Faculty Collaboration Database

Volatile anaesthetics restore bradykinin and serotonin-induced coronary vasodilation after blocking nitric oxide synthase: lack of anaesthetic effects on KATP channels and prostaglandin pathways. Eur J Anaesthesiol 2001 Apr;18(4):219-30

Date

05/15/2001

Pubmed ID

11350459

DOI

10.1046/j.0265-0215.2000.00853.x

Scopus ID

2-s2.0-0035054513 (requires institutional sign-in at Scopus site)   5 Citations

Abstract

BACKGROUND AND OBJECTIVE: Volatile anaesthetic effects on altering tone after blocking nitric oxide synthase, cyclo-oxygenase-prostaglandin synthase and KATP channel pathways are controversial. We examined in isolated guinea pig hearts whether anaesthetics alter bradykinin and 5-hydroxytryptamine-induced effects on coronary flow and percentage oxygen extraction after blocking these pathways.

METHODS: Before and during exposure to sevoflurane, halothane or isoflurane, hearts were infused with 10-13-10-8 M bradykinin, or 10-8-10-6 M 5-hydroxytryptamine (serotonin), with either L-NAME, indomethacin, or glibenclamide. Bradykinin or 5-hydroxytryptamine alone increased flow and decreased percentage oxygen extraction in a concentration-dependent manner; these effects were largely blocked by L-NAME (nitro-L-arginine methylester), which also decreased basal flow and increased basal percentage oxygen extraction.

RESULTS: The anaesthetics restored bradykinin and 5-hydroxytryptamine-induced increases in flow or decreases in percentage oxygen extraction after inhibition by L-NAME. Indomethacin or glibenclamide alone had little effect on basal flow and percentage oxygen extraction. The anaesthetics restored bradykinin and 5-hydroxytryptamine-induced increases in flow or decreases in percentage oxygen extraction after inhibition by L-NAME. Indomethacin or glibenclamide alone had little effect on basal flow and percentage oxygen extraction. Drug-induced increases in flow and decreases in percentage oxygen extraction in the absence or presence of glibenclamide or indomethacin were not altered at either of the two concentrations of anaesthetics.

CONCLUSIONS: Endothelium-dependent vasodilatation is not affected by blocking prostaglandin release or KATP channels in the intact heart even in the presence of an anaesthetic. However, the diminished responses to vasodilators after nitric oxide synthase inhibition is largely restored or enhanced by anaesthetics.

Author List

Stowe DF, Heisner JS, Chung WW, Fujita S

Author

David F. Stowe MD, PhD Professor in the Anesthesiology department at Medical College of Wisconsin

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

ATP-Binding Cassette Transporters
Anesthetics, Inhalation
Animals
Bradykinin
Coronary Circulation
Cyclooxygenase Inhibitors
Enzyme Inhibitors
Glyburide
Guinea Pigs
Heart
Hypoglycemic Agents
In Vitro Techniques
Indomethacin
KATP Channels
Male
Myocardium
NG-Nitroarginine Methyl Ester
Nitric Oxide Synthase
Nitric Oxide Synthase Type III
Potassium Channel Blockers
Potassium Channels
Potassium Channels, Inwardly Rectifying
Prostaglandin Antagonists
Serotonin
Vasodilation