No abstract

Ileum displays little active transcellular calcium (Ca2+) absorption but is credited with the bulk of Ca2+ absorbed in vivo. We examined the effect of taurodeoxycholic acid (TDC, 2 mM), a bile salt, on mannitol (MN, a marker of intercellular solute traffic) and Ca2+ fluxes in rat ileum. In the absence of electrochemical gradients between the mucosal (M) and serosal (S) bathing media in an Ussing chamber, net flux (Jnet) was observed in the S-to-M direction for both MN and Ca2+, i.e., the unidirectional secretory S-to-M flux (Js-->m) exceeded the absorptive M-to-S flux (Jm-->s). Mucosal TDC caused simultaneous increase in transepithelial conductance and Js-->m for both MN and Ca2+. This was followed by even greater increases in MN and Ca2+ Jm-->s, so that ultimately Jm-->s equaled Js-->m in each case. In control tissue, Js-->m for Ca2+ appeared to permeate exclusively through the intercellular MN pathway while part of Jm-->s for Ca2+ appeared to traverse through a non-MN route. After the TDC-induced increase in intercellular solute permeability, both Ca2+ fluxes appeared to traverse through the aqueous MN conduit. During the postprandial state, the presence of bile salts and the relative abundance of Ca2+ in ileal lumen can cause bulk Ca2+ absorption through the intercellular pathway.

Chronic lead exposure may cause hypertension in normotensive rats. This hypertensinogenic effect has been attributed to perturbations in the renin-angiotensin axis, the contractile response of the vascular smooth muscle, or the intracellular Ca2+ homeostasis as a consequence of the inhibition of Na(+)-K(+)-ATPase activity. In this study we examined the short-term effect of lead exposure on blood pressure, plasma renin activity, vascular contractility, and renal Na(+)-K(+)-ATPase activity and abundance in the spontaneously hypertensive rat. Our data indicate that modest lead exposure caused blood pressure elevation within two weeks in this rat strain that is genetically susceptible to the development of hypertension. This rapid blood pressure-elevating effect did not appear to depend on the mechanisms described in hypertension associated with more chronic lead exposure listed above. This acute model provides an additional approach to the study of lead-induced hypertension.

Aimed at the present maintenance training in the army, the virtual maintenance training system frame of a certain type of power station was designed by using the object model and virtual reality technology. The key technologies to build simulation models based on NGrain were studied, and the virtual maintenance training system was developed finally. Results show that the system has lots of advantages such as multiple training modes, friendly operation and low requests to hardware.

Partial correction of uraemic anaemia restores the baseline hyperkinetic haemodynamics toward normal, reduces left ventricular size and mass and improves exercise tolerance in dialysis patients. These effects may, in large part, be attributed to increases in haematocrit. Information on whether erythropoietin also acts directly on the heart, as it does on the peripheral vasculature, is not available. Also remaining unanswered is the question as to whether the effects of erythropoietin on the heart reduce cardiovascular mortality in end-stage renal disease (ESRD) patients. In addition, we do not know whether complete (vs partial) correction of uraemic anaemia will further enhance the beneficial effect of erythropoietin, or whether such gains could be counterbalanced by side effects of erythropoietin, such as the development or exacerbation of hypertension. Studies in the peripheral vasculature suggest erythropoietin also acts directly on the vascular smooth muscle cells, exerting both vasopressive and growth effects. Better understanding of the mechanism and control of such non-erythropoietic actions of erythropoietin can optimize the beneficial effect and minimize the side effect of this hormone on the cardiovascular system.