Release of Antidiuretic Hormone from Neurohypophysis in Response to Hemorrhage and Infusion of Hypertonic Saline in Dogs

Abstract

Plasma hypertonicity and hemorrhage cause release of antidiuretic hormone (ADH) from neurohypophysis. In order to elucidate the location of the pathways through which osmotic and hemorrhagic stimuli influence the neurohypophysis, hypertonic saline in-fusion and hemorrhage experiments were performed in dogs.
Mongrel dogs of both sexes were used and the following seven groups of dogs were prepared.
(1) Intact dogs : Experiments were performed under anesthesia with pentobarbital sodium.
(2) Decorticated dogs : After craniotomy the telencephalon was removed by suction.
(3) Decerebrated dogs : The transection of the midbrain was performed at the level of colliculus superior by suction.
(4) Dogs with diencephalic islands : The telencephalon was removed and the transection of the midbrain was performed by suction.
(5) Dogs with spinal cord sectioned : The spinal cord was sectioned at the level of C-1 by suction.
(6) Dogs with cervical vagus nerves sectioned : The bilateral cervical vagus nerves were sectioned a few centimeters cephalad to the caudal cervical ganglion.
(7) Dogs with abdominal vagus nerves sectioned : The abdominal vagus nerves (i.e. ventral and dorsal gastric nerve) were sectioned.
The experiments on the intact dogs, decorticated dogs and dogs with cervical or abdominal vagus nerves sectioned were performed under pentobarbital sodium anesthesia. The decerebrated dogs, dogs with diencephalic islands and dogs with their spinal cord sectioned were not anesthetised during the experiments.
In hemorrhage experiments each animal was allowed to bleed freely through an open cannula inserted into the femoral artery until the mean arterial blood pressure fell to a level below 50% of the initial value and less than 50 mmHg. The experiments of intravenous infusion of hypertonic saline were performed by infusing 2.5% saline at a speed of 0.25 ml/min/Kg B.W. for 45 minutes. The ADH titers in jugular vein plasma were measured by the method of Yoshida et al before and after the hemorrhage or infusion of saline.
In intact dogs hemorrhage caused a marked increase in plasma ADH titer from 41.4 ±11.0 μU/ml to 360±74.6 μU/ml. Hemorrhage that was performed in the same way as that in the intact dogs caused an increase in plasma ADH level, from 26.9±9.0 μU/ml to 206±60.7 μU/ml in the decorticated dogs and from 28.1±7.5 μU/ml to 476±149 μU/ml in the spinal dogs. These increases are statistically highly significant. In two group of dogs whose midbrains were sectioned, i.e., the decerebrated dogs and the dogs with diencephalic islands, concentration of ADH did not increase significantly following hemorrhage.
The dogs with abdominal vagus nerves sectioned also showed a marked increase in ADH levels in plasma in response to hemorrhage. Significant rises in ADH titers in plasma after hemorrhage were also observed in the dogs with cervical vagus nerves sectioned. However, these responses were markedly attenuated compared with those observed in the dogs with abdominal vagus nerves sectioned.
The intravenous infusion of hypertonic saline in the intact dogs resulted in an increase in plasma ADH titer from 34.4±8.4 μU/ml to 72.2 ±12.3μU/ml. In the dogs with diencephalic islands the concentration of ADH rose from a control level 26.2±3.6 μU/ml concentration of ADH rose from a control level 26.2±3.6 μU/ml to 55.9±12.5, μU/ml after the hypertonic saline infusion. These increases in plasma ADH titers are statistically significant. There was no significant difference in the increment in plasma ADH titers between these two groups of dogs.
These results suggested that isolated diencephalon could release ADH in response to an osmotic stimulus without nervous connection with the adjacent nervous system. On the contrary,