title: Evaluation of ventricular and arterial hemodynamics in anesthetized closed-chest mice.
abstract: Transgenic and knock-out mice with cardiovascular phenotypes have created the need for methods to measure murine arterial and ventricular mechanics. The aims of this study were (1) to develop a method for the assessment of wall stress (sigma es)-rate corrected velocity of fiber shortening (Vcfc) relation and (2) to assess the feasibility of quantifying global arterial function in normal mice. This method can thus serve as a reference for future studies in genetically altered mice by establishing normal values for comparison. Ten anesthetized closed-chest mice were studied with targeted M-mode echocardiography of the left ventricle recorded simultaneously with high-fidelity aortic pressures. Data were acquired at baseline and during infusions of methoxamine and isoproterenol. Tracings were digitized to obtain end-systolic wall stress (sigma es) and rate-corrected velocity of fiber shortening (Vcfc) relationships and plots of systolic meridional wall stress. Instantaneous aortic pressures and continuous wave aortic Doppler velocities were digitized to study arterial hemodynamics. The Vcfc-sigma es relationship was inverse and linear in all mice studied with a median value of r2 = 0.94. Isoproterenol resulted in an upward shift from the baseline contractility line obtained with methoxamine (mean shift = 2.0 +/- 0.3 circ/sec). Relative to baseline the integral of wall stress decreased with isoproterenol and increased with methoxamine. Methoxamine increased mean arterial pressure and total vascular resistance and decreased heart rate, cardiac output, and arterial compliance. Isoproterenol decreased total vascular resistance and increased cardiac output. Stress-shortening relationships, systolic wall stress, and evaluation of vascular function can be obtained in a closed-chest mouse model.
authors.affiliation: Department of Medicine, University of Chicago, IL 60637, USA.
authors.forename: R C
authors.initials: RC
authors.lastname: Fentzke
authors.forename: C E
authors.initials: CE
authors.lastname: Korcarz
authors.forename: S G
authors.initials: SG
authors.lastname: Shroff
authors.forename: H
authors.initials: H
authors.lastname: Lin
authors.forename: J
authors.initials: J
authors.lastname: Sandelski
authors.forename: J M
authors.initials: JM
authors.lastname: Leiden
authors.forename: R M
authors.initials: RM
authors.lastname: Lang
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000502:physiology*; D005240:Feasibility Studies; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging*; D006439:Hemodynamics / Q000187:drug effects; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D008729:Methoxamine / Q000494:pharmacology; D051379:Mice; D008815:Mice, Inbred Strains; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D014463:Ultrasonography; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology
chemical_list: D000316:Adrenergic alpha-Agonists; D000318:Adrenergic beta-Agonists; D008729:Methoxamine; D007545:Isoproterenol