Different response of oxygen consumption and cardiac output to various endogenous and synthetic catecholamines in awake dogs.
OBJECTIVE
To determine whether catecholamines with different adrenergic receptor affinities are characterized by individual relationships between cardiac output (Q) and oxygen consumption (VO2).


METHODS
Comparison of the dose-effect relationships and Q/VO2 relationships of four different catecholamines in the same awake dogs.


METHODS
University research department of experimental anesthesiology.


METHODS
Ten trained, healthy dogs in the basal metabolic state with chronically implanted ultrasonic flow transducers around the pulmonary artery for the continuous measurement of cardiac output.


METHODS
Increasing doses of norepinephrine, epinephrine, dobutamine, or dopexamine were infused in a randomly varied sequence on separate days until VO2 and Q reached a maximum.


RESULTS
VO2 was measured by indirect calorimetry, and Q was measured via the pulmonary artery by ultrasonic flowmetry. In healthy dogs, catecholamines increased both VO2 and Q in a dose-dependent manner until a plateau was reached when VO2 had doubled and Q had quadrupled compared with baseline conditions. Regardless of the catecholamine, the resulting Q/VO2 relationships were linear up to the maximal effects, but their slopes (s) differed significantly between agents (p < .05, paired sign test) and increased approximately three-fold in the order norepinephrine (s = 34), epinephrine (s = 54), dobutamine (s = 86), and dopexamine (s = 105). Except for norepinephrine, the catecholamines also increased oxygen delivery more than VO2, so that O2 extraction decreased to 40% below baseline.


CONCLUSIONS
Catecholamines are characterized by linear Q/VO2 relationships with drug-specific slopes. All agents (except norepinephrine) increased oxygen delivery more than oxygen demand. For the practice of catecholamine therapy, our experiments imply that synthetic agents such as dobutamine and particularly dopexamine may be preferred in the treatment of low cardiac output states because they increase Q with the least metabolic effects.
Scheeren
T W
TW
Department of Experimental Anesthesiology, Heinrich-Heine University of Düsseldorf, Germany.
Arndt
J O
JO
D000322:Adrenergic Agonists / Q000494:pharmacology*; D000818:Animals; D001481:Basal Metabolism; D001783:Blood Flow Velocity / Q000187:drug effects; D002153:Calorimetry, Indirect; D002302:Cardiac Output / Q000187:drug effects*; D002316:Cardiotonic Agents / Q000494:pharmacology*; D002395:Catecholamines / Q000494:pharmacology* / Q000502:physiology*; D002407:Catheterization, Swan-Ganz; D004280:Dobutamine / Q000494:pharmacology*; D004285:Dogs; D004298:Dopamine / Q000031:analogs & derivatives* / Q000494:pharmacology* / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D004353:Drug Evaluation, Preclinical; D004837:Epinephrine / Q000494:pharmacology* / Q000502:physiology*; D005260:Female; D016014:Linear Models; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology* / Q000502:physiology*; D010101:Oxygen Consumption / Q000187:drug effects*; D011897:Random Allocation; D011941:Receptors, Adrenergic / Q000187:drug effects; D012212:Rheology; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000494:pharmacology*; D014665:Vasodilator Agents / Q000494:pharmacology*; D014851:Wakefulness / Q000502:physiology
D000322:Adrenergic Agonists; D002316:Cardiotonic Agents; D002395:Catecholamines; D011941:Receptors, Adrenergic; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; C046318:dopexamine; D004280:Dobutamine; D004298:Dopamine; D009638:Norepinephrine; D004837:Epinephrine