Beneficial effects of vasopressors on right ventricular function in experimental acute right ventricular failure in a rabbit model.
BACKGROUND
An acute increase in right ventricular (RV) afterload leads to RV dilation, reduced systolic function, and low cardiac output. It has previously been shown, experimentally, that an additional increase of left ventricular afterload by aortic constriction can reverse some of these changes. We studied the clinically more relevant effects of intravenous vasopressors on this phenomenon in an animal model.


METHODS
Acute RV failure was induced by pulmonary artery constriction in adult New Zealand white rabbits. We then assessed the effect of aortic constriction on the functional performance of the failing RV using conductance catheters. We compared the impact of aortic constriction on RV contractility with the effects of 0.05, 0.1, 0.5, and 1 mcg/kg × min(-1) norepinephrine and epinephrine.


RESULTS
Aortic constriction lead to increased RV end-systolic pressure-volume relation (RVESPVR 3.2 (±0.6) versus 5.2 (±0.7) mm Hg/mL (p = 0.0002). Cardiac output (131 (±23.7) versus 134.8 (±32.5) mL/min), and heart rate remained unchanged. Administration of norepinephrine and epinephrine lead to similar effects on RV contractility with the maximum increase in RVESPVR observed with 0.5 mcg/kg × min(-1) norepinephrine (RVESPVR 4.8 (±0.4) mm Hg/mL, p = 0.007). However, in contrast to aortic constriction, cardiac output also markedly increased during vasopressor therapy, the most significant effect seen with 1 mcg/kg × min(-1) epinephrine (214.8 (±46.8) mL/min, p = 0.04).


CONCLUSIONS
Aortic constriction improves RV contractility but not cardiac output in acute right heart failure. A comparable effect on RV functional performance with increased cardiac output was achieved by administration of systemic vasopressors. These data may have implications for management of clinical right heart failure.
Pediatric Heart Centre, University Childrens Hospital, Giessen, Germany.
Christian
C
Apitz
Osami
O
Honjo
Mark K
MK
Friedberg
Renato S
RS
Assad
Glen
G
Van Arsdell
Tilman
T
Humpl
Andrew N
AN
Redington
D000208:Acute Disease; D000818:Animals; D001011:Aorta / Q000503:physiopathology / Q000601:surgery; D002302:Cardiac Output / Q000187:drug effects; D004195:Disease Models, Animal; D004837:Epinephrine / Q000008:administration & dosage / Q000494:pharmacology*; D006333:Heart Failure / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D007262:Infusions, Intravenous; D008026:Ligation; D009200:Myocardial Contraction / Q000187:drug effects; D009638:Norepinephrine / Q000008:administration & dosage / Q000494:pharmacology*; D011651:Pulmonary Artery / Q000601:surgery; D011817:Rabbits; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000008:administration & dosage / Q000494:pharmacology*; D018497:Ventricular Dysfunction, Right / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D016278:Ventricular Function, Right / Q000187:drug effects*
D014662:Vasoconstrictor Agents; D009638:Norepinephrine; D004837:Epinephrine