Faculty Collaboration Database

Anesthetic preconditioning attenuates mitochondrial Ca2+ overload during ischemia in Guinea pig intact hearts: reversal by 5-hydroxydecanoic acid. Anesth Analg 2002 Dec;95(6):1540-6, table of contents

Date

11/29/2002

Pubmed ID

12456413

DOI

10.1097/00000539-200212000-00013

Scopus ID

2-s2.0-0036897277 (requires institutional sign-in at Scopus site)   74 Citations

Abstract

UNLABELLED: Cardiac ischemia/reperfusion (IR) injury is associated with mitochondrial (m)Ca(2+) overload. Anesthetic preconditioning (APC) attenuates IR injury. We hypothesized that mCa(2+) overload is decreased by APC in association with mitochondrial adenosine triphosphate-sensitive K(+) (mK(ATP)) channel opening. By use of indo-1 fluorescence, m[Ca(2+)] was measured in 40 guinea pig Langendorff-prepared hearts. Control (CON) hearts received no treatment for 50 min before IR; APC hearts were exposed to 1.2 mM (8.8 vol%) sevoflurane for 15 min; APC + 5-hydroxydecanoate (5-HD) hearts received 200 micro M 5-HD from 5 min before to 15 min after sevoflurane exposure; and 5-HD hearts received 5-HD for 35 min. Sevoflurane was washed out for 30 min and 5-HD for 15 min before 30 min of global ischemia and 120 min of reperfusion. During ischemia, the peak m[Ca(2+)] accumulation was decreased by APC from 489 +/- 37 nM (CON) to 355 +/- 28 nM (P < 0.05); this was abolished by 5-HD (475 +/- 38 nM m[Ca(2+)]). APC resulted in improved function and reduced infarct size on reperfusion, which also was blocked by 5-HD. 5-HD pretreatment alone did not affect m[Ca(2+)] (470 +/- 34 nM) or IR injury. Thus, preservation of function and morphology on reperfusion is associated with attenuated mCa(2+) accumulation during ischemia. Reversal by 5-HD suggests that APC may be triggered by opening mK(ATP) channels.

IMPLICATIONS: Myocardial ischemia/reperfusion injury is associated with mitochondrial Ca(2+) overload. Mitochondrial [Ca(2+)] and function were measured in guinea pig isolated hearts. Anesthetic preconditioning attenuated mitochondrial Ca(2+) overload during ischemia, improved function, and reduced infarct size. Reversal by 5-hydroxydecanoate suggests that anesthetic preconditioning may be triggered by mitochondrial adenosine triphosphate-sensitive K channel opening.

Author List

Riess ML, Camara AK, Novalija E, Chen Q, Rhodes SS, Stowe DF

Authors

Amadou K. Camara PhD Professor in the Anesthesiology department at Medical College of Wisconsin
David F. Stowe PhD, MA, MA Emeritus Professor in the Anesthesiology department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Anesthetics
Animals
Calcium
Decanoic Acids
Guinea Pigs
Heart Rate
Hydroxy Acids
Ischemic Preconditioning, Myocardial
Methyl Ethers
Mitochondria, Heart
Myocardial Ischemia