We determined regional myocardial blood flow (MBF: 15 μm tracer microspheres) and hemodynamics in 12 unanesthetized normal calves and 10 unanesthetized calves with severe right ventricular hypertrophy (RVH). RVH was produced by banding the main pulmonary artery of 24- to 48-hour-old calves 25-30 weeks prior to the study. Measurements were made in six normal calves and seven calves with RVH at control (baseline), during isoproterenol infusion (0.2 μg/kg per min), and during acute volume overload produced before and after propranolol pretreatment. In six normal calves and three RVH calves, these parameters also were determined before and during maximal coronary vasodilation produced by intraventricular infusion of adenosine (4 μM/kg per min). In this model of RVH, right ventricular (RV) MBF was significantly increased whereas the left ventricular (LV) mass and LV MBF were normal. Minimal coronary vascular resistance per unit weight of the hypertrophied RV was identical to that in the normal RV myocardium. This suggested that, although functional cross-sectional area of the vascular bed supplying RV myocardium, hypertrophied from soon after birth, kept pace with increasing muscle mass, higher baseline perfusion in the hypertrophied RV myocardium occurred at the expense of decreased available coronary vascular reserve. Isoproterenol infusion resulted in subendocardial underperfusion in both ventricles of calves with RVH, but this did not occur in the normal RV myocardium. Acute volume expansion of a similar magnitude was perceived as a more severe stress in calves with RVH as reflected by a larger increase in their RV and LV MBF. Propranolol pretreatment significantly blunted these increments in MBF despite markedly higher ventricular filling pressures. Throughout the study, blood flow in right and left sides of the interventricular septum closely resembled that in RV and LV, respectively.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine