title: Cardiac Catheterization in Mice to Measure the Pressure Volume Relationship: Investigating the Bowditch Effect.
abstract: Animal models that mimic human cardiac disorders have been created to test potential therapeutic strategies. A key component to evaluating these strategies is to examine their effects on heart function. There are several techniques to measure in vivo cardiac mechanics (e.g., echocardiography, pressure/volume relations, etc.). Compared to echocardiography, real-time left ventricular (LV) pressure/volume analysis via catheterization is more precise and insightful in assessing LV function. Additionally, LV pressure/volume analysis provides the ability to instantaneously record changes during manipulations of contractility (e.g., β-adrenergic stimulation) and pathological insults (e.g., ischemia/reperfusion injury). In addition to the maximum (+dP/dt) and minimum (-dP/dt) rate of pressure change in the LV, an accurate assessment of LV function via several load-independent indexes (e.g., end systolic pressure volume relationship and preload recruitable stroke work) can be attained. Heart rate has a significant effect on LV contractility such that an increase in the heart rate is the primary mechanism to increase cardiac output (i.e., Bowditch effect). Thus, when comparing hemodynamics between experimental groups, it is necessary to have similar heart rates. Furthermore, a hallmark of many cardiomyopathy models is a decrease in contractile reserve (i.e., decreased Bowditch effect). Consequently, vital information can be obtained by determining the effects of increasing heart rate on contractility. Our and others data has demonstrated that the neuronal nitric oxide synthase (NOS1) knockout mouse has decreased contractility. Here we describe the procedure of measuring LV pressure/volume with increasing heart rates using the NOS1 knockout mouse model.
authors.affiliation: Department of Physiology & Cell Biology, Davis Heart and Lung Research Institute, The Ohio State University; Institute of Organ Transplantation, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology.
authors.forename: Bo
authors.initials: B
authors.lastname: Zhang
authors.affiliation: Department of Physiology & Cell Biology, Davis Heart and Lung Research Institute, The Ohio State University.
authors.forename: Jonathan P
authors.initials: JP
authors.lastname: Davis
authors.affiliation: Department of Physiology & Cell Biology, Davis Heart and Lung Research Institute, The Ohio State University; Mark.Ziolo@osumc.edu.
authors.forename: Mark T
authors.initials: MT
authors.lastname: Ziolo
mesh_terms: D000818:Animals; D006328:Cardiac Catheterization / Q000379:methods*; D006321:Heart / Q000502:physiology*; D006339:Heart Rate / Q000502:physiology; D051379:Mice; D018345:Mice, Knockout; D023421:Models, Animal; D052248:Nitric Oxide Synthase Type I / Q000172:deficiency; D016277:Ventricular Function, Left
chemical_list: D052248:Nitric Oxide Synthase Type I; C496321:Nos1 protein, mouse