TY - JOUR
T1 - Hypoxia-induced vasodilation in the right coronary circulation of conscious dogs
T2 - Role of adrenergic activation
AU - Setty, Srinath
AU - Zong, Pu
AU - Sun, Wei
AU - Tune, Johnathan D.
AU - Downey, H. Fred
N1 - Funding Information:
The expert surgical assistance of Jian Bi, M.D. and the expert technical assistance of Arthur G. Williams, Jr., are gratefully acknowledged. This investigation was supported by National Institutes of Health Grant HL-64785.
PY - 2008/2/29
Y1 - 2008/2/29
N2 - The role of adrenergic activation in the right coronary (RC) flow response to hypoxia has not been previously delineated, and limited information from left coronary studies is inconsistent. Seven dogs were instrumented with catheters implanted in the aorta and in the right ventricle to measure aortic pressure and right ventricular (RV) pressure, respectively. A flow transducer was placed around the RC artery to measure RC flow. After recovery from surgery, the dogs were exposed to systemic hypoxia in a Plexiglas chamber ventilated with N2. Percent O2 in the chamber was monitored, and blood samples and hemodynamic data were collected as chamber O2 was progressively reduced to ∼ 6%. The chamber was then opened, and the dog breathed room air. Phentolamine, 1 mg/kg, and propranolol, 2 mg/kg, were then administered via the RV catheter to achieve adrenergic blockade, and the hypoxia protocol was repeated. During hypoxia, arterial PO2 progressively fell from 87 ± 3 to 25 ± 1 mmHg during untreated control condition and from 90 ± 4 to 23 ± 1 mmHg during adrenergic blockade. In the unblocked condition, hypoxia caused increases in aortic pressure, heart rate, RV pressure, and RV dP/dtmax. After adrenergic blockade, normoxic aortic pressure was reduced; heart rate and RV dP/dtmax tended to be lower. Aortic pressure rose during hypoxia, but to lesser values than before blockade. Heart rate and RV dP/dtmax also increased, but only at more severe hypoxia, and these values were less than before blockade. Normoxic flow and hypoxia-induced increases in RC flow and conductance were not altered by blockade. The relationship between RC conductance and RV triple product, an index of RV O2 demand, was steeper after blockade. These findings indicate that in the normal, unblocked condition, RC flow during hypoxia is restrained by an adrenergic-mediated increase in RC vasomotor tone.
AB - The role of adrenergic activation in the right coronary (RC) flow response to hypoxia has not been previously delineated, and limited information from left coronary studies is inconsistent. Seven dogs were instrumented with catheters implanted in the aorta and in the right ventricle to measure aortic pressure and right ventricular (RV) pressure, respectively. A flow transducer was placed around the RC artery to measure RC flow. After recovery from surgery, the dogs were exposed to systemic hypoxia in a Plexiglas chamber ventilated with N2. Percent O2 in the chamber was monitored, and blood samples and hemodynamic data were collected as chamber O2 was progressively reduced to ∼ 6%. The chamber was then opened, and the dog breathed room air. Phentolamine, 1 mg/kg, and propranolol, 2 mg/kg, were then administered via the RV catheter to achieve adrenergic blockade, and the hypoxia protocol was repeated. During hypoxia, arterial PO2 progressively fell from 87 ± 3 to 25 ± 1 mmHg during untreated control condition and from 90 ± 4 to 23 ± 1 mmHg during adrenergic blockade. In the unblocked condition, hypoxia caused increases in aortic pressure, heart rate, RV pressure, and RV dP/dtmax. After adrenergic blockade, normoxic aortic pressure was reduced; heart rate and RV dP/dtmax tended to be lower. Aortic pressure rose during hypoxia, but to lesser values than before blockade. Heart rate and RV dP/dtmax also increased, but only at more severe hypoxia, and these values were less than before blockade. Normoxic flow and hypoxia-induced increases in RC flow and conductance were not altered by blockade. The relationship between RC conductance and RV triple product, an index of RV O2 demand, was steeper after blockade. These findings indicate that in the normal, unblocked condition, RC flow during hypoxia is restrained by an adrenergic-mediated increase in RC vasomotor tone.
KW - Alpha adrenergic blockade
KW - Beta adrenergic blockade
KW - Conscious dogs
KW - Right coronary circulation
KW - Systematic hypoxia
UR - http://www.scopus.com/inward/record.url?scp=38149033580&partnerID=8YFLogxK
U2 - 10.1016/j.autneu.2007.10.004
DO - 10.1016/j.autneu.2007.10.004
M3 - Article
C2 - 18055275
AN - SCOPUS:38149033580
SN - 1566-0702
VL - 138
SP - 76
EP - 82
JO - Autonomic Neuroscience: Basic and Clinical
JF - Autonomic Neuroscience: Basic and Clinical
IS - 1-2
ER -