Vitamin C augments the inotropic response to dobutamine in humans with normal left ventricular function

Authors
Citation
S. Mak et Ge. Newton, Vitamin C augments the inotropic response to dobutamine in humans with normal left ventricular function, CIRCULATION, 103(6), 2001, pp. 826-830
Citations number
35
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CIRCULATION
ISSN journal
00097322 → ACNP
Volume
103
Issue
6
Year of publication
2001
Pages
826 - 830
Database
ISI
SICI code
0009-7322(20010213)103:6<826:VCATIR>2.0.ZU;2-M
Abstract
Background-We studied the effect of an antioxidant, the intracoronary infus ion of vitamin C, on basal and dobutamine-stimulated left ventricular (LV) contractility. Methods and Results-Nineteen patients with normal ventricular function part icipated in this study. A micromanometer-tipped catheter was inserted into the LV. In the experimental group (n=10), an infusion catheter was position ed in the left main coronary artery. LV peak +dP/dt (LV +dP/dt) was measure d in response to the intravenous infusion of dobutamine before (Dob) and du ring (Dob+vit C) the intracoronary infusion of vitamin C, The intracoronary infusion of vitamin C had no effect on basal LV +dP/dt or any other hemody namic parameter. The infusion of vitamin C augmented the LV +dP/dt response to dobutamine by 22+/-4% (Dob, 1680+/-76 mm Hg/s; Dob+vit C, 1814+/-97 mm Hg/s, P<0.01). In the control group (n=9), LV +dP/dt was measured in respon se to sequential infusions of dobutamine (Dob, Dob-2) given at the same tim e intervals as in the experimental group but without the intracoronary infu sion of vitamin C. In contrast to the experimental group, no difference in LV +dP/dt was observed between the 2 infusions of dobutamine (Dob, 1706+/-1 31 mm Hg/s; Dob-2, 1709+/-138 mm Hg/s, P=NS). Conclusions-The administration of the antioxidant vitamin C augments the in otropic response to dobutamine in humans. This suggests that redox environm ent contributes to the adrenergic regulation of ventricular contractility.