losartan-potassium and dexamethasone-21-phosphate

losartan-potassium has been researched along with dexamethasone-21-phosphate* in 2 studies

Other Studies

2 other study(ies) available for losartan-potassium and dexamethasone-21-phosphate

Article	Year
In vitro effect of dexamethasone phosphate on hematopoietic progenitor cells in preterm infants. Archives of disease in childhood. Fetal and neonatal edition, 1998, Volume: 78, Issue:1 The in vitro effect of dexamethasone on the clonal growth of haematopoietic progenitors in preterm infants was investigated. Concentrations of 10(6)M to 10(9)M were associated with a dose dependent inhibition of colony formation, with the most clinically important effects seen on the earliest erythroid and granulocyte-macrophage colonies. Because of the potential clinical implications of these observations, studies are needed to determine the effects of dexamethasone on haematopoiesis in preterm infants. Topics: Adult; Cell Culture Techniques; Colony-Forming Units Assay; Dexamethasone; Dose-Response Relationship, Drug; Erythroid Precursor Cells; Erythropoietin; Fetal Blood; Glucocorticoids; Hematopoietic Stem Cells; Humans; Infant, Newborn; Infant, Premature	1998
Effect of dexamethasone on fetal liver erythroid colony-forming cells in vivo. Experimental hematology, 1985, Volume: 13, Issue:9 Pretreatment of pregnant mice (CD-1) with intravenous dexamethasone phosphate (10(-3)-10(-7) g/mouse), a synthetic glucocorticoid, reduced the number of erythroid colonies that formed when 15-day-old fetal liver erythroid progenitor cells (3 X 10(4] were cultured for two days in plasma clots containing exogenous erythropoietin (Epo) (25 mU). The proliferative rate of fetal liver erythroid colony-forming cells (CFU-E), obtained from pregnant mice treated 24 h earlier with dexamethasone phosphate (1 mg/mouse), was reduced from 76% (control) to 46% as measured by a decrease in the percentage of fetal liver CFU-E lost following a 20-min exposure to high-specific-activity tritiated thymidine (50 microCi, 50-77 Ci/mmol). In addition, pretreatment of pregnant mice with lower doses of dexamethasone phosphate (10(-5)-10(-7) g/mouse) resulted in a higher percentage of fetal liver CFU-E lost following exposure to high-specific-activity tritiated thymidine (64% and 67%, respectively). Concomitantly, the inhibitory effect of dexamethasone on erythroid colony formation by these fetal liver cells in response to exogenous Epo is reduced. These results appear to indicate that the dexamethasone-mediated reduction in erythroid colony formation is inversely related to the fraction of fetal liver CFU-E lost after exposure to high-specific-activity tritiated thymidine. Furthermore, this observation suggests that glucocorticoids inhibit erythroid colony formation by decreasing the proliferative rate of the fetal liver CFU-E. Topics: Animals; Cell Division; Dexamethasone; Erythrocytes; Erythropoietin; Female; Hematopoietic Stem Cells; Humans; Interphase; Liver; Maternal-Fetal Exchange; Mice; Pregnancy; Thymidine	1985

Article

Year

In vitro effect of dexamethasone phosphate on hematopoietic progenitor cells in preterm infants.

Archives of disease in childhood. Fetal and neonatal edition, 1998, Volume: 78, Issue:1

The in vitro effect of dexamethasone on the clonal growth of haematopoietic progenitors in preterm infants was investigated. Concentrations of 10(6)M to 10(9)M were associated with a dose dependent inhibition of colony formation, with the most clinically important effects seen on the earliest erythroid and granulocyte-macrophage colonies. Because of the potential clinical implications of these observations, studies are needed to determine the effects of dexamethasone on haematopoiesis in preterm infants.

Topics: Adult; Cell Culture Techniques; Colony-Forming Units Assay; Dexamethasone; Dose-Response Relationship, Drug; Erythroid Precursor Cells; Erythropoietin; Fetal Blood; Glucocorticoids; Hematopoietic Stem Cells; Humans; Infant, Newborn; Infant, Premature

1998

Effect of dexamethasone on fetal liver erythroid colony-forming cells in vivo.

Experimental hematology, 1985, Volume: 13, Issue:9

Pretreatment of pregnant mice (CD-1) with intravenous dexamethasone phosphate (10(-3)-10(-7) g/mouse), a synthetic glucocorticoid, reduced the number of erythroid colonies that formed when 15-day-old fetal liver erythroid progenitor cells (3 X 10(4] were cultured for two days in plasma clots containing exogenous erythropoietin (Epo) (25 mU). The proliferative rate of fetal liver erythroid colony-forming cells (CFU-E), obtained from pregnant mice treated 24 h earlier with dexamethasone phosphate (1 mg/mouse), was reduced from 76% (control) to 46% as measured by a decrease in the percentage of fetal liver CFU-E lost following a 20-min exposure to high-specific-activity tritiated thymidine (50 microCi, 50-77 Ci/mmol). In addition, pretreatment of pregnant mice with lower doses of dexamethasone phosphate (10(-5)-10(-7) g/mouse) resulted in a higher percentage of fetal liver CFU-E lost following exposure to high-specific-activity tritiated thymidine (64% and 67%, respectively). Concomitantly, the inhibitory effect of dexamethasone on erythroid colony formation by these fetal liver cells in response to exogenous Epo is reduced. These results appear to indicate that the dexamethasone-mediated reduction in erythroid colony formation is inversely related to the fraction of fetal liver CFU-E lost after exposure to high-specific-activity tritiated thymidine. Furthermore, this observation suggests that glucocorticoids inhibit erythroid colony formation by decreasing the proliferative rate of the fetal liver CFU-E.

Topics: Animals; Cell Division; Dexamethasone; Erythrocytes; Erythropoietin; Female; Hematopoietic Stem Cells; Humans; Interphase; Liver; Maternal-Fetal Exchange; Mice; Pregnancy; Thymidine

1985