ADENOSINE-RECRUITABLE FLOW RESERVE IS ABSENT DURING MYOCARDIAL-ISCHEMIA IN UNANESTHETIZED DOGS STUDIED IN THE BASAL STATE

We conducted the present study to determine if pharmacologically recru itable flow reserve was present during ischemia in unanesthetized dogs studied in the absence of adrenergic activation. Microsphere measurem ents of regional perfusion at reduced coronary pressures in a distal c ircumflex region subjected to intracoronary adenosine infusion (0.265 mg/min IC) were compared with measurements in a proximal circumflex re gion where pressure was reduced but flow was being autoregulated norma lly. Ischemia began when coronary pressure was reduced below 40 mm Hg. At a coronary pressure of 28+/-1 (mean+/-SEM) mmHg, subendocardial fl ow with autoregulation intact was 0.59+/-0.05 mL . min . g(-1) and sim ilar to that in the region receiving adenosine, which averaged 0.61+/- 0.05 mL . min(-1). g(-1) (P=NS). Although adenosine increased subepica rdial flow from 0.81+/-0.05 to 1.16+/-0.09 mL . min(-1). g(-1) (P<.001 ), the magnitude of the increase was minimal when coronary pressure fe ll to a level that caused subepicardial flow during autoregulation to be reduced below resting values. These results demonstrate that the su bstantially lower autoregulatory break point found in unanesthetized d ogs studied in the basal state reflects the ability of intrinsic autor egulatory mechanisms to match local vasodilator reserve to that recrui table pharmacologically. This contrasts with the presence of pharmacol ogically recruitable subendocardial flow reserve in anesthetized anima ls and is most likely related to a low level of circulating catecholam ines and lack of sympathetic activation in unanesthetized animals stud ied under basal conditions.