Comparison of the role of endothelin, vasopressin and angiotensin in arterial pressure regulation during sevoflurane anaesthesia in dogs.
BACKGROUND
In this study we aimed to clarify the role of endothelin in arterial pressure regulation during anaesthesia with increasing concentrations of sevoflurane (1-3 MAC) and compare it with those of vasopressin and angiotensin.


METHODS
After an awake control period, on different days, six dogs underwent each of the following four interventions: sevoflurane anaesthesia alone (1-3 MAC), sevoflurane after block of either endothelin receptors using tezosentan (3 mg kg(-1) followed by 3 mg kg(-1) h(-1)), vasopressin V(1a) receptors using [d(CH(2))(5)Tyr(Me(2))]AVP (40 micro g kg(--1)) or angiotensin receptors using losartan (6 mg kg(-1) h(-1)). Plasma concentrations of endothelin, big endothelin, vasopressin and renin were measured. Effects of sevoflurane in the presence and absence of the respective receptor block were analysed and compared using analysis of variance for repeated measures (ANOVA followed by Fisher's PLSD (protected least significant difference) (P<0.05)).


RESULTS
Mean arterial pressure decreased in a dose-dependent manner with sevoflurane during all interventions. At 1 MAC, this decrease was greatest during angiotensin receptor block (mean (SEM), -41 (3) mm Hg), intermediate during vasopressin and endothelin receptor block (-31 (4) and -30 (2) mm Hg respectively), and least during sevoflurane alone (-24 (3) mm Hg). The course of systemic vascular resistance mirrored the course of arterial pressure, while cardiac output did not differ between groups. Plasma concentrations of endothelin, big endothelin and renin did not change during any intervention, whereas vasopressin concentration increased from approximately 0.5 to 40 ng litre(-1) at 3 MAC as arterial pressure decreased in all groups.


CONCLUSIONS
At 1 MAC, angiotensin attenuated the decrease in arterial pressure during sevoflurane anaesthesia more than endothelin and vasopressin. However, at higher MAC only vasopressin was specifically activated to partly compensate for the arterial pressure decrease.
Picker
O
O
Department of Anaesthesiology, Universitätsklinikum Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany. olaf.picker@uni-duesseldorf.de
Schwarte
L A
LA
Roth
H J
HJ
Greve
J
J
Scheeren
T W L
TW
D000704:Analysis of Variance; D018685:Anesthetics, Inhalation / Q000494:pharmacology*; D000809:Angiotensins / Q000097:blood / Q000502:physiology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects* / Q000502:physiology; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output / Q000187:drug effects; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D065128:Endothelin Receptor Antagonists; D016232:Endothelins / Q000097:blood / Q000502:physiology*; D005260:Female; D006727:Hormone Antagonists / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration / Q000187:drug effects; D008297:Male; D008738:Methyl Ethers / Q000494:pharmacology*; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D000077149:Sevoflurane; D014655:Vascular Resistance / Q000187:drug effects; D014667:Vasopressins / Q000097:blood / Q000502:physiology
D018685:Anesthetics, Inhalation; D000809:Angiotensins; D065128:Endothelin Receptor Antagonists; D016232:Endothelins; D006727:Hormone Antagonists; D008738:Methyl Ethers; D014667:Vasopressins; D002245:Carbon Dioxide; D000077149:Sevoflurane; D010100:Oxygen