Parathyroid hormone reduces acute ischemic injury of the myocardium

Synthetic parathyroid hormone (PTH), particularly the molecular fragment containing amino acids one to 34 (1-34), has been shown to produce coronary vasodilation and systemic vasodilation without tachycardia. On this basis, we tested the hypothesis that PTH(1-34) would favorably affect oxygen balance in acutely ischemic myocardium and reduce the extent of injury after coronary occlusion. Experiments were done upon the left anterior descending coronary artery which was ligated through a thoracotomy in anesthetized dogs subjected to ligation of the left anterior descending coronary artery. After 30 minutes of ischemia, the dogs were randomly assigned to either a group which received an intracoronary infusion of 0.008 nanomoles per kilogram of body weight per minute of PTH (1-34) for ten minutes at intervals of 30 minutes or a control group which received intracoronary saline solution. PTH(1-34) increased circumflex artery blood flow 290 +/- 62 per cent (p less than 0.005) and coronary venous return from the ischemic area 190 +/- 12 per cent (p less than 0.005) while reducing mean arterial pressure 12.5 +/- 1.7 per cent (p less than 0.05) without a change in the heart rate. These hemodynamic changes resulted in a 54.3 +/- 3.7 per cent (p less than 0.005) decrease in ischemic myocardial oxygen extraction and a reduction of infarct size (25 +/- 5 per cent of myocardium at risk in treated versus 75 +/- 10 per cent in the control group). It is concluded that PTH given after coronary artery occlusion increases collateral blood flow and oxygen supply to the ischemic myocardium while reducing oxygen requirements. Thus, PTH may offer significant protection for the acutely ischemic myocardium.