardiothoracic and vascular anesthesia
5
27
925
932
http://hdl.handle.net/2241/120031
1053-0770
AA10801216
https://tsukuba.repo.nii.ac.jp/record/29427/files/JCVA_27-5.pdf
eng
23266286
10.1053/j.jvca.2012.09.019
© 2013 Elsevier Inc. “NOTICE: this is the author’s version of a work that was accepted for publication in Journal of Cardiothoracic and Vascular Anesthesia. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Journal of Cardiothoracic and Vascular Anesthesia,27,5,2013 http://dx.doi.org/10.1053/j.jvca.2012.09.019.