Hypoxia-induced vasodilation in the right coronary circulation of conscious dogs: role of adrenergic activation.
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 N(2). Percent O(2) in the chamber was monitored, and blood samples and hemodynamic data were collected as chamber O(2) was progressively reduced to approximately 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 PO(2) 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/dt(max). After adrenergic blockade, normoxic aortic pressure was reduced; heart rate and RV dP/dt(max) tended to be lower. Aortic pressure rose during hypoxia, but to lesser values than before blockade. Heart rate and RV dP/dt(max) 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 O(2) 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.
Department of Integrative Physiology, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, Texas 76107, USA.
Srinath
S
Setty
Pu
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Zong
Wei
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Sun
Johnathan D
JD
Tune
H Fred
HF
Downey
D018674:Adrenergic Antagonists / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002395:Catecholamines / Q000378:metabolism*; D003243:Consciousness / Q000502:physiology; D003331:Coronary Vessels / Q000187:drug effects / Q000294:innervation* / Q000502:physiology*; D004285:Dogs; D004837:Epinephrine / Q000378:metabolism; D005260:Female; D007839:Functional Laterality / Q000502:physiology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D009638:Norepinephrine / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects / Q000502:physiology; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects / Q000378:metabolism; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology*; D017779:Sympathetic Fibers, Postganglionic / Q000187:drug effects / Q000378:metabolism*; D014160:Transducers, Pressure; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*
D018674:Adrenergic Antagonists; D002395:Catecholamines; D011942:Receptors, Adrenergic, alpha; D009638:Norepinephrine; D004837:Epinephrine