Faculty Collaboration Database

Increases in coronary collateral blood flow produced by sevoflurane are mediated by calcium-activated potassium (BKCa) channels in vivo. Anesthesiology 2002 Sep;97(3):725-31

Date

09/10/2002

Pubmed ID

12218541

DOI

10.1097/00000542-200209000-00028

Scopus ID

2-s2.0-0036725422 (requires institutional sign-in at Scopus site)   15 Citations

Abstract

BACKGROUND: Sevoflurane enhances coronary collateral blood flow independent of adenosine triphosphate-regulated potassium channels. The authors tested the hypothesis that this volatile anesthetic increases coronary collateral blood flow by either opening calcium-activated potassium channels or by directly stimulating nitric oxide synthesis in the canine coronary collateral circulation.

METHODS: Twelve weeks after left anterior descending coronary artery ameroid constrictor implantation, barbiturate-anesthetized dogs (n = 22) were instrumented for measurement of hemodynamics and retrograde coronary flow. Dogs received sevoflurane ([0.5 and 1.0 minimum alveolar concentration [MAC]) during intracoronary infusions of drug vehicle (0.9% saline), the calcium-activated potassium channel antagonist iberiotoxin (13 microg/min), or the nitric oxide synthase inhibitor -nitro-l-arginine methyl ester (l-NAME, 300 microg/min). Retrograde coronary collateral blood flow was measured under baseline conditions, during and after administration of sevoflurane, and during intracoronary infusion of bradykinin. Data are mean +/- SEM.

RESULTS: Sevoflurane increased (* < 0.05) retrograde coronary collateral blood flow (from 65 +/- 11 during control to 67 +/- 12* and 71 +/- 12* ml/min during 0.5 and 1.0 MAC, respectively). Iberiotoxin but not l-NAME attenuated these sevoflurane-induced increases in retrograde flow (6 +/- 1*, 7 +/- 2*, and 3 +/- 2 ml/min during vehicle, l-NAME, and iberiotoxin, respectively). After discontinuation of sevoflurane, retrograde flow returned to baseline values in each group. Bradykinin increased retrograde flow in vehicle- (63 +/- 12 to 69 +/- 12* ml/min) but not in iberiotoxin- (61 +/- 7 to 62 +/- 5 ml/min) or l-NAME-treated dogs (64 +/- 11 to 63 +/- 10 ml/min).

CONCLUSIONS: The results demonstrate that sevoflurane increases coronary collateral blood flow, in part, through activation of calcium-activated potassium channels. This action occurs independent of nitric oxide synthesis.

Author List

Kehl F, Krolikowski JG, Tessmer JP, Pagel PS, Warltier DC, Kersten JR

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

Anesthetics, Inhalation
Animals
Bradykinin
Collateral Circulation
Constriction, Pathologic
Coronary Circulation
Dogs
Hemodynamics
In Vitro Techniques
Methyl Ethers
NG-Nitroarginine Methyl Ester
Nitric Oxide Synthase
Nitric Oxide Synthase Type III
Potassium Channels, Calcium-Activated