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Cardiovascular Research 1998 39(1):34-49; doi:10.1016/S0008-6363(98)00073-X
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

Cardiovascular phenotyping in mice

Pieter A Doevendansa, Mat J. Daemenb, Ebo D de Muincka and Jos F Smitsc,*

aDepartment of Cardiology, Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands
bDepartment of Pathology, Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands
cDepartment of Pharmacology, Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands

* Corresponding author. Address for correspondence: Dept of Pharmacology, Cardiovascular Research Institute Maastricht, Universiteit Maastricht, PO BOX 616, 6200MD Maastricht, The Netherlands. Tel.: +31 (43) 388 1421; Fax: +31 (43) 367 0940; E-mail: j.smits@farmaco.unimaas.nl

Progress in molecular genetics has changed cardiovascular research. The mouse has turned out to be an invaluable model for mammalian genetic modifications to mimic and analyse cardiovascular pathology. Through the introduction of transgene and gene targeting technology, regulatory systems can be studied at the molecular level. Recent technical developments have down-sized the equipment for physiological measurements to the mouse level. Micro-surgery has developed to the level where most manipulations previously performed in larger animals can now be applied to mice. However, different investigators report considerable differences in values for physiological parameters. Whether these differences are related to the variation in mouse strains or experimental procedures remains to be established, but awareness of the variation can be relevant for prospective mouse investigators. In the present review, the physiological measurements performed in mice to date are discussed and complemented with results from genetically manipulated animals. In addition the various surgical procedures and their practical application are illustrated.

KEYWORDS AAR, area at risk; ACE, angiotensin converting enzyme; ANF, atrial natriuretic factor; AT, angiotensin receptor; AV node, atrioventricular node; AWTh, anterior wall thickness; βARK, β-adrenergic receptor kinase; C/F ratio, capilliary-fiber ratio; ECG, electrocardiogram; EC-SOD, extracellular superoxide dismutase; EDP, End-diastolic pressure; EP, electrophysiology; ET-1, endothelin-1; FS, fractional shortening; GFR, glomerular filtration rate; IS, infarct size; LVEDD, left ventricular end-diastolic diameter; LVESD, left ventricular end-systolic diameter; MAP, mean arterial pressure; MI, myocardial infarction; PWTh, posterior wall thickness; SERCA, sarcoplasmatic reticulum Ca2+ ATPase; SIP, systolic intraventricular pressure; SNGFR, single nephron glomerular filtration rate; SR, sarcoplasmatic reticulum; SW, Swiss Webster; TGF, tubuloglomerular feedback; TPP, time to peak pressure per unit pressure; Vcf, velocity of circumferential shortening


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