The Influence of Low Calcium Concentration Hemodialysis on Cardiovascular Response / 대한신장학회잡지

OBJECTIVE: Arterial compliance (AC) reflects the buffering function of the vessel. Low AC caused by arterial stiffness increases pulse pressure amplitude. Therefore, Low AC must be correlated with high cardiovascular mobidity and mortality in HD patients. Dialysate calcium concentration is potentially a main determinant of serum ionized calcium level and the vasoconstriction is associated with high calcium concentration. Therefore, We conducted a study for evaluation of the interdialytic effects of treatment with a low dialysate calcium (LdCa) concentration and high dialysate calcium (HdCa) concentration on the changes of AC, BP, biochemical parameters. METHODS: Eight HD patient (mean age 45.5, sex ratio 1 : 1) were studied. The mean HD period was 3 years. Arterial Compliance, stroke Volume, SBP, DBP, PP, MAP, Ionized Ca, T-CO2, P and CaxP product were compared after treatment with a LdCa and HdCa concentration for each 10 sessions. RESULTS: AC were 0.143+/-0.076 mm2/kPa in baseline, 0.166+/-0.097 mm2/kPa in LdCa (1.25 mmol/L) dialysate, 0.142+/-0.082 mm2/kPa in HdCa (1.75 mmol/L) dialysate. SBP, DBP, MAP and PP were 157.75+/-15.97, 94.25+/-9.48, 114.12+/-10.56, 63.50+/-10.87 mmHg in baseline and 135.25+/-13.00, 78.75+/-11.24, 98.37+/-15.14, 56.50+/-5.95 mmHg in LdCa dialysate and 160.50+/-15.36, 94.05+/-10.34, 115.75+/-9.64, 62.00+/-15.71 mmHg in HdCa dialysate. Ionized Ca were 4.66+/-0.40 mg/dL in baseline, 4.45+/-0.28 mg/dL in LdCa dialysate and 4.65+/-0.43 mg/dL in HdCa dialysate. However, there were no changes of other biochemical parameters. CONCLUSION: Treatment with LdCa dialysis, by minimizing the risk for LdCa-induced hypocalcemia, may have a beneficial role in the prevention of the ongoing reduction of arterial compliance in HD patients and thus improve cardiovascular prognosis.

Expression of ICAM-1 on the Hantaan virus-infected human umbilical vein endothelial cells

OBJECTIVES: In HFRS, there is a varying degree of disseminated intravascular coagulation which was evident in the early phase of the illness. It is believed also that DIC would be the consequence, at least in part, of functional changes of endothelium resulting in kinin activation and clinical syndrome. This study investigated the role of adhesion molecule in the pathogenesis of Hantaan virus-related disease. METHODS: The expression of ICAM-1 antigen on the cell membrane of human umbilical vein endothelial cells was assessed by immunohistochemistry, and ICAM-1 mRNA in the endothelial cells was assessed by in situ hybridization after Hantaan virus infection (2.6 x 10(4) PFU/mL) with the time course. RESULTS: In immunohistochemistry, the number of ICAM-1 positive cells increased with time during the 12 or 24 hours after infection. 5 to 10% of HUVECs had been positive after 12-24 hours and the number of positive cells decreased abruptly after 24 hours. Hantaan antigen had been noticed after 12 hours focally on the HUVECs but continued to proliferate into day 7 post-infection when most of HUVECs were infected by Hantaan virus. In situ hybridization showed identical patterns of ICAM-1 mRNA expression after Hantaan virus infection. CONCLUSION: It implies that the Hantaan virus infection on HUVECs would express more ICAM-1 on their surface and implicated in the pathogenesis of early clinical syndrome of HFRS.