The hypothesis that severe lung damage generated by acid aspiration or a 50-hour exposure to 100% oxygen aggravates ethanol-induced hemorrhagic mucosal lesions in the stomach was examined in the rat. Animals were either given intratracheally with pyrogen-free saline or HCl (pH 1.75) or exposed for 50 h to 100% oxygen before the intragastric application of 1 ml of 50 or 75% ethanol. All rats receiving 50% ethanol were also given 3% monastral blue, 3 min before ethanol administration as a vascular tracer. Lung acid damage and inflammation as assessed by bronchopulmonary lavage were severe. We observed a significant increase in extracellular lactate dehydrogenase beta-glucosaminidase, albumin and the number of polymorphonuclear leukocytes in the lavage fluid. The number of resident macrophages decreased significantly. Blood gas analysis was not influenced. Hemorrhagic gastric mucosal lesions after 50 or 75% ethanol increased from 4.4 or 8.2% to 9.8 or 13.1% after HCl and from 6.7 or 18.2% to 10.6 or 21.6% of the glandular stomach following oxygen exposure. The area of mucosal vascular damage caused by 50% ethanol as revealed by monastral blue labelling was 3.3 and 2.6 times larger in rats with lung damage induced by HCl or hyperoxia, respectively. Thus, severe lung damage predisposes to microvascular damage and aggravates chemically induced hemorrhagic mucosal lesions.

OBJECTIVE:To test the hypothesis that an early increase in vascular permeability is correlated with later gastric mucosal protection in the rat. METHODS:Histamine, its agonists (H1, H2, H3) and bradykinin, were either given subcutaneously or intragastrically before the intragastric administration of ethanol. The extravasation of intravenously injected 99mTc-glucoheptonate into the gastric wall and into the gastric contents was used as an indicator of increased permeability. Gastric haemorrhagic lesions where measured by computerized planimetry and ethanol absorption was determined by an ACA Clinical Analyzer. RESULTS:Histamine and bradykinin increased vascular permeability in the glandular stomach and provided significant gastroprotection, similar to H1-, H2- and H3-agonists, against ethanol-induced gastric haemorrhagic lesions. This gastroprotection was accompanied by low blood levels of ethanol, probably indicating decreased ethanol absorption and the creation of a histodilutional barrier in the stomach by histamine. CONCLUSIONS:These data indicate that an increase in vascular permeability dissipates the concentration, and may delay the absorption, of ethanol in gastric mucosa by creating a perivascular histodilutional barrier. Vascular injury, which is an early pathogenetic factor in the development of ethanol-induced gastric haemorrhagic erosions, may thus be prevented.

Duodenal ulcer is a disease characterized by very high rates of recurrence: up to 80% at 1 year, 95% at 2 years. Maintenance therapy will reduce relapse rates. However, when therapy directed against gastric acid is stopped, the slope of the recurrence curve is identical whether therapy is stopped after 6 weeks, 8 weeks, 3 months, 6 months, 1 year, or 2 years. This suggests that therapy directed against acid does nothing to change the natural history of ulcer disease. Cytoprotective therapy is equally successful as H2-blockers at healing ulcer or reducing relapse rates, but the time to recurrence is significantly prolonged after either acute or maintenance cytoprotective therapy is stopped. This suggests that cytoprotective therapy has a beneficial effect that does improve the natural history of ulcer disease. The mechanism by which maintenance therapy reduces ulcer relapse could be masking symptoms (analgesic), accelerated healing, or true prevention of ulcer recurrence. By using frequent endoscopic assessment combined with complex statistical evaluation (calculating traditional ulcer prevalence, point prevalence, and maximal ulcer prevalence), we showed that sucralfate cytoprotection genuinely prevents ulcer recurrence. The incidence of asymptomatic ulcer recurrence after sucralfate is 10% but is up to 40% after H2-blocker therapy.

Hepatic artery aneurysm is a rare vascular lesion that accounts for nearly 10% of hemobilia cases. Its etiology is most often atherosclerosis, trauma, or infection. Autoaggressive disorders are rarely associated with hepatic artery aneurysm as is thyroid dysfunction. Presented here is a case of hemobilia secondary to a rupture of one of multiple aneurysms of both right and left hepatic arteries in a women with a history of rheumatoid arthritis, hypothyroidism, and hypertension. Surgical intervention has been the rule in the past. Selective transcatheter embolization has gained clinical application in recent years, especially in the treatment of intrahepatic aneurysms. Its efficacy and safety are demonstrated by this case.

Intestinal ischemia is either occlusive or nonocclusive. Occlusive intestinal ischemia is caused by complete or very high grade obstruction of a major mesenteric artery or one or more of its principal segmental branches, usually by a thrombus (often on a plaque) or an embolus. Nonocclusive intestinal ischemia is associated with low flow states, mesenteric vasoconstriction, and mucosal hypoperfusion without actual obstruction to arterial inflow; it frequently coexists with congestive cardiac failure and generalized arteriosclerotic vascular disease (including arteriosclerosis of mesenteric arteries) but the degree of stenosis in the mesenteric vasculature is insufficient alone to account for the sudden development of this acute and often fatal ischemia. Another useful distinction is that of small intestinal ischemia as opposed to colonic ischemia. Either may be occlusive or nonocclusive. Ischemia of the small intestine is associated with a much poorer prognosis,1and may be the event that leads to irreversibility in many

Seven patients with cardiovascular disease had clinical episodes and marked transaminase elevations that suggested viral hepatitis, but all had morphologic evidence (from liver biopsy or autopsy specimens) that documented centrilobular necrosis (ischemic hepatitis) with no evidence of viral or drug injury. Several also had moderate or marked passive congestion of the liver so the liver biopsies of 15 additional patients were retrospectively reviewed. In this latter group congestion alone was associated with normal or minimal elevation in transaminases while all patients with notable (>5 times normal) transaminase elevations had centrilobular necrosis. Congestion alone, no matter how severe or prolonged, seems to do little if any damage to the liver. Centrilobular necrosis, or ischemic hepatitis, correlates with significant hypertransaminasemia, appears to result from failure of hepatic perfusion (with or without preceding hypotension), and presents with clinical and laboratory manifestations that suggest viral hepatitis.

In order to avoid the use of adhesive appliance for patients with enterostomy, colostomy or ileostomy, we use the magnetic continent colostomy device already described (1).Technique.This study includes 27 patients (20 males and 7

Hypocalcemia following jejunoileal bypass for morbid obesity is not an uncommon occurrence. Three cases of severe hypocalcemia after bypass operation are presented with emphasis on the altered physiology of calcium homeostasis. Recognition and treatment of bypass hypocalcemia can avert a potentially serious complication.

Pepsin secretion is stimulated by the back-diffusion of acid across the mucosa of the vagally denervated canine pouch. If back-diffusion is enhanced by damage, pepsin secretion increases. The current study investigates whether this mechanism exists in man. The stomachs of normal human volunteers were irrigated for 1 hour with either buffer or 0.01 N HCl, 1 hour with 0.2 N HCl, and a final hour with buffer or 0.01 N HCl. During the middle hour both the concentration and output of pepsin increased three- or fourfold. From these studies it appears that the human gastric mucosa contains a mechanism similar to the dog's which results in the stimulation of pepsin secretion when exposed to acid. This mechanism could be of etiologic significance in gastric ulcer disease, which has been shown to be associated with increased gastric-musocal permeability.