Post-hypoxic hypoperfusion is associated with suppression of cerebral metabolism and increased tissue oxygenation in near-term fetal sheep.

Secondary cerebral hypoperfusion is common following perinatal hypoxia-ischaemia. However, it remains unclear whether this represents a true failure to provide sufficient oxygen and nutrients to tissues, or whether it is simply a consequence of reduced cerebral metabolic demand. We therefore examined the hypothesis that cerebral oxygenation would be reduced during hypoperfusion after severe asphyxia, and further, that the greater neural injury associated with blockade of the adenosine A(1) receptor during the insult would be associated with greater hypoperfusion and deoxygenation. Sixteen near-term fetal sheep received either vehicle or 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) for 1 h, followed by 10 min of severe asphyxia induced by complete occlusion of the umbilical cord. Infusions were discontinued at the end of the occlusion and data were analysed for the following 8 h. A transient, secondary fall in carotid artery blood flow and laser Doppler flow was seen from approximately 1-4 h after occlusion (P < 0.001), with no significant differences between vehicle and DPCPX. Changes in laser Doppler blood flow were highly correlated with carotid blood flow (r(2)= 0.81, P < 0.001). Cortical metabolism was suppressed, reaching a nadir 1 h after occlusion and then resolving. Cortical tissue P(O(2)) was significantly increased at 1, 2 and 3 h after occlusion compared to baseline, and inversely correlated with carotid blood flow (r(2)= 0.69, P < 0.001). In conclusion, contrary to our initial hypothesis, delayed posthypoxic hypoperfusion was associated with suppression of cerebral metabolism and increased tissue P(O(2)), and was not significantly affected by preceding adenosine A1 blockade. These data suggest that posthypoxic hypoperfusion is actively mediated and reflects suppressed cerebral metabolism.

The role of endoscopy in the evaluation of iron deficiency anemia in patients over the age of 50.

OBJECTIVE: To determine the prevalence of various etiologies of iron deficiency anemia in patients over the age of 50 yr in order to better define the role of endoscopy in the evaluation of these patients and to see whether historical features are predictive of subsequent diagnostic findings. METHODS: We retrospectively reviewed the records of all patients referred for endoscopic evaluation of anemia between 1986 and 1990. To be included in the study, patients had to meet the following criteria: they must be more than 50 yr old and must have anemia and documented iron deficiency. Data collected included historical features, endoscopic or radiological procedures performed, and diagnostic findings. RESULTS: Of a total of 375 patients referred, 170 patients (119 men, 51 women), with a mean age of 69 yr, met the inclusion criteria. A lower gastrointestinal source of iron deficiency was identified in only 30 patients (18%), with carcinoma of the colon (9%), colitis (4%), and arteriovenous malformations (3%) being most common. An upper gastrointestinal source of iron deficiency was identified in 70 patients (41%). Peptic ulcer disease (15%), erosive esophagitis (8%) or gastritis (7%), previous partial gastrectomy (6%), and sprue (3%) were found most often. The etiology of iron deficiency was not identified in 70 patients (41%). In addition, historical features, including gastrointestinal symptoms, fecal occult blood testing, or a history of smoking, excessive alcohol intake, or use of nonsteroidal anti-inflammatory drugs, were poor predictors of diagnostic findings. CONCLUSION: A minority of patients over 50 yr of age have a colonic etiology for iron deficiency. Upper gastrointestinal sources of iron deficiency are prevalent and are frequently asymptomatic, but often they can be identified by upper endoscopy. Therefore, esophagogastroduodenoscopy with small bowel biopsies should be included in the evaluation of iron deficiency anemia in older patients, especially when a colonic source has not been identified.