Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1999;100:1562-1568

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 PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Karunanithi, M. K.
Right arrow Articles by Feneley, M. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Karunanithi, M. K.
Right arrow Articles by Feneley, M. P.
Related Collections
Right arrow Contractile function
Right arrow Animal models of human disease
Right arrow Coronary circulation

(Circulation. 1999;100:1562-1568.)
© 1999 American Heart Association, Inc.


Basic Science Reports

Response of the Intact Canine Left Ventricle to Increased Afterload and Increased Coronary Perfusion Pressure in the Presence of Coronary Flow Autoregulation

Mohanraj K. Karunanithi, BE, MBiomedE; Jason A. Young, BE, MBiomedE; Wally Kalnins, BE; Scott Kesteven, BSci, Grad Dip BiomedE; Michael P. Feneley, MD, FRACP

From the Victor Chang Cardiac Research Institute and Cardiology Department, St. Vincent's Hospital, Sydney, Australia.

Correspondence to Michael P. Feneley, MD, FRACP, FACC, Cardiology Department, St. Vincent's Hospital, Darlinghurst NSW 2010, Australia.

Background—Increased left ventricular (LV) contractile force or oxygen consumption has been documented with increased coronary arterial pressure (CAP) and flow (Gregg phenomenon). We investigated whether the increase in contractile force with increased LV afterload might be mediated by the concomitant increase in CAP when coronary autoregulation is intact.

Methods and Results—The LV of 6 autonomically blocked open-chest dogs was perfused through the left main coronary artery by a cannula with a side gate to the aortic root. With the gate open, CAP increased from 77±20 to 93±20 mm Hg (P<0.05) with aortic constriction (AC). With the gate closed, CAP was maintained at a constant level of 100 mm Hg. A small reduction in the slope of the preload recruitable stroke work (PRSW) relationship was observed with AC, but this response was not altered by the coronary perfusion gate position. The end-systolic pressure-volume (ESPV) relationship shifted upward significantly with AC (P<0.001), but this shift was not greater with open-gate perfusion than with closed-gate perfusion. Furthermore, with coronary autoregulation intact, wide changes in CAP (between 60 and 180 mm Hg, n=5) did not alter either the PRSW or ESPV relationship. In contrast, when autoregulation was abolished with intracoronary adenosine (n=6), both indexes of contractility increased progressively with increased CAP.

Conclusions—The concomitant increase in CAP with increased afterload in the intact canine LV does not contribute to the afterload-induced increase in contractile force. Coronary perfusion pressure per se does not influence LV contractile function. Coronary perfusion pressure influences contractility only when coronary flow changes.


Key Words: contractility • ventricles • perfusion • pressure • physiology




This article has been cited by other articles:


Home page
Physiol. Rev.Home page
N. Westerhof, C. Boer, R. R. Lamberts, and P. Sipkema
Cross-talk between cardiac muscle and coronary vasculature.
Physiol Rev, October 1, 2006; 86(4): 1263 - 1308.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
E. I. Tikh, R. A. Fenton, and J. G. Dobson Jr.
Contractile effects of adenosine A1 and A2A receptors in isolated murine hearts
Am J Physiol Heart Circ Physiol, January 1, 2006; 290(1): H348 - H356.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
S. Schenk, Z. B. Popovic, Y. Ochiai, F. Casas, P. M. McCarthy, R. C. Starling, M. W. Kopcak Jr., R. Dessoffy, J. L. Navia, N. L. Greenberg, et al.
Preload-adjusted right ventricular maximal power: concept and validation
Am J Physiol Heart Circ Physiol, October 1, 2004; 287(4): H1632 - H1640.
[Abstract] [Full Text] [PDF]


Home page
Eur J Heart FailHome page
G. Cotter, Y. Moshkovitz, E. Kaluski, O. Milo, Y. Nobikov, A. Schneeweiss, R. Krakover, and Z. Vered
The role of cardiac power and systemic vascular resistance in the pathophysiology and diagnosis of patients with acute congestive heart failure
Eur J Heart Fail, August 1, 2003; 5(4): 443 - 451.
[Abstract] [Full Text] [PDF]


Home page
Eur Heart JHome page
G. Cotter, E. Kaluski, O. Milo, A. Blatt, A. Salah, A. Hendler, R. Krakover, A. Golick, and Z. Vered
LINCS: L-NAME (a NO synthase inhibitor) In the treatment of refractory Cardiogenic Shock: A prospective randomized study
Eur. Heart J., July 2, 2003; 24(14): 1287 - 1295.
[Abstract] [Full Text] [PDF]


Home page
J. Thorac. Cardiovasc. Surg.Home page
M. K. Karunanithi, J. Michniewicz, J. A. Young, and M. P. Feneley
Effect of acutely increased left ventricular afterload on work output from the right ventricle in conscious dogs
J. Thorac. Cardiovasc. Surg., January 1, 2001; 121(1): 0116 - 124.
[Abstract] [Full Text] [PDF]


Home page
Circ. Res.Home page
F. Lin, W. A. Owens, S. Chen, M. E. Stevens, S. Kesteven, J. F. Arthur, E. A. Woodcock, M. P. Feneley, and R. M. Graham
Targeted {alpha}1A-Adrenergic Receptor Overexpression Induces Enhanced Cardiac Contractility but not Hypertrophy
Circ. Res., August 17, 2001; 89(4): 343 - 350.
[Abstract] [Full Text] [PDF]