Experiments were carried out to investigate the effect of intracerebroventricular administration of a prostaglandin synthesis inhibitor on the osmotic control of vasopressin (ADH) secretion. During ventriculocisternal perfusion with indomethacin (7.6 μg/min) or vehicle, dogs were infused intravenously with either 2.5 or 0.15 M NaCl. Hypertonic saline infusion elevated plasma osmolality approximately 60 mosm/kg H2O. In accordance, the plasma ADH concentration increased substantially in animals perfused ventriculocisternally with the vehicle (from 2.1 ± 0.7 to 7.3 ± 1.3 μU/ml); this response was markedly attenuated, however, in animals perfused with indomethacin (from 1.0 ± 0.2 to 2.2 ± 0.4 μU/ml). Isotonic saline infusion caused a decline in plasma ADH concentration which was similar in the indomethacin- and vehicle-perfused groups. Mean arterial blood pressure was unchanged during the experiments. In a companion study, ventriculocisternal perfusion with 152 ng PGE2/min was found to be as effective in stimulating ADH release in the presence of indomethacin as in its absence, indicating that the action of indomethacin in the first study was not nonspecific. The suppression of osmotically induced ADH release by intracerebroventricular indomethacin suggests that endogenous brain prostaglandins play a critical intermediary role in the osmotic control of ADH secretion.

Objective-To evaluate a new cross sectional echocardiographic method for estimating the volume of pericardial effusions.Design-The volume of pericardial fluid removed by surgical drainage or paracentesis was compared with the volume estimated by the echocardiographic method. The pericardial sac volume and cardiac volume were calculated by applying the formula for the volume of a prolate ellipse (i x 4/3 x L/2 x D1/2 x D2/2) where L is the major axis and Dl and D2 are the minor axes. The pericardial fluid volume was calculated as the pericardial sac volume minus the cardiac volume.Patients-13 patients with 14 large pericardial effusions (one recurrence) all of whom had tamponade and cross sectional echocardiography just before therapeutic full drainage of the effusion.Results-The volumes of pericardial fluid drained ranged from 05 to 2-1 1. The correlation between these actual volumes and the volumes estimated by echocardiography was excellent (r = 097); the correlation was good in four patients with intrapericardial adhesions.Conclusions-Because of certain approximations in measuring quantity of pericardial fluid drained, the echocardiographic estimations cannot be claimed to be definite. The data, however, indicate that the echocardiographic method is sufficiently reliable to provide useful estimates for practical clinical purposes.

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Experiments were carried out to determine the effect of intracerebroventricular (icv) administration of the angiotensin-converting enzyme inhibitor, captopril, on osmotically stimulated vasopressin secretion. During icv infusion of captopril (3.1 μg/kg·min), dogs were infused intravenously (iv) with either 2.5 or 0.15 MNaCl. Control groups received an osmotically equivalent mannitol solution icv with the 2.5 or 0.15 M NaCl iv infusion. As a result of the iv hypertonic saline infusion, plasma vasopressin concentrations increased progressively and in concert with the plasma osmolality; this response was not altered by icv captopril. Plasma vasopressin levels were unchanged during iv isotonic saline infusion, and, again, icv captopril was without effect. At the completion of the icv infusions, injection of angiotensin I icv (310 ng/kg) produced a markedly greater increase in plasma vasopressin levels in animals which had received mannitol icv, compared to those which had received captopril icv. On the basis of these findings, a role for an intrinsic brain renin-angiotensin system, if such a system exists, in the osmotic control of vasopressin secretion is seriously questioned, but not ruled out.

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