Experimental Coronary Artery Occlusion: Ventricular Fibrillation and Survival as Affected by Selected Drugs and Ionic Alterations

¹ Public Health Research Fellow of the National Heart Institute. The Surgical Experimental Laboratory and the Department of Surgery, University of Mississippi School of Medicine.
² The Surgical Experimental Laboratory and the Department of Surgery, University of Mississippi School of Medicine.

1. The effect of selected drugs and various inorganic ions on ventricular fibrillation and mortality following experimental coronary artery occlusion has been investigated.

2. Control mortality of 80 per cent and early fibrillation of 30 per cent was obtained following ligation of the left anterior descending coronary artery immediately at its origin.

3. When coronary occlusion was delayed for 20 days post-pericardotomy in three animals there was no mortality and two of the three animals failed to demonstrate any change in the pre and postocclusion electrocardiogram.

4. Mortality of 80 per cent and fibrillation of 40 per cent resulted when acidosis was produced by hydrochloric acid.

5. Mortality of 80 per cent and fibrillation of 60 per cent resulted when alkalosis was produced by the infusion of sodium bicarbonate.

6. A mortality rate of 60 per cent and a fibrillation rate of 60 per cent resulted when hyperkaliemia was produced.

7. Hypercalcemia produced a mortality of 80 per cent and fibrillation of 60 per cent.

8. Following the infusion of a relatively small amount of sodium chloride an unexpected 100 per cent mortality and 80 per cent fibrillation rate resulted.

9. A mortality rate of 100 per cent and a fibrillation rate of 100 per cent followed the infusion of procaine.

10. The intravenous administration of papaverine produced mortality and fibrillation rates of 60 per cent.

11. Quinidine administered intravenously yielded a mortality rate of 60 per cent and fibrillation rate of 60 per cent.

12. The influence of infusion of certain ions and drugs upon the concentration of other ions was determined.

13. It would appear from this study that if potassium is the excitatory agent for ventricular fibrillation that myocardial potassium in ischemia is unaffected by the plasma concentration of potassium and is on a metabolic basis.

14. If potassium is the agent inciting ventricular fibrillation it would appear from this study that myocardial metabolism of potassium in myocardial ischemia is unaffected by blood pH insofar as decreasing early fibrillation is concerned.

15. None of the drugs or ions employed in this study showed any beneficial effect on reducing mortality or ventricular fibrillation following coronary artery occlusion.