A series of 45 patients with chylous ascites has been reviewed. The age at presentation ranged from 1 to 80 (median 12) years; 23 patients were aged < or = 15 years. Thirty-five patients had an abnormality of the lymphatics (primary chylous ascites); in the remaining ten, the ascites was secondary to other conditions, principally non-Hodgkin's lymphoma (six patients). Two principal mechanisms of ascites formation were identified using lymphangiography and inspection at laparotomy: leakage from retroperitoneal megalymphatics, usually through a visible lymphoperitoneal fistula (14 patients); and leakage from dilated subserosal lymphatics of the small intestine, invariably associated with leaking lacteals causing protein-losing enteropathy (24 patients). Both sites of leakage were present in a further five patients. In the remaining two patients, chyle was leaking from normal mesenteric lymphatics, in one via a ruptured mesenteric lymph cyst and in the other from the site of a previous lymph node biopsy. Other associated lymphatic abnormalities were present in 36 patients, lymphoedema of the leg being the commonest (26 patients). All patients were initially treated conservatively with dietary manipulation; this was the most satisfactory treatment for those with leaking small bowel lymphatics. Surgery (fistula closure, bowel resection or insertion of a peritoneovenous shunt) was performed in 30 patients. Closure of a retroperitoneal fistula, when present, was the most successful operation, curing seven of the 12 patients so treated.
1. Twenty-seven young subjects used their right hand to perform sustained, isometric contractions at 40% of maximum for 2 min while lying supine. 2. During the last 30 s of exercise, mean arterial blood pressure increased by 38 +/- 4 mmHg (mean +/- S.E.M.) and heart rate by 27 +/- 2 beats/min. 3. Nineteen of the subjects respired eucapnically during exercise, increasing ventilation by 4.1 +/- 0.5 litres/min. Eight subjects hyperventilated (7.1-19.6 litres/min) and decreased end-tidal PCO2 by 8.2 to 15.1 mmHg during the last minute of exercise. 4. In the eucapnic subjects mean flow velocity in the right (i.e. contralateral to the activated cortex) middle cerebral artery increased by 11.4 +/- 1.0 cm/s, a change of 17%, during the contraction. This represents an increase in volume flow to the territory of this vessel, but an increase in global flow to the brain cannot be inferred. 5. In the eight subjects who hyperventilated during exercise, there was no rise of flow velocity in the middle cerebral artery, and in some subjects there was a fall during the first 2 min of recovery. These findings suggest that if subjects hyperventilate during handgrip exercise there could be a fall in volume flow to many regions of the brain during and after the exercise.
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