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Biomedical subjects

S J Piliero

Publications and source records attributed to S J Piliero.

34 records · Page 2Linked to original sources
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Mechanisms underlying the suppression of erythropoiesis by hyperoxia.

The possible mechanisms underlying the suppression of erythropoiesis in hyperoxic animals were studied. Male Long-Evans rats were injected with cobaltous chloride hexahydrate, a known erythropoietic stimulant. One group was exposed to a hyperoxic environment for ten hours. Both serum levels of erythropoietin (Ep) and renal levels of erythrogenin were significantly lower (p less than 0.005) in the hyperoxic animals compared to those left at room air. In addition, inhibitors to Ep or erythrogenin could not be detected in either the serum or renal tissue of the hyperoxic rats. These results indicate that the primary factor responsible for the erythropoietic suppression observed in a hyperoxic environment is a decreased production of erythrogenin which results in turn, in a lowered level of circulating Ep.

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PubMedDate not supplied

Isoproterenol-induced changes in cell cycle kinetics of parotid gland acinar cells in 8-day-old rats.

Isoproterenol (IPR) was shown to alter some parameters of the parotid gland acinar cell cycle in 8-year-old rats. Although the deoxyribonucleic acid (DNA) synthetic period (S) was decreased and the pre-DNA synthetic (G1) period was lengthened, there were no differences in the total cycle time. There was an increase in the 3H-thymidine labeling index from 35.7 to 50.8% combined with a decrease in the value of the mitotic index from 2.64 to 2.16% after IPR was administered. The results suggest that noncycling (G0) cells may be involved in the normal differentiation of the parotid gland and that IPR alters the transition of acinar cells between the cycling and noncycling state.

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PubMedDate not supplied

Recovery of an erythropoietin inducing factor from the regenerating rat liver.

The perfusion of livers of partially hepatectomized (H mean) rats lends support to earlier findings that the regenerating rat liver is the source of an erythropoietin-inducing hepatic factor (Ep-IHF) which stimulates hepatic production of extrarenal erythropoietin (Ep). Blood plasma was collected from perfused livers of rats that were partially hepatectomized (H mean) 48 to 72 hrs prior to perfusion with whole blood from normal rats. This plasma, when injected into normal rats which were nephrectomized (N mean) and rendered hypoxic 18 hrs after injection, evoked a significant increase in Ep values when compared to blood plasma collected from perfused livers of normal rats. Ep values were significantly higher when regenerating livers were perfused with blood collected from nephrectomized (N mean) rats than when such livers were perfused with blood of normal rats. The highest Ep values resulting from the liver perfusions were obtained when the liver donor and blood donor rats were both H mean and N mean. The results demonstrate that the liver is the principal source of an Ep-inducing factor since perfusion of the liver eliminated other potential tissue sources of activity in the rat. This was achieved by perfusing the livers directly through the portal vein and collecting the perfusate from the hepatic vein, thereby eliminating potential contributions from organs draining into other parts of the systemic circulation. In addition, it was shown that the kidney inhibits the activity and/or production of the Ep-IHF which is evoked by H mean.

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