The oxygen wasting effect of isoproterenol is altered by chemical denervation and cardiac hypertrophy.
We tested the hypothesis that isoproterenol would increase myocardial work and O2 consumption at reduced efficiency and that both left ventricular hypertrophy and chemical sympathectomy would lead to changes in this myocardial efficiency response. Left ventricular hypertrophy was produced by aortic valve plication in 23 puppies. Six months later, sympathetic denervation (6-hydroxydopamine) was produced in 12 hypertrophied and 10 non-hypertrophied dogs, 5 days prior to acute experiments. Ten non-hypertrophied and 11 hypertrophied animals were not denervated. Measurements were made before and during an isoproterenol infusion (0.5 microgram/kg/ min). Regional myocardial work was calculated as the integrated product of force (miniature transducer) and segment shortening (ultrasonic crystals). Regional O2 consumption was calculated from regional blood flow (microspheres) and regional O2 saturations (microspectrophotometry). In all groups, regional O2 consumption increased with isoproterenol (non-hypertrophied, non-sympathectomized 6.5 +/- 0.8 to 20.3 +/- 5 ml O2/min/100 g, non-hypertrophied, sympathectomized 5.0 +/- 0.7 to 10.0 +/- 1.5, hypertrophied, non-sympathectomized 9.8 +/- 1.3 to 16.2 +/- 2.2, hypertrophied, sympathectomized 6.1 +/- 0.5 to 13.3 +/- 1.6). Regional segment work also increased in all groups with isoproterenol stimulation (non-hypertrophied, non-sympathectomized 781 +/- 73 to 1197 +/- 61 g.mm/min, non-hypertrophied, sympathectomized 996 +/- 221 to 2118 +/- 412, hypertrophied, non-sympathectomized 1031 +/- 145 to 3262 +/- 753, hypertrophied, sympathectomized 721 +/- 116 to 1745 +/- 402). In the non-hypertrophied, non-sympathectomized group, efficiency (work/O2 consumption) was significantly decreased from 122 +/- 17 to 76 +/- 9 g.mm/ml O2/100 g demonstrating an "oxygen wasting" effect. In the hypertrophied, non-sympathectomized group, segment efficiency significantly increased from 94 +/- 19 to 250 +/- 63. In both sympathectomized groups, efficiency was not altered by isoproterenol. Thus the oxygen wasting effect of beta-adrenergic stimulation was reversed by left ventricular hypertrophy and blocked by sympathectomy.
Scholz
P M
PM
UMDNJ-Robert Wood Johnson Medical School, Heart and Brain Circulation Laboratory, Piscataway, New Jersey 08854-5635, USA.
Kedem
J
J
Cheinberg
B V
BV
Weiss
H R
HR
D000818:Animals; D004285:Dogs; D006321:Heart / Q000187:drug effects / Q000294:innervation / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology / Q000662:veterinary*; D007545:Isoproterenol / Q000494:pharmacology*; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology; D016627:Oxidopamine; D010100:Oxygen / Q000378:metabolism*; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D013562:Sympathectomy; D013564:Sympathetic Nervous System / Q000503:physiopathology
D016627:Oxidopamine; D007545:Isoproterenol; D010100:Oxygen