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ROGIERS ET AL.young DI rats than in young SO rats and adult DI and SO rats. We also found that this hypotension could be prevented by the continuous infusion of AVP (2000 pg·lOO g-I min-I). The adult 01 rats were more resistant to hemorrhagic hypotension than the infant 01 rats. The reason for this is not known. In addition to AVP, angiotensin has also been thought to prevent hemorrhagic hypotension. The angiotensin levels were the same in the adult DI and SO rats both during control conditions and following bleeding. It is therefore likely that the relative resistance to hemorrhagic hypotension, observed in adult DI rats, is independent of angiotensin.The serum AVP levels were measured in the SO rats. The capacity to release AVP was at least as good in young as in adult rats. Previous studies on fetal lambs have shown that the capacity to release AVP in response to blood volume contraction is well developed even in fetal life (12). The AVP levels recorded under basal conditions were high in both the adult and the infant 01 rats; they were 21 and 45 pg-ml", respectively. In adult rats that have been dehydrated for 48 h, the AVP concentration has been reported to be around 30 pg.ml-I (5). The SO rats in this study had been dehydrated for 10 h and subjected to anesthesia and blood vessel cannulation which might have caused the blood volume contraction. Great care had, however, been taken not to use animals that had been bled prior to carrying out the procedure. Following bleeding, the AVP levels increased in both groups, but the increase was significant only in the adult rats. It is possible, however, that the AVP levels in the infant rats were already so high during basal conditions that they represented maximal levels. SummaryA study was carried out in order to investigate whether the abnormal in vitro turnover of fatty acids in the phospholipids of the red blood cell membranes of cystic fibrosis patients is intrinsic to the membrane, or whether it is induced by extrinsic serum factors. Red blood cells of cystic fibrosis patients and healthy subjects were labeled in vitro with 1 14 q linoleic acid, bound to albumin. The labeled cells were reincubated in autologous and homologous serum. The radioactivity present in the serum lipids and in the major phospholipid fractions of the red cell membranes was measured.Conclusions of this study are: 1) not all of the cystic fibrosis patients examined individually show an abnormal in vitro turnover of the red cell fatty acids, although they all presented abnormal fatty acid patterns for the red blood cell phospholipids,

In our previous work it was found that in cystic fibrosis patients with and without pancreatic insufficiency, the fatty acid pattern of the plasma long chain, non-esterified fatty acid fraction is strikingly abnormal in comparison with the corresponding pattern of healthy subjects. However, other investigators have shown abnormal fatty acid patterns only in patients with pancreatic insufficiency. Therefore, we studied the plasma cholesterol ester fraction in cystic fibrosis patients of both types by gas liquid chromatography. It was found that the absolute total concentration of the plasma cholesterol esters in cystic fibrosis patients with and also without pancreatic insufficiency is significantly lower than in healthy subjects. Furthermore, the fatty acid pattern of this lipid fraction is significantly abnormal in both groups of patients, although to a lesser extent in patients without pancreatic insufficiency.

Glutathione S-transferases (GSTs) are subject to regulation by thyroid and sex hormones and by GH. We have used an in vitro experimental system comprising adult rat hepatocytes co-cultured with rat liver epithelial cells of primitive biliary origin, to distinguish between direct and indirect effects of various hormones on GSTs; to identify the GST subunits affected by individual hormones; and to investigate the level at which the hormones act. Triiodothyronine (T 3 ), thyroxine (T 4 ) and 17 -oestradiol (OE 2 ) reduced GST activities, whereas testosterone, dihydrotestosterone, and human growth hormone (hGH) had little effect on total GST activity. HPLC separation of the various GST subunits revealed that T 3 and T 4 reduced total GST content, in particular the abundance of subunits M1 and M2. The amount of the Pi-class subunit P1 was reduced by OE 2 . Treatment of the co-cultured cells with this hormone altered the GST subunit profile to one that is more similar to that observed in freshly isolated hepatocytes. Analysis of mRNAs demonstrated that some of the hormones act at a pre-translational level, whereas others act at a translational or post-translational level to regulate the expression of various GST subunits.