Universität zu Köln

Behmenburg, Friederike, Trefz, Lara, Dorsch, Marianne, Stroethoff, Martin, Mathes, Alexander, Raupach, Annika, Heinen, Andre, Hollmann, Markus W., Berger, Marc M. and Huhn, Ragnar (2018). Milrinone-Induced Postconditioning Requires Activation of Mitochondrial Ca2+-sensitive Potassium (mBK(ca)) Channels. J. Cardiothorac. Vasc. Anesth., 32 (5). S. 2142 - 2149. PHILADELPHIA: W B SAUNDERS CO-ELSEVIER INC. ISSN 1532-8422

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Abstract

Objectives: Cardioprotection by postconditioning requires activation of mitochondrial large-conductance Ca2+-sensitive potassium (mBK(ca)) channels. The involvement of these channels in milrinone-induced postconditioning is unknown. The authors determined whether cardioprotection by milrinone-induced postconditioning involves activation of mBK(ca) channels in the rat heart in vitro. Design: Randomized, prospective, blinded laboratory investigation. Setting: Experimental laboratory. Participants: Male Wistar rats. Interventions: Hearts of male Wistar rats were randomized, placed on a Langendorff system, and perfused with Krebs-Henseleit buffer at a constant pressure of 80 mmHg. All hearts were subjected to 33 minutes of global ischemia and 60 minutes of reperfusion. At the onset of reperfusion, hearts were perfused with different concentrations of milrinone (0.3-100 mu M) for determination of a dose-effect curve. In a second set of experiments, 3 pM milrinone was administered in combination with the mBK(ca) channel inhibitor paxilline (1 mu M). Infarct size was determined by triphenyltetrazoliumchloride staining. Measurements and Main Results: In control animals, infarct size was 37 +/- 7%. Milrinone at a concentration of 3 mu M reduced infarct size to 22 +/- 7% (p < 0.05 v control). Higher milrinone concentrations did not confer stronger protection. Paxilline completely blocked milrinone-induced cardioprotection whereas paxilline alone had no effect on infarct size. Conclusions: This study shows that activation of mBK(ca) channels plays a pivotal role in milrinone-induced postconditioning. (C) 2017 Elsevier Inc. All rights reserved.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Behmenburg, Friederike UNSPECIFIED UNSPECIFIED UNSPECIFIED Trefz, Lara UNSPECIFIED UNSPECIFIED UNSPECIFIED Dorsch, Marianne UNSPECIFIED UNSPECIFIED UNSPECIFIED Stroethoff, Martin UNSPECIFIED UNSPECIFIED UNSPECIFIED Mathes, Alexander UNSPECIFIED UNSPECIFIED UNSPECIFIED Raupach, Annika UNSPECIFIED UNSPECIFIED UNSPECIFIED Heinen, Andre UNSPECIFIED UNSPECIFIED UNSPECIFIED Hollmann, Markus W. UNSPECIFIED UNSPECIFIED UNSPECIFIED Berger, Marc M. UNSPECIFIED UNSPECIFIED UNSPECIFIED Huhn, Ragnar UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-171088
DOI:	10.1053/j.jvca.2017.11.048
Journal or Publication Title:	J. Cardiothorac. Vasc. Anesth.
Volume:	32
Number:	5
Page Range:	S. 2142 - 2149
Date:	2018
Publisher:	W B SAUNDERS CO-ELSEVIER INC
Place of Publication:	PHILADELPHIA
ISSN:	1532-8422
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language CA2+-ACTIVATED K+ CHANNELS; PROTEIN-KINASE-A; REPERFUSION INJURY; HEART-FAILURE; INOTROPIC AGENTS; INHIBITION; CARDIOPROTECTION; MYOCARDIUM; MECHANISM; ISCHEMIA Multiple languages Anesthesiology; Cardiac & Cardiovascular Systems; Respiratory System; Peripheral Vascular Disease Multiple languages
Refereed:	Yes
URI:	http://kups.ub.uni-koeln.de/id/eprint/17108