This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Palacios, I. Articles by Powell, W. J. Search for Related Content PubMed PubMed Citation Articles by Palacios, I. Articles by Powell, W. J., Jr

Circulation, Vol 53, 428-436, Copyright © 1976 by American Heart Association

ARTICLES

Left ventricular end-diastolic pressure volume relationships with experimental acute global ischemia

I Palacios, RA Johnson, JB Newell and WJ Powell Jr

The mechanism of elevation of left ventricular end-diastolic pressure during acute global ischemia was evaluated by examiniation of the relative contributions of a decrease in contractility and an alteration of the pressure-volume relationship. The external circumference (mercury-in-silastic gauge) pressure relationship, as an index of the pressure-volume relationship, was studied in beta adrenergic and ganglionic blocked, open chest dogs on right heart bypass at constant heart rate ane aortic pressure. Ischemia of one and two hours' duration was produced by reducing total coronary blood flow in cannulated left and right coronary arteries until left ventricular end-diastolic pressure rose significantly. At a constant stroke work, left ventricular end-diastolic pressure rose from 5.0 +/- 0.5 to 15.0 +/- 0.5 cm H2O in the experiments of one hour of ischemia, and from 7.0 +/- 1.0 to 17.0 +/- 1.0 cm H2O in experiments of two hours of ischemia. Ischemia was followed by one hour of restoration of coronary blood flow. Ischemia produced a marked depression of ventricular function: stroke work, considered at a left ventricular end-diastolic pressure of 15 cm H2O, decreased from 21.0 +/- 3.0 to 3.5 +/- 0.5 gm-m, and from 15.0 +/- 2.0 to 2.5 +/- 0.5 gm-m, in the experiments of one and two hours, respectively. Neither ischemia nor reflow changed the pressure- volume relationship. Thus, the elevation of left ventricular end- diastolic pressure during ischemia in an otherwise normal canine myocardium is due to a decrease in systolic performance of the heart rather than to an alteration of the pressure-volume relationship.

This article has been cited by other articles:

				S. Savonitto, M. G. Cohen, A. Politi, M. P. Hudson, D. F. Kong, Y. Huang, K. S. Pieper, F. Mauri, G. S. Wagner, R. M. Califf, et al. Extent of ST-segment depression and cardiac events in non-ST-segment elevation acute coronary syndromes Eur. Heart J., October 2, 2005; 26(20): 2106 - 2113. [Abstract] [Full Text] [PDF]