|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Cardiology Division, Department of Medicine, University of California, San Francisco, California, United States
2 Cardiology Division, Department of Medicine, University of California, SanFrancisco, San Francisco, California, United States
3 Cardiology, UCSF, San Francisco, California, United States
4 Cardiology Division, Veterans Affairs Medical Center, San Francisco, California, United States
5 Cardiology Division, Department of Medicine, University of California, San Francisco, San Francisco, California, United States
* To whom correspondence should be addressed. E-mail: grossman{at}medicine.ucsf.edu.
With the availability of transgenic models, the mouse has become an increasingly important subject for genetic-hemodynamic studies. Recently, we developed a technique to measure left ventricular (LV) pressure in conscious mice with an implanted LV polyethylene tube. We extended our new method by evaluating the LV pressure-volume relationship and examined feasibility in this study. We studied 17 mice with a conductance catheter inserted into the LV through the polyethylene tube. Load-independent parameters of contractility {slope of the end-systolic pressure-volume relationship (Ees), slope of the dP/dtmax - end-diastolic volume relation and preload-recruitable stroke work} were evaluated by inferior vena caval occlusion with an implanted snare. LV function on two different days showed that the parameters were very similar, indicating reproducibility. Contractility was enhanced by isoproterenol, depressed by atenolol and isoflurane, significantly. CONCLUSION: This is the first description of the LV pressure-volume relationship in conscious mice. These findings suggest that this method is feasible to detect changes of contractility in conscious state, allowing serial assessment of pressure-volume derived cardiac function indices over time without anesthesia or repeated surgery.
This article has been cited by other articles:
![]() |
P. Pokreisz, G. Marsboom, and S. Janssens Pressure overload-induced right ventricular dysfunction and remodelling in experimental pulmonary hypertension: the right heart revisited Eur. Heart J. Suppl., December 1, 2007; 9(suppl_H): H75 - H84. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. J. Chess, B. Lei, B. D. Hoit, A. M. Azimzadeh, and W. C. Stanley Deleterious effects of sugar and protective effects of starch on cardiac remodeling, contractile dysfunction, and mortality in response to pressure overload Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1853 - H1860. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |