title: Equine coronary hemodynamics during brief coronary occlusions at three levels of collateral function.
abstract: Adult-grade ponies were surgically instrumented with a Doppler flow probe and pneumatic cuff occluder on the left anterior descending coronary artery (LAD), sonomicrometry crystals and intraventricular micromanometer in the left ventricle, and catheters in the left atrium, anterior interventricular vein, and, in some animals, the LAD. Conscious-animal studies were begun 2 wk after surgery. Measured variables included regional left ventricular systolic function, end-diastolic wall thickness, oxygen extraction, lactate extraction, and hydrogen ion release. Changes in collateral perfusion were deduced from changes in these variables. Serial data were obtained during a 3-min LAD occlusion before stimulation of collateral function by the intermittent coronary occlusion method and during a 10-min LAD occlusion after 14 +/- 2 and 27 +/- 2 days of stimulation. Hemodynamic interpretation of data was based on a model of the equine coronary circulation consisting of collateral and arteriolar resistances in series. It was concluded that 1) chronic stimulation of collateral function leads to the emergence of a time-dependent reduction in total collateral resistance during acute coronary occlusion; 2) with enhancement of collateral function, the major resistance controlling collateral blood flow shifts from the collateral circulation to the recipient vessel arterioles; and 3) at a certain level of enhanced collateral function, coronary occlusion results in a triphasic blood flow response in collateral-dependent myocardium consisting of early hypoperfusion, transient hyperperfusion, and late autoregulated perfusion. This study demonstrates that chronic stimulation of collateral function is accompanied by specific alterations in coronary hemodynamics during acute coronary occlusion that hasten the recovery of ischemic myocardium.
authors.affiliation: Department of Physiology, University of Missouri, Columbia 65211, USA.
authors.forename: D O
authors.initials: DO
authors.lastname: Williams
authors.forename: R B
authors.initials: RB
authors.lastname: Boatwright
authors.forename: K S
authors.initials: KS
authors.lastname: Rugh
authors.forename: C R
authors.initials: CR
authors.lastname: Ross
authors.forename: R D
authors.initials: RD
authors.lastname: Sarazan
authors.forename: H E
authors.initials: HE
authors.lastname: Garner
authors.forename: D M
authors.initials: DM
authors.lastname: Griggs
mesh_terms: D000818:Animals; D001794:Blood Pressure; D003097:Collateral Circulation; D003326:Coronary Circulation; D003327:Coronary Disease / Q000503:physiopathology*; D006321:Heart / Q000503:physiopathology; D006439:Hemodynamics; D006706:Homeostasis; D006736:Horses; D009206:Myocardium / Q000378:metabolism