The effect of parathyroid hormone on the acutely ischemic myocardium

Parathyroid hormone (PTH) is reported to be a potent vasodilator. To determine if this action is beneficial in acute myocardial infarction (AMI) and is due to changes in prostacyclin or thomboxane, thirty dogs were anesthetized and instrumented (left atrial, coronary sinus, left main coronary, pulmonary artery and femoral artery catheters). AMI was induced by ligating the left anterior descending coronary artery. Either pentobarbital or alpha chloralose anesthesia was randomly assigned. Following LAD ligation, animals were randomized to receive PTH 0.008 nm/kg over 10 minutes every 30 minutes during the ischemic period or an equal volume of saline. Cardiac index, regional myocardial blood flow, O2 consumption and lactate production were measured. Infarct size was determined by computerized planimetry. PTH bioactivity was verified by adenyalate cyclase stimulating activity in rat osteosarcoma cells. Myocardial blood flow ranged from 81.5 to 155.2 ml/min/kg for normal myocardium. Cardiac index, O2 consumption, lactate production and myocardial perfusion was unaltered by the PTH administration. PTH reduced infarct size in dogs receiving pentobarbital but was deleterious in those receiving alpha chloralose. There was no difference in prostacyclin and thromboxane levels among groups.

PTH is not beneficial in acute myocardial infarction.