J.A. Solís-Herruzo

Effect of intrathoracic pressure on plasma arginine vasopressin levels

Abdominal distention during pneumoperitoneum results in a marked increase in plasma arginine vasopressin levels, which has been ascribed to an increase in intrathoracic pressure. Because of this relationship, tense ascites could contribute to nonosmotic release of antidiuretic hormone, to the development of hyponatremia, and eventually to further ascites formation. The effect of pneumoperitoneum, thoracocentesis, and paracentesis on plasma arginine vasopressin levels was studied in three groups of patients, and the mechanism by which these maneuvers may induce these changes was investigated. Patients with pleural effusion, pneumothorax, or ascites showed a significant increase in plasma arginine vasopressin levels, and thoracocentesis or paracentesis resulted in a decrease in these levels. Plasma vasopressin levels increased significantly during pneumoperitoneum, as did intrathoracic and atrial pressures; the atrial transmural pressure gradient declined. However, no changes in plasma levels of norepinephrine, aldosterone, and renin activity were observed during pneumoperitoneum. Changes in plasma arginine vasopressin levels correlated with the changes in intrathoracic and atrial pressures and transmural pressure gradient. The authors conclude that increased intrathoracic pressure is associated with an increase in plasma arginine vasopressin levels and propose that ascites could be a factor promoting vasopressin release by acting on intrathoracic volume receptors in decompensated cirrhotics.

Antidiuretic Hormone and Renal Function after Water Loading in Patients with Cirrhosis of the Liver

Renal function and plasma antidiuretic hormone (ADH) levels were studied basally and after oral water load in four groups of subjects: 15 healthy controls (group I), 15 cirrhotics without ascites (group II), 15 cirrhotics with ascites (group III), and 10 decompensated cirrhotics with hyponatremia (group IV). Renal function and ADH levels were normal in group II. In groups III and IV water diuresis and fractional proximal sodium excretion were significantly decreased, whereas fractional distal sodium resorption and fractional excretion of potassium did not differ from those of controls. Basal ADH was significantly increased only in patients of group IV. In these patients ADH remained abnormally high after water loading. ADH did not correlate with water diuresis, plasma osmolality, mean arterial pressure, and plasma renin activity. We conclude that impaired water excretion in decompensated cirrhotics without hyponatremia cannot be ascribed to high serum levels of ADH. On the contrary, it seems to be related mainly to a reduced delivery of filtrate to the diluting segment of the nephron. In cirrhotic patients with hyponatremia high levels of ADH may play an additional role.

Rhabdomyolysis and cutaneous necrosis following intravenous vasopressin infusion

A continuous IV infusion of vasopressin was administrated to a patient with cirrhosis of the liver and acute gastrointestinal bleeding from esophageal varices. In the first 24 hours, the patient developed rhabdomyolysis and cutaneous necrosis. Stopping vasopressin infusion resulted in relief of these lesions. The rarity of these complications suggests an idiosyncratic reaction of susceptible individuals that may be related to previous vascular disease or a failure in baroreceptor regulation.

Plasma arginine vasopressin response to oral, gastric, and intravenous water load in patients with cirrhosis

BACKGROUND/AIMS Hepatic osmoreceptors are sensitive to changes in portal blood osmolality and cause variations in plasma antidiuretic hormone and water diuresis, which prevent major systemic osmotic changes. Insensitivity of hepatic osmoreceptors might contribute to maintaining increased plasma levels of antidiuretic hormone and negative free water clearance after oral hydration in some cirrhotic patients. METHODS We measured free water clearance and plasma arginine vasopressin levels in basal conditions and after oral, intravenous, and intragastric water overload in control subjects (group I) and patients with cirrhosis (some with a positive [group II] and some a negative [group III] free water clearance). RESULTS In groups I and II, no significant differences in plasma arginine vasopressin levels were found regardless of the route used for hydration. In group III, plasma levels were significantly higher between 0 and 75 minutes after intragastric hydration than after oral or intravenous hydration. No significant changes in plasma osmolality were detected between minute 0 and 20 after the end of oral or intragastric hydration, although plasma arginine vasopressin decreased significantly only 5 minutes after the oral hydration. Group III patients showed evidence of autonomic neuropathy. However, this dysfunction was unrelated to the insensitivity to gastric hydration. CONCLUSIONS Hepatic osmoreceptors seem to be disturbed in some cirrhotic patients, although this dysfunction may be compensated for by normally functioning oropharyngeal and hypothalamic osmoreceptors.