title: Middle cerebral artery blood velocity during exercise with beta-1 adrenergic and unilateral stellate ganglion blockade in humans.
abstract: A reduced ability to increase cardiac output (CO) during exercise limits blood flow by vasoconstriction even in active skeletal muscle. Such a flow limitation may also take place in the brain as an increase in the transcranial Doppler determined middle cerebral artery blood velocity (MCA V(mean)) is attenuated during cycling with beta-1 adrenergic blockade and in patients with heart insufficiency. We studied whether sympathetic blockade at the level of the neck (0.1% lidocaine; 8 mL; n=8) affects the attenuated exercise - MCA V(mean following cardio-selective beta-1 adrenergic blockade (0.15 mg kg(-1) metoprolol i.v.) during cycling. Cardiac output determined by indocyanine green dye dilution, heart rate (HR), mean arterial pressure (MAP) and MCA V(mean) were obtained during moderate intensity cycling before and after pharmacological intervention. During control cycling the right and left MCA V(mean) increased to the same extent (11.4 +/- 1.9 vs. 11.1 +/- 1.9 cm s(-1)). With the pharmacological intervention the exercise CO (10 +/- 1 vs. 12 +/- 1 L min(-1); n=5), HR (115 +/- 4 vs. 134 +/- 4 beats min(-1)) and delta MCA V(mean) (8.7 +/- 2.2 vs. 11.4 +/- 1.9 cm s(-1) were reduced, and MAP was increased (100 +/- 5 vs. 86 +/- 2 mmHg; P < 0.05). However, sympathetic blockade at the level of the neck eliminated the beta-1 blockade induced attenuation in delta MCA V(mean) (10.2 +/- 2.5 cm s(-1)). These results indicate that a reduced ability to increase CO during exercise limits blood flow to a vital organ like the brain and that this flow limitation is likely to be by way of the sympathetic nervous system.
authors.affiliation: Department of Anaesthesia, The Copenhagen Muscle Research Centre, University of Copenhagen, Rigshospitalet, Denmark.
authors.forename: K
authors.initials: K
authors.lastname: Ide
authors.forename: R
authors.initials: R
authors.lastname: Boushel
authors.forename: H M
authors.initials: HM
authors.lastname: Sørensen
authors.forename: A
authors.initials: A
authors.lastname: Fernandes
authors.forename: Y
authors.initials: Y
authors.lastname: Cai
authors.forename: F
authors.initials: F
authors.lastname: Pott
authors.forename: N H
authors.initials: NH
authors.lastname: Secher
mesh_terms: D000293:Adolescent; D058671:Adrenergic beta-1 Receptor Antagonists; D000328:Adult; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002302:Cardiac Output / Q000187:drug effects / Q000502:physiology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D020768:Middle Cerebral Artery / Q000187:drug effects* / Q000502:physiology; D005082:Physical Exertion / Q000502:physiology*; D018342:Receptors, Adrenergic, beta-1 / Q000502:physiology; D018709:Statistics, Nonparametric; D013233:Stellate Ganglion / Q000187:drug effects* / Q000502:physiology; D013565:Sympatholytics / Q000494:pharmacology*
chemical_list: D058671:Adrenergic beta-1 Receptor Antagonists; D018342:Receptors, Adrenergic, beta-1; D013565:Sympatholytics