Angiotensin II does not mediate the pressor response to PGD2 (icv).

The objective of the present studies was to examine the interaction between brain-derived angiotensin II (Ang II) and prostaglandins in order to identify the mechanisms mediating the pressor response produced by these neuroregulators. Inhibiting synthesis of prostaglandins with indomethacin [indocin, 200 microg/ 5 microl artificial cerebrospinal fluid (aCSF)], administered intracerebroventricularly (icv) to conscious adult male Sprague-Dawley rats, reduced blood pressure to values below basal levels. When injected prior to Ang II (50 ng/5 microl aCSF; icv), indomethacin completely abolished the pressor response induced by the octapeptide. The increase in blood pressure produced by prostaglandin D(2) (PGD(2), 20 microg/5 microl; icv), the most prominent prostaglandin in the rat brain, however, was not prevented by losartan (25 microg/5 microl; icv), an Ang II AT(1)-receptor antagonist. Collectively, these results indicate that prostaglandins produced tonically in the brain maintain resting arterial blood pressure and that the pressor action of Ang II is dependent on de novo synthesis of a prostaglandin.

Helicobacter pylori infection among patients with alcoholic and nonalcoholic cirrhosis.

BACKGROUND: The prevalence of Helicobacter pylori in patients with alcoholic and nonalcoholic cirrhosis is uncertain. The present study was aimed at determining the prevalence of H. pylori infection among cirrhotic patients and to explore its relationship to demography, etiology of cirrhosis, and liver function. MATERIALS AND METHODS: Thirty-three cirrhotic patients were included. H. pylori infection was determined by the 14C urea breath test (n = 30) and endoscopy with antral biopsy (n = 4). Etiology of cirrhosis was classified as alcoholic or nonalcoholic. The rate of H. pylori infection was related to age, gender, etiology, Child-Pugh grading, portal hypertension, and portal-systemic encephalopathy (PSE). None of the patients received antibiotics for at least the last 3 months. RESULTS: Twelve alcoholic and 21 nonalcoholic cirrhotics, with a median age of 57 years and a male:female ratio of 1:1.4 were studied. Overall H. pylori prevalence was 45.5%. This prevalence varied from 47.1% to 43.8% in those younger and older than the median age, and from 35.7% to 52.6% in men and women, respectively. Fifty percent of alcoholic and 42.9% of nonalcoholic cirrhotics were H. pylori-positive. According to Child-Pugh grading, 69% of grade A, 40% of grade B, and 0% of grade C were infected (p = .03). Among patients with PSE, 25% were H. pylori-positive compared to 52% of those without PSE (p = .24). CONCLUSIONS: The prevalence of H. pylori infection in cirrhotics is 45.5%. Prevalence was unrelated to age, gender, and etiology of cirrhosis. An inverse relation to the Child-Pugh grading and a tendency to a lower prevalence in PSE was found.