Blood pressure reactivity in young children: comparing three stressors.

Blood pressure (BP) reactivity in children, the transient elevation of BP after an acute stressor, is a stable characteristic that may predict cardiovascular disease (CVD) and hypertension. The purpose of the present study was to assess the generalizability of BP reactivity across various stressors in young children. BP reactivity was measured in 85 children (ages 3 to 6 years) after each of three different stressors. Systolic BP reactivity level was highest after physical exertion (104 mm Hg), followed by competitive task (95 mm Hg) and cognitive task (93 mm Hg). Resting systolic BP was 90. The 2-week test-retest reliability was higher for physical stress systolic BP reactivity level (r = .66) than for baseline systolic BP (r = .58) and the other two stressors. The reliability of the systolic BP change score was significant only for physical stressor (r = .33). Correlations among the three stressors ranged from .75 to .79 for systolic BP reactivity level and from .37 to .50 for change in systolic BP. Change in systolic BP after physical stress correlated with skin-fold thickness (r = .32). There was evidence of generalizability across stressors. The physical task is the most promising for future study of BP reactivity in young children.     

A novel 37-Kd adhesive membrane protein from cloned murine bone marrow stromal cells and cloned murine hematopoietic progenitor cells

The adhesion of hematopoietic progenitor cells to bone marrow stromal cells is critical to hematopoiesis and involves multiple effector molecules. Stromal cell molecules that participate in this interaction were sought by analyzing the detergent-soluble membrane proteins of GBI/6 stromal cells that could be adsorbed by intact FDCP-1 progenitor cells. A single-chain protein from GBI/6 cells having an apparent molecular weight of 37 Kd was selectively adsorbed by FDCP-1 cells. This protein, designated p37, could be surface-radiolabeled and thus appeared to be exposed on the cell membrane. An apparently identical 37- Kd protein was expressed by three stromal cell lines, by Swiss 3T3 fibroblastic cells, and by FDCP-1 and FDCP-2 progenitor cells. p37 was selectively adsorbed from membrane lysates by a variety of murine hematopoietic cells, including erythrocytes, but not by human erythrocytes. Binding of p37 to cells was calcium-dependent, and was not affected by inhibitors of the hematopoietic homing receptor or the cell-binding or heparin-binding functions of fibronectin. It is proposed that p37 may be a novel adhesive molecule expressed on the surface of a variety of hematopoietic cells that could participate in both homotypic and heterotypic interactions of stromal and progenitor cells.     

Retardation of calcification of bovine pericardium used in bioprosthetic heart valves by phosphocitrate and a synthetic analogue

The purpose of this study was to determine if phosphocitrate (PC), a naturally occurring inhibitor of calcification, and its synthetic analogue, N-sulpho-2-amino tricarballylate (SAT), administered either by daily injection or local delivery via Alzet osmotic minipump, could inhibit calcification of glutaraldehyde-preserved bovine pericardium used in bioprosthetic heart valves, subcutaneously implanted in rats. Local drug delivery, but not systemic administration, was effective. PC, administered by Alzet minipump (12 mg.kg-1.day-1), inhibited calcification significantly (tissue calcium = 5 +/- 2 micrograms/mg dry tissue, mean +/- SEM), compared with untreated or saline-treated controls (89 +/- 9 and 49 +/- 9 micrograms/mg, respectively). SAT, administered by the same route at both the same and a higher molar dosage, was less potent (tissue calcium = 26 +/- 9 micrograms/mg and 17 +/- 5 micrograms/mg, respectively). PC and SAT therapy were not associated with adverse effects. We conclude that locally administered PC and SAT can inhibit intrinsic calcification of bovine pericardium, with PC being more potent.