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Abstract-We studied the effect of hyperbaric oxygen (HBO) treatment on the extent of diet-induced accumulation of lipid oxidation products in rabbit plasma and tissues, on plasma paraoxonase activity, and on the extent of progression and regression of atherosclerotic lesions in the rabbit aorta. HBO treatment of cholesterol-fed rabbits dramatically reduces the development of arterial lesions despite having little or no effect on plasma or individual lipoprotein cholesterol concentrations. Compared with no treatment in cholesterol-fed animals, HBO treatment also substantially reduces the accumulation of lipid oxidation products (conjugated dienes, trienes, and thiobarbituric acid-reactive substances) in plasma, in the low density lipoprotein and high density lipoprotein fractions of plasma, in the liver, and in the aortic tissues. In addition, HBO treatment prevents the decrease in plasma paraoxonase activity observed in rabbits fed cholesterol-rich diets. Similarly, in regression studies, HBO treatment has no effect on the rate of plasma (or lipoprotein) cholesterol decline but significantly accelerates aortic lesion regression compared with no treatment. Direct measures of aortic cholesterol content support these morphological observations. On the basis of these results, we conclude that repeated, but relatively short, exposure to HBO induces an antioxidant defense mechanism(s) that is responsible for retarding the development or accelerating the regression of atherosclerotic lesions.

SUMMARY Mucus was sampled from the gastric mucosal surface of anaesthetised rats. Three weeks later these rats were orally dosed each day with aspirin (375 mg/kg) for six months. Then the number and size of the aspirin induced chronic gastric ulcers were assessed. Gel filtration chromatography of the mucus samples showed that mucus glycoprotein was present in both high and low molecular weight forms. There was a natural variation between individual rats in the percentage of glycoprotein in the high molecular weight form (mean=58-9%; SD=9.6%; n=23). This variation correlated strongly with the degree of subsequent aspirin induced chronic gastric ulceration (r=-0 85, p<0001). This is the first time that a pre-existent variability in a mucosal defence factor has been shown to predict susceptibility of the stomach to chronic ulceration.It has been previously noted with some animal models of chronic gastric ulceration, that a wide range of responses, between individual animals, is obtained with a constant dose per unit weight of an ulcerogenic agent. Hence, Pfeiffer and MacPherson postulated that this might be because of the variability in some aspect of mucosal defence. ' The surface mucus layer is one of the gastric mucosal defence factors, and it has been shown to be different in the presence of gastric ulcer in man. Gastrectomy specimens from patients with this condition had a mucus layer which contained a smaller percentage of high molecular weight mucus glycoprotein, than similar specimens removed from patients with non-ulcer disease. It is not known, however, if this difference in the gastric mucus predates or follows the ulceration. We wished to investigate which might be the case, but as there was no obvious way to do this in man, an animal model of chronic gastric ulceration was used. Of those available, the chronic aspirin dosed rat' was chosen for study.The aims of the present study were: (1) to develop a method for sampling rat gastric epithelial mucus that permitted recovery of the animal for subsequent

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The role of genetic factors in controlling CR1 quantitative expression on erythrocytes (E) of patients with systemic lupus erythematosus (SLE) was reexamined by determining the temporal stability of CR1 numbers and the frequency of a CR1 genomic restriction fragment length polymorphism (RFLP). The mean number of binding sites/(E) for Yz-1 monoclonal anti-CR1 correlated with the number of sites for polyclonal anti-CR1 that had been determined 2 to 4 yr previously in 18 normal persons (p less than 0.001), 18 patients (p less than 0.001), and 28 relatives (p less than 0.001), indicating that CR1 sites/E was a stable characteristic in all three groups. The mean number of Yz-1 sites/E was 281 +/- 34 (+/- SEM) in 28 probands with SLE and 457 +/- 21 in 93 relatives, both determinations being less than that for 100 normal persons, 553 +/- 21 (p less than 0.002). Thirty-six patients and 51 normal individuals were also assessed for the presence of the 7.4 kb and 6.9 kb HindIII CR1 allelic restriction fragments that correlate with high and low expression, respectively, of CR1 on E. The distribution of patients differed from normal (p less than 0.05), with a smaller proportion being homozygous for the 7.4 kb allele. In addition, the mean numbers of Yz-1 sites/E for patients and relatives who were homozygous (p less than 0.02) and heterozygous (p less than 0.05) for the 7.4 kb allele were significantly lower than those for normal persons matched for the HindIII RFLP, suggesting the existence of additional heritable factors that decrease CR1 expression. The stability over time of the CR1 deficiency among patients, the finding of decreased CR1 number among an expanded group of relatives, the altered frequency among patients of CR1 alleles defined by the HindIII RFLP, and the decreased expression of CR1 on E among patients and relatives compared with normal individuals having the same HindIII RFLP indicate a role for genetic factors in CR1 deficiency in SLE.