Abstract
It is well known that the infusion of hypertonic saline or hemorrhage causes a release of antidiuretic hormone (ADH) from the neurohypophysis. The quantitative difference between the responses of ADH release to these 2 maneuvers was investigated in dogs. The levels of ADH in plasma after infusion with 10 and 30 % saline (4.0 ml fkg) averaged 22.2 and 19.6 /iU/ml, respectively. On the other hand, ADH levels attained after hemorrhage following saline infusion were much higher than the level after hypertonic saline infusion: 204.0 /uU/ml in the dogs infused with normal saline and 274.8 and 325.7 juU/ml in dogs infused with hypertonic saline. The mechanisms were discussed concerning the attenuated responses to hypertonic saline infusion as compared to hemorrhage. {Endocrinology 88: 1512, 1971) I IS WELL KNOWN that ADH release induced by a reduction in blood volume is extremely massive (1, 2). The present experiments were carried out in order to evaluate the magnitude of ADH release in response to the infusion of hypertonic saline in comparison to that in response to hemorrhage. The results are presented, which show a marked attenuation in ADH release in response to infusion of hypertonic saline as compared with hemorrhage. Materials and Methods Mongrel dogs of both sexes weighing between 7.0 and 15.8 kg were anesthetized with pentobarbital sodium (30 mg/kg body wt) and fixed in a supine position. Cannulae were inserted into both femoral arteries, the right external jugular vein and the right antecubital vein after the general administration of heparin. Ten min after cannulation the saline infusion was started. In the control group 10 dogs were infused with 0.9 % saline at a rate of 4.0 ml/kg body wt in 10 min through the right antecubital vein. In the experiments with hypertonic saline infusion 13 dogs were infused with 10 % saline and the other 10 dogs were infused with 30 % saline by the same maneuver as the control group. Five min after the end of infusion each animal was allowed to bleed freely through Received May 27, 1970. This work was supported in part by Research Grant AM-11278 from the NIH, USPHS. an open cannula inserted into the right femoral artery until the mean arterial blood pressure measured via the left femoral artery fell to 50 mm Hg. For measuring the ADH concentration and osmolality of plasma and the hematocrit value, approximately 40 ml of blood was collected from the right external jugular vein just prior to and 30 sec after the end of hemorrhage. During the collection about the same amount of 0.9% saline was infused through the right antecubital vein in order to minimize the influence of the blood collection upon ADH release. Plasma ADH concentrations were determined by the method of Yoshida et al. (3). Recovery of ADH was examined regularly and it averaged 55% during the period of these experiments. The plasma ADH titers were not corrected according to the recovery rate in this report. Plasma osmolality was measured with an Advanced osmometer and blood pressure was recorded with a strain gauge. Hematocrit values were obtained by means of heparinized microhematocrit tubes. In 22 dogs the degree of plasma dilution induced by the infusion of saline solutions was estimated by the change in the concentration of plasma protein measured with a refractometer. The statistical significance of the observations was evaluated by Student's i-test. Paired analysis was applied for the evaluation of differences in ADH titers in plasma before and after the infusion of hypertonic saline or hemorrhage, while the differences of the ADH titers between the 2 groups were evaluated by unpaired observations. TABLE 1. Effect of infusion of saline solutions and subsequent hemorrhage on the concentration of ADH in jugular vein plasma (mean ±SEM) Solutions No. of experiments ADH concentration (/xU/ml) Before infusion After infusion After hemorrhage Normal saline 10 % saline 30% saline 10 13 10 10.2±3.4 12.9+3.0 12.8+2.6 8.4+1.4 22.2+7.3 19.6±3.4 204.0 ± 60.41 274.8+ 70.8 325.7+112.1
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