Universität zu Köln

Truse, Richard ORCID: 0000-0001-6650-5800, Grewe, Steven, Herminghaus, Anna, Schulz, Jan, Weber, Andreas P. M., Mettler-Altmann, Tabea, Bauer, Inge, Picker, Olaf and Vollmer, Christian (2019). Exogenous vasopressin dose-dependently modulates gastric microcirculatory oxygenation in dogs via V1A receptor. Crit. Care, 23 (1). LONDON: BMC. ISSN 1364-8535

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Abstract

Background Hypercapnia improves gastric microcirculatory oxygenation (mu HbO(2)) and increases vasopressin plasma levels, whereas V1A receptor blockade abolishes the increase of mu HbO(2). The aim of this study was to evaluate the effect of exogenous vasopressin (AVP) in increasing doses on microcirculatory perfusion and oxygenation and systemic hemodynamic variables. Furthermore, we evaluated the role of the vasopressin V1A receptor in mediating the effects. Methods In repetitive experiments, six anesthetized dogs received a selective vasopressin V1A receptor inhibitor ([Pmp(1), Tyr (Me)(2)]-Arg(8)-Vasopressin) or sodium chloride (control groups). Thereafter, a continuous infusion of AVP was started with dose escalation every 30 min (0.001 ng/kg/min-1 ng/kg/min). Microcirculatory variables of the oral and gastric mucosa were measured with reflectance spectrometry, laser Doppler flowmetry, and incident dark field imaging. Transpulmonary thermodilution was used to measure systemic hemodynamic variables. AVP plasma concentrations were measured during baseline conditions and 30 min after each dose escalation. Results During control conditions, gastric mu HbO(2) did not change during the course of experiments. Infusion of 0.001 ng/kg/min and 0.01 ng/kg/min AVP increased gastric mu HbO(2) to 87 +/- 4% and 87 +/- 6%, respectively, compared to baseline values (80 +/- 7%), whereas application of 1 ng/kg/min AVP strongly reduced gastric mu HbO(2) (59 +/- 16%). V1A receptor blockade prior to AVP treatment abolished these effects on mu HbO(2). AVP dose-dependently enhanced systemic vascular resistance (SVR) and decreased cardiac output (CO). After prior V1A receptor blockade, SVR was reduced and CO increased (0.1 ng/kg/min + 1 ng/kg/min AVP). Conclusions Exogenous AVP dose-dependently modulates gastric mu HbO(2), with an increased mu HbO(2) with ultra-low dose AVP. The effects of AVP on mu HbO(2) are abolished by V1A receptor inhibition. These effects are independent of a modulation of systemic hemodynamic variables.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Truse, Richard UNSPECIFIED orcid.org/0000-0001-6650-5800 UNSPECIFIED Grewe, Steven UNSPECIFIED UNSPECIFIED UNSPECIFIED Herminghaus, Anna UNSPECIFIED UNSPECIFIED UNSPECIFIED Schulz, Jan UNSPECIFIED UNSPECIFIED UNSPECIFIED Weber, Andreas P. M. UNSPECIFIED UNSPECIFIED UNSPECIFIED Mettler-Altmann, Tabea UNSPECIFIED UNSPECIFIED UNSPECIFIED Bauer, Inge UNSPECIFIED UNSPECIFIED UNSPECIFIED Picker, Olaf UNSPECIFIED UNSPECIFIED UNSPECIFIED Vollmer, Christian UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-127777
DOI:	10.1186/s13054-019-2643-y
Journal or Publication Title:	Crit. Care
Volume:	23
Number:	1
Date:	2019
Publisher:	BMC
Place of Publication:	LONDON
ISSN:	1364-8535
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language ARGININE-VASOPRESSIN; BLOOD-FLOW; GASTROINTESTINAL PERFUSION; SPLANCHNIC HEMODYNAMICS; MUCOSAL OXYGENATION; HORMONE-LEVELS; SEPTIC SHOCK; PRESSURE; PLASMA; TISSUE Multiple languages Critical Care Medicine Multiple languages
Refereed:	Yes
URI:	http://kups.ub.uni-koeln.de/id/eprint/12777