AJP - Heart Calcium Transients and Cell-Sarcomere
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Heart Circ Physiol 278: H8-H15, 2000;
0363-6135/00 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (12)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Champion, H. C.
Right arrow Articles by Hyman, A. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Champion, H. C.
Right arrow Articles by Hyman, A. L.
Vol. 278, Issue 1, H8-H15, January 2000

A novel right-heart catheterization technique for in vivo measurement of vascular responses in lungs of intact mice

Hunter C. Champion, Douglas J. Villnave, Allen Tower, Philip J. Kadowitz, and Albert L. Hyman

Department of Pharmacology, Tulane University School of Medicine, New Orleans, Louisiana, 70112; and Nu-Med Inc., Hopkinton, New York 12940

The present study employed a new right-heart catheterization technique to measure pulmonary arterial pressure, pulmonary arterial wedge pressure, and pulmonary vascular resistance in anesthetized intact-chest, spontaneously breathing mice. Under fluoroscopic guidance, a specially designed catheter was inserted via the right jugular vein and advanced to the main pulmonary artery. Cardiac output was determined by the thermodilution technique, and measured parameters were stable for periods of equal3 h. Pressure-flow curves in vivo were curvilinear, with mean pulmonary arterial pressure increasing more rapidly at low pulmonary blood flows of 5-10 ml/min and less rapidly at higher blood flow rates. The pressure-flow relationship was shifted to the left by the nitric oxide synthase inhibitor nitro-L-arginine methyl ester (L-NAME) at higher blood flow levels, whereas the cyclooxygenase inhibitor sodium meclofenamate was without effect. The increase in pulmonary arterial pressure in response to acute hypoxia (fractional inspired O2 10%) was augmented by L-NAME but unaltered by sodium meclofenamate. The present results demonstrate that the right-heart catheterization technique can be used to measure pulmonary vascular pressures and responses in the mouse. This is, to our knowledge, the first report of a right-heart catheterization technique to measure pulmonary vascular pressures and responses in the intact-chest, spontaneously breathing mouse and should prove useful for the investigation of pulmonary vascular responses in transgenic mice.

cardiac output; pulmonary vascular bed; mouse; vascular resistance; pressure-flow relationship; acute hypoxia; nitric oxide


This article has been cited by other articles:


Home page
Eur Heart J SupplHome page
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]


Home page
BloodHome page
L. L. Hsu, H. C. Champion, S. A. Campbell-Lee, T. J. Bivalacqua, E. A. Manci, B. A. Diwan, D. M. Schimel, A. E. Cochard, X. Wang, A. N. Schechter, et al.
Hemolysis in sickle cell mice causes pulmonary hypertension due to global impairment in nitric oxide bioavailability
Blood, April 1, 2007; 109(7): 3088 - 3098.
[Abstract] [Full Text] [PDF]


Home page
HypertensionHome page
P. Pokreisz, I. Fleming, L. Kiss, E. Barbosa-Sicard, B. Fisslthaler, J. R. Falck, B. D. Hammock, I.-H. Kim, Z. Szelid, P. Vermeersch, et al.
Cytochrome P450 Epoxygenase Gene Function in Hypoxic Pulmonary Vasoconstriction and Pulmonary Vascular Remodeling
Hypertension, April 1, 2006; 47(4): 762 - 770.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
S. R. Baber, W. Deng, J. Rodriguez, R. G. Master, T. J. Bivalacqua, A. L. Hyman, and P. J. Kadowitz
Vasoactive prostanoids are generated from arachidonic acid by COX-1 and COX-2 in the mouse
Am J Physiol Heart Circ Physiol, October 1, 2005; 289(4): H1476 - H1487.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
J. C. Parker and M. I. Townsley
Evaluation of lung injury in rats and mice
Am J Physiol Lung Cell Mol Physiol, February 1, 2004; 286(2): L231 - L246.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
L. A. Ortiz, H. C. Champion, J. A. Lasky, F. Gambelli, E. Gozal, G. W. Hoyle, M. B. Beasley, A. L. Hyman, M. Friedman, and P. J. Kadowitz
Enalapril protects mice from pulmonary hypertension by inhibiting TNF-mediated activation of NF-kappa B and AP-1
Am J Physiol Lung Cell Mol Physiol, June 1, 2002; 282(6): L1209 - L1221.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online