Abstract

1. The first intravenous injection of pitressin in unanesthetized dogs was followed in all of our experiments by a fall in arterial blood pressure (confirmation of Gruber). Similar findings were noted following the intravenous injection of pitressin in dogs under either ether or chloretone anesthesia.

2. The normal blood pressures in twenty-four unanesthetized dogs of various weights and ages were studied. In these a wide variation was noted the lowest being 110 and the highest 230 mm. mercury the average being 154, the normal variation in each animal however being less than 10 mm. above or below the control level.

In a small group of animals with both vagi cut the average was less than that noted in the normal animals. In a still smaller group with the carotid arteries tied off the average blood pressure was higher than the average found in the normal animals.

3. In the unanesthetized dog following the injection of pitressin the heart rate at first decreases during the primary rise in blood pressure, then it accelerates during the drop in blood pressure and decreases again during the secondary prolonged rise in blood pressure. Similar findings were recorded in dogs under either chloretone or ether anesthesia.

4. Neither the injection of atropine nor the cutting of both vagi before the injection of pitressin completely prevents the changes in cardiac rate.

5. In the normal animal the intravenous injection of atropine after the injection of pitressin, increases the rate of heart beat above the control rate.

6. In those dogs in which the vagi were cut, atropine injected intravenously had no effect upon the slowed cardiac rate caused by the injection of pitressin.

7. The acceleration in heart rate which occurs during the fall in blood pressure after the injection of pitressin is mainly if not wholly a reflex compensatory phenomenon. The sudden fall in blood pressure reflexly exciting the cardio accelerator center, is an attempt on the part of the cardio-vascular system to maintain a normal blood pressure.

8. The slowed heart rate caused by the injection of pitressin is partly a reflex due to stimulation of the cardio-inhibitory center through the depressor nerve, and partly due to a direct action upon the heart muscle itself, the latter due probable to injury through vaso-constriction of the coronaries.

9. The secondary rise in blood pressure was higher in our dogs which had received atropine before the injection of pitressin. Likewise it was higher in those in which the vagi had been severed before the injection. We believe this to be due to the fact that the heart rate does not slow as much in these cases following the injection of pitressin as it does in the other experiments.

10. Ligating both carotid arteries did not change the action of pitressin upon either the blood pressure or heart rate.

11. Ligation and excision of both adrenal bodies had no influence on the effect of pitressin upon either the blood pressure or heart rate.

12. Pitressin like whole extract of the posterior lobe of the pituitary when injected intravenously in unanesthetized dogs causes a Cheyne-Stokes type of respiration.