Increased susceptibility to mucosal damage is a prominent feature of portal hypertensive gastropathy. Since the portal hypertensive gastric mucosa has extensive microvascular changes, we postulated that the increased sensitivity to mucosal damage could have an ischemic basis. We measured distribution of gastric serosal and mucosal oxygenation in a group of portal hypertensive and sham-operated rats, and then studied the effects of intragastric aspirin. In the basal state, gastric mucosa of portal hypertensive rats had significantly reduced oxygenation compared to controls (24 +/- 5 vs 45 +/- 7 mm Hg PO2, P less than 0.02), while serosal oxygenation was similar between the two groups. Intragastric aspirin produced significantly greater mucosal damage to portal hypertensive rats and mucosal oxygenation was almost one third that of sham-operated controls. Systemic arterial pressures and oxygenation were similar between the two groups. We conclude that there is impairment of gastric mucosal oxygenation and increased mucosal damage by aspirin in portal hypertensive rats compared with sham-operated controls. These results support our hypothesis that the increased sensitivity of the portal hypertensive mucosa to damage is a consequence of impaired mucosal oxygenation.
Thirty-four episodes of pneumococcal bacteremia were identified in 15 patients over 5 years in 10 hospitals in Franklin County, Ohio. Twelve patients each had 2 episodes of pneumococcal bacteremia, 2 had 3, and 1 had 4. All patients had predisposing conditions, with lymphoma, multiple myeloma, and chronic obstructive pulmonary disease being the most frequent. The mean interval between the first and second episode was 268 days. Serotyping and genotyping were performed on 29 isolates. The same serotypic and genotypic patterns were found for sequential isolates from four patients; three of these patients had a recurrence between 22 and 90 days after a previous episode. Seven (24%) of the 29 isolates were serotype 23F; four isolates (14%) were not susceptible to penicillin. All of our patients received appropriate antimicrobial therapy and appeared to be clinically cured of their initial infection. For patients with recurrent pneumococcal disease, alternate preventive measures such as immunization with conjugate pneumococcal vaccine and/or prophylactic antibiotic therapy should be considered.
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