Circulation, Vol 81, 1644-1653, Copyright © 1990 by American Heart Association
WH Gaasch, MR Zile, PK Hoshino, EO Weinberg, DR Rhodes and CS Apstein
Tolerance of the canine heart to prolonged ischemic arrest was studied in
10 hearts from normal control dogs and 15 hearts from dogs with left
ventricular hypertrophy (LVH); experiments were performed 1 year after
banding the aorta in 8-week-old puppies. At 1 year, hemodynamic studies
revealed decreased left ventricular (LV) fiber shortening and elevated
end-diastolic pressure (EDP) in five dogs (group with LVH failure); 10 dogs
exhibited normal shortening and normal EDP (group with LVH compensation).
The left ventricle-to-body weight ratio (g/kg) was 4.4 +/- 0.8 in the
control group of dogs, 7.7 +/- 1.0 in the group with LVH compensation, and
10 +/- 2.5 in the group with LVH failure. The tolerance to 60 minutes of
global ischemia (37 degrees C) followed by 90 minutes of reperfusion was
studied in an isolated blood-perfused heart apparatus (isovolumic left
ventricle, coronary perfusion pressure of 100 mm Hg). In the baseline
(preischemic) state, coronary blood flow, myocardial oxygen consumption,
lactate extraction, and myocardial high-energy phosphate content were
essentially equal in the three groups; with LV volume adjusted to produce a
systolic pressure of 100 mm Hg, there were no significant differences in
LVEDP among the three groups. During ischemia, the diastolic (asystolic)
pressure increased from 11 +/- 3 to 28 +/- 16 mm Hg (p less than 0.05) in
the group with LVH failure; however, it did not increase in the control or
the LVH compensation groups. Myocardial ATP levels declined equally in all
three groups. During early reperfusion, lactate washout was lowest in the
group with LVH failure. By 90 minutes of reperfusion, there were no
significant differences in coronary blood flow, myocardial oxygen
consumption, lactate extraction, or high-energy phosphate levels. High
diastolic pressure persisted at 90 minutes of reperfusion in the LVH
failure group (EDP was 34 +/- 19 mm Hg); however, there was no significant
change in EDP during reperfusion in the control or with LVH compensation
groups. After 90 minutes of reperfusion, developed pressures in the control
(54 +/- 9 mm Hg), the LVH compensation (49 +/- 18 mm Hg), and the LVH
failure (67 +/- 17 mm Hg) groups were not significantly different. These
data indicate that hearts with compensated LVH do not exhibit an impaired
tolerance to ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)
ARTICLES
Tolerance of the hypertrophic heart to ischemia. Studies in compensated and failing dog hearts with pressure overload hypertrophy
Department of Medicine, Medical Center of Central Massachusetts, Boston.
This article has been cited by other articles:
![]() |
T. Mihaljevic, E. R. Nowicki, J. Rajeswaran, E. H. Blackstone, L. Lagazzi, J. Thomas, B. W. Lytle, and D. M. Cosgrove Survival after valve replacement for aortic stenosis: Implications for decision making. J. Thorac. Cardiovasc. Surg., June 1, 2008; 135(6): 1270 - 1279.e12. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. B. Donnelly Cardiac Valvular Pathology: Comparative Pathology and Animal Models of Acquired Cardiac Valvular Diseases Toxicol Pathol, February 1, 2008; 36(2): 204 - 217. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Barillas, I. Friehs, H. Cao-Danh, J. F. Martinez, and P. J. del Nido Inhibition of Glycogen Synthase Kinase-3{beta} Improves Tolerance to Ischemia in Hypertrophied Hearts Ann. Thorac. Surg., July 1, 2007; 84(1): 126 - 133. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. O. Bonow, B. A. Carabello, K. Chatterjee, A. C. de Leon Jr, D. P. Faxon, M. D. Freed, W. H. Gaasch, B. W. Lytle, R. A. Nishimura, P. T. O'Gara, et al. ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease) Developed in Collaboration With the Society of Cardiovascular Anesthesiologists Endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons J. Am. Coll. Cardiol., August 1, 2006; 48(3): e1 - e148. [Full Text] [PDF] |
||||
![]() |
J. R. B. Dyck and G. D. Lopaschuk AMPK alterations in cardiac physiology and pathology: enemy or ally? J. Physiol., July 1, 2006; 574(1): 95 - 112. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Galinanes and A. G Fowler Role of clinical pathologies in myocardial injury following ischaemia and reperfusion Cardiovasc Res, February 15, 2004; 61(3): 512 - 521. [Abstract] [Full Text] [PDF] |
||||
![]() |
I. Friehs and P. J. del Nido Increased susceptibility of hypertrophied hearts to ischemic injury Ann. Thorac. Surg., February 1, 2003; 75(2): S678 - 684. [Abstract] [Full Text] [PDF] |
||||
![]() |
I. Friehs, C. Stamm, H. Cao-Danh, F. X. McGowan Jr, and P. J. del Nido Insulin-like growth factor-1 improves postischemic recovery in hypertrophied hearts Ann. Thorac. Surg., November 1, 2001; 72(5): 1650 - 1656. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. B. Wambolt, G. D. Lopaschuk, R. W. Brownsey, and M. F. Allard Dichloroacetate improves postischemic function of hypertrophied rat hearts J. Am. Coll. Cardiol., October 1, 2000; 36(4): 1378 - 1385. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Yokoyama, S. Gunasegaram, S. E. Harding, and M. Avkiran Sarcolemmal Na+/H+ exchanger activity and expression in human ventricular myocardium J. Am. Coll. Cardiol., August 1, 2000; 36(2): 534 - 540. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. W. Saupe, C. C. Lim, J. S. Ingwall, C. S. Apstein, and F. R. Eberli Comparison of Hearts With 2 Types of Pressure-Overload Left Ventricular Hypertrophy Hypertension, May 1, 2000; 35(5): 1167 - 1172. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. M. Hoffmeister, M. Strobele, M. E Beyer, S. Kazmaier, M. Fischer, A. Bassler, and L. Seipel Inotropic response of stunned hypertrophied myocardium: responsiveness of hypertrophied and normal postischemic isolated rat hearts to calcium and dopamine stimulation Cardiovasc Res, April 1, 1998; 38(1): 149 - 157. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. O. Schonekess, M. F. Allard, S. L. Henning, R. B. Wambolt, and G. D. Lopaschuk Contribution of Glycogen and Exogenous Glucose to Glucose Metabolism During Ischemia in the Hypertrophied Rat Heart Circ. Res., October 19, 1997; 81(4): 540 - 549. [Abstract] [Full Text] |
||||
![]() |
M. F. Allard, S. L. Henning, R. B. Wambolt, S. R. Granleese, D. R. English, and G. D. Lopaschuk Glycogen Metabolism in the Aerobic Hypertrophied Rat Heart Circulation, July 15, 1997; 96(2): 676 - 682. [Abstract] [Full Text] |
||||
![]() |
H. L. Lazar, X. Zhang, S. Rivers, S. Bernard, and R. J. Shemin Limiting Ischemic Myocardial Damage Using Glucose-Insulin-Potassium Solutions Ann. Thorac. Surg., August 1, 1995; 60(2): 411 - 416. [Abstract] [Full Text] |
||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1990 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |