Effects of isoproterenol-induced tachycardia on myocardial blood flow and glycogen in the fetal lamb.

In utero tachycardia is a cause of fetal congestive heart failure and fetal hydrops. We investigated the effects of isoproterenol-induced tachycardia (IIT) on cardiac output and its distribution, on myocardial blood flow and intramyocardial blood flow distribution as well as on regional myocardial glycogen in 8 chronically prepared, near-term fetal lambs and 3 control twins (for myocardial glycogen only). Blood flows were measured by the radioactive microsphere method, myocardial glycogen by an enzymatic method. In animals with IIT (heart rate 200-280), cardiac output (excluding lung flow) increased from 0.399 to 0.544 ml/g/tissue/min (+36%), blood flow to the carcass increased from 0.19 to 0.32 ml/g/tissue/min (+68%) and myocardium increased from 2.31 to 7.72 ml/g/tissue/min (+234%), while kidney blood flow decreased from 1.34 to 0.72 ml/g/tissue/min (-46%). The normal intramyocardial blood flow distribution and predominance of flow to the endocardium of both ventricles was preserved during IIT. In the three sets of twins, glycogen was lower in the right (RV) and left (LV) ventricular walls of each animal stressed by IIT (mean RV = 0.19, mean LV = 0.44) than of its unstressed twin (mean RV = 0.75, mean LV = 0.70). Furthermore, a metabolic acidemia (mean pH 7.21, mean BE -8.4) developed in the stressed animals. Although we were unable to demonstrate regional myocardial ischemia at the maximal fetal heart rates achieved by isoproterenol infusion, our data suggest that metabolic acidemia and myocardial glycogen depletion are consequences of severe inotropic and chronotropic stress in the fetal lamb.