title: Cerebral oxygenation during changes in vascular resistance and flow in patients on cardiopulmonary bypass - a physiological proof of concept study.
abstract: Despite a rise in blood pressure, cerebral oxygenation decreases following phenylephrine administration, and we hypothesised that phenylephrine reduces cerebral oxygenation by activating cerebral α1receptors. We studied patients on cardiopulmonary bypass during constant flow. Phenylephrine raised mean arterial pressure (α1-mediated) from mean (SD) 69 (8) mmHg to 79 (8) mmHg; p = 0.001, and vasopressin raised mean arterial pressure (V1mediated) from 69 (8) mmHg to 83 (6) mmHg; p = 0.001. Both drugs elicited a comparable decrease in cerebral oxygenation from 61 (7)% to 60 (7)%; p = 0.023 and 61 (8)% to 59 (8)%; p = 0.022, respectively. This implies that after phenylephrine or vasopressin administration, cerebral oxygenation declines as a result of cerebral vasoconstriction, due to either both cerebral α1and V1receptors being equipotentially activated or to an intrinsic myogenic mechanism of cerebral vasculature in reaction to blood pressure elevation.
authors.affiliation: Department of Anaesthesiology, Academic Medical Center, Amsterdam, The Netherlands.
authors.forename: N H
authors.initials: NH
authors.lastname: Sperna Weiland
authors.affiliation: Department of Anaesthesiology, Academic Medical Center, Amsterdam, The Netherlands.
authors.forename: D
authors.initials: D
authors.lastname: Brevoord
authors.affiliation: Department of Anaesthesiology, Academic Medical Center, Amsterdam, The Netherlands.
authors.forename: D A
authors.initials: DA
authors.lastname: Jöbsis
authors.affiliation: Department of Anaesthesiology, Academic Medical Center, Amsterdam, The Netherlands.
authors.forename: E M F H
authors.initials: EM
authors.lastname: de Beaumont
authors.affiliation: Department of Anaesthesiology, Academic Medical Center, Amsterdam, The Netherlands.
authors.forename: V
authors.initials: V
authors.lastname: Evers
authors.affiliation: Department of Anaesthesiology, Academic Medical Center, Amsterdam, The Netherlands.
authors.forename: B
authors.initials: B
authors.lastname: Preckel
authors.affiliation: Department of Anaesthesiology, Academic Medical Center, Amsterdam, The Netherlands.
authors.forename: M W
authors.initials: MW
authors.lastname: Hollmann
authors.affiliation: Department of Anaesthesiology, Academic Medical Center, Amsterdam, The Netherlands.
authors.forename: S
authors.initials: S
authors.lastname: van Dieren
authors.affiliation: Department of Cardiothoracic Surgery, Academic Medical Center, Amsterdam, The Netherlands.
authors.forename: B A J M
authors.initials: BA
authors.lastname: de Mol
authors.affiliation: Department of Anaesthesiology, Academic Medical Center, Amsterdam, The Netherlands.|Laboratory for Clinical Cardiovascular Physiology, Department of Anatomy and Embryology, Academic Medical Center, Amsterdam, The Netherlands.
authors.forename: R V
authors.initials: RV
authors.lastname: Immink
mesh_terms: D000368:Aged; D062186:Arterial Pressure / Q000187:drug effects; D002245:Carbon Dioxide / Q000097:blood; D006348:Cardiac Surgical Procedures; D002315:Cardiopulmonary Bypass; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption / Q000187:drug effects / Q000502:physiology*; D010313:Partial Pressure; D010656:Phenylephrine / Q000494:pharmacology; D000075082:Proof of Concept Study; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014667:Vasopressins / Q000494:pharmacology
chemical_list: D014662:Vasoconstrictor Agents; D014667:Vasopressins; D002245:Carbon Dioxide; D010656:Phenylephrine; D010100:Oxygen
keywords: arginine vasopressin; cardiopulmonary bypass management; cerebral autoregulation; inotropes: alpha-1 activity