Disuse inhibition of newly functional coronary collateral circulation in ponies.
We evaluated the loss of coronary collateral function in the absence of stimulation (disuse inhibition) by doubling the interval between successive left anterior descending coronary artery (LAD) occlusions in ponies in which collateral function initially had been enhanced by 2-min occlusions at 30-min intervals. Before collateralization, occlusion caused segment systolic shortening, velocity of shortening, and stroke work index in the LAD-dependent left ventricular apex to decrease, whereas heart rate and left ventricular end-diastolic pressure increased. After 476 +/- 102 occlusions, segment function recovered to preocclusion levels and hemodynamics were unchanged during occlusion. Occlusion did not elicit sustained functional deterioration until the occlusion interval was greater than or equal to 32 h. During the occlusion after the 128-h interval, segment systolic shortening, velocity of shortening, and stroke work index were reduced 69 +/- 8, 38 +/- 9, and 46 +/- 13%, respectively. Percent recovery of systolic shortening during successive occlusions declined exponentially (T1/e = 102.0 +/- 17.3 h). Thus, in ponies collateral function progressively declines when the occlusion interval is greater than or equal to 32 h, but complete inhibition does not occur even after 128 h without occlusion. This indicates that collateral function in ponies can be maintained by occlusions that are far less frequent than those needed for initial collateral development. The long time constant of collateral disuse inhibition suggests that equine collaterals are quite resistant to the effects of occlusion cessation and differ from canine collaterals in that respect.
Rugh
K S
KS
John M. Dalton Research Center, Department of Physiology, University of Missouri-Columbia 65211.
Ross
C R
CR
Sarazan
R D
RD
Boatwright
R B
RB
Williams
D O
DO
Garner
H E
HE
Griggs
D M
DM
D000818:Animals; D003097:Collateral Circulation; D003326:Coronary Circulation; D003327:Coronary Disease / Q000503:physiopathology*; D006736:Horses / Q000502:physiology*; D009200:Myocardial Contraction; D012008:Recurrence; D013599:Systole; D013997:Time Factors