Baroreflex function in conscious rats submitted to iron overload

Our hypothesis is that iron accumulated in tissue, rather than in serum, may compromise cardiovascular control. Male Fischer 344 rats weighing 180 to 220 g were divided into 2 groups. In the serum iron overload group (SIO, N = 12), 20 mg elemental iron was injected ip daily for 7 days. In the tissue iron overload group (TIO, N = 19), a smaller amount of elemental iron was injected (10 mg, daily) for 5 days followed by a resting period of 7 days. Reflex heart rate responses were elicited by iv injections of either phenylephrine (0.5 to 5.0 µg/kg) or sodium nitroprusside (1.0 to 10.0 µg/kg). Baroreflex curves were determined and fitted to sigmoidal equations and the baroreflex gain coefficient was evaluated. To evaluate the role of other than a direct effect of iron on tissue, acute treatment with the iron chelator deferoxamine (20 mg/kg, iv) was performed on the TIO group and the baroreflex was re-evaluated. At the end of the experiments, evaluation of iron levels in serum confirmed a pronounced overload for the SIO group (30-fold), in contrast to the TIO group (2-fold). Tissue levels of iron, however, were higher in the TIO group. The SIO protocol did not produce significant alterations in the baroreflex curve response, while the TIO protocol produced a nearly 2-fold increase in baroreflex gain (-4.34 ± 0.74 and -7.93 ± 1.08 bpm/mmHg, respectively). The TIO protocol animals treated with deferoxamine returned to sham levels of baroreflex gain (-3.7 ± 0.3 sham vs -3.6 ± 0.2 bpm/mmHg) 30 min after the injection. Our results indicate an effect of tissue iron overload on the enhancement of baroreflex sensitivity.

Neuronal protein biosynthesis by neonatally malnourished and nutritionally recovered rats

1. The objective of the present study was to examine the reversibility of the effect of neonatal malnutritiona on in vivo neuronal protein synthesis. 2. Neonatal malnutrition was achieved by letting the pups suckle mothers fed a low casein diet (6.4%) which decreased the amount of milk produced. The control group was composed of pups from mothers fed a 17% casein diet and kept on the same diet after weaning. A group of pups was undernourished during the suckling period, as above, but fed a 17% casein dietafter weaning (recovered group). All animals were killed at 60 days of age. 3. Neuronal cell bodies were separated from forebraim by mechanical disruption of the tissue and centrifugation in a sucrose gradient. 4. Protein biosynthesis was measured by the incorporation of [14C] - leucine into proteins of neuronal cell bodies, after correcting for the specific activity of the precursor. 5. Forebrain cell number and cell size were evaluated by DNA content and the protein/ DNA ratio, respectively. 6. The forebrains of the recovered group weighed less than those of the controls, perhaps due to a lower number of cells, which exhibited an average size similar to that of the control group. 7. The rate of protein biosynthesis was similar in malnourished and recovered groups, but both were only 57% of the rate of the control group. 8. We conclude that neonatal malnutrition promotes an irreversible adverse effect on in vivo neuronal protein synthesis by rats