Differences in aortic impedance between normotensives and hypertensives are not well characterized. We examined impedance in 8 normotensive and 11 hypertensive (mean 96.7 vs. 122.2 mmHg) age-matched, Chinese patients undergoing cardiac catheterization at rest, during nitroprusside, and handgrip exercise before and after beta blockade (propranolol). Hypertensives had higher resistance (2,295 vs. 1713 dyn-s/cm5), characteristic impedance (145.7 vs. 93.9 dyn-s/cm5), total external power (1,579 vs. 1174 mW), peripheral reflections (ratio of backward to forward wave components of 0.54 vs. 0.44), and first zero crossing of impedance phase angle (4.15 vs. 2.97 Hz). These abnormalities were eliminated with vasodilatation. Differences between groups were not further exacerbated when pressure was increased during handgrip exercise. Beta blockade further increased resistance and reflections. Thus, hemodynamic abnormalities of essential hypertension (increased resistance, reflections, and pulse wave velocity, and decreased compliance) are compatible with an increased vasomotor tone that is further unmasked during generalized beta blockade.

Essential hypertension affects the regional properties of the aortic wall. These alterations are manifested by increased peripheral wave-speed and increased wave reflections along the aorta. The differences in wavespeed but not reflection properties are eliminated when the pressures are matched by handgrip, suggesting that factors other than the level of blood pressure per se are responsible for the alterations in reflection properties.

The role of infectious agents in the pathogenesis of autoimmune diseases has long been a matter of debate. This study investigated the possible role of Epstein-Barr virus (EBV) and human cytomegalovirus (HCMV) infections in the pathogenesis of autoimmune diseases by an attempt to demonstrate the presence of the viral genome in the leukocyte of 21 juvenile rheumatoid arthritis (JRA) patients, 20 childhood-onset systemic lupus erythematosus (SLE) patients, and 20 age-matched normals, using polymerase chain reaction (PCR) and DNA probes. The results showed: (1) there was no difference in serum IgG anti-EBV antibody titers among three groups; (2) the EBV PCR-positive rates for JRA and SLE patients and normal controls were 5% (1/21), 10 (2/20), and 0% (0/20), respectively; (3) the HCMV PCR-positive rates for JRA and SLE patients and normal controls were 33% (7/21), 25 (5/20), and 10% (2/20), respectively, and (4) the HCMV-positive rate was 25% for JRA patients with steroid treatment and 33% for those without steroid treatment. It is, therefore, concluded that: (1) the data do not support the participation of EBV and HCMV in the pathogenesis of childhood-onset SLE and JRA; (2) steroid therapy does not increase the frequency of HCMV infection in JRA patients, and (3) immunoincompetence might be one of the major factors contributing to increased susceptibility to HCMV infection in JRA and SLE patients.

alpha-Adrenergically mediated vasoconstriction cannot account for all of the hemodynamic alterations seen in essential hypertension.

Twenty-three patients with systemic lupus erythematosus (SLE) were studied in order to understand the mechanism of increased susceptibility to infection in SLE patients. We found that phagocytosis by polymorphonuclear leucocytes (PMN) was significantly defective in untreated (24.2 +/- 3.1%) and immunosuppressant-treated SLE patients (30.0 +/- 3.6%) compared with normals (47.9 +/- 0.6%), while the generation of superoxide anion radicals was normal. The defective phagocytosis in SLE could be increased by human recombinant tumour necrosis factor alpha (TNF-alpha). However, the percentages of phagocytosis in SLE before and after TNF-alpha stimulation were 56.6% and 60.7% of the normal values. This indicates that certain populations of PMN in SLE are not only defective as regards phagocytosis but also unresponsive to TNF-alpha stimulation. In an ELISA, TNF-alpha production by phorbol myristate acetate (PMA)-stimulated mononuclear cells from SLE patients was significantly decreased (181.4 +/- 22.7 pg/ml vs. 533.0 +/- 81.9 pg/ml, p = 0.002). In addition, the percentage of phytohaemagglutinin (PHA)-stimulated mononuclear cells in S phase in the cell cycle was deficient in patients with SLE (17.2 +/- 1.8% vs. 29.7 +/- 2.9%, p less than 0.001). These results lead us to propose that defective PMN in spontaneous and TNF-alpha-induced phagocytosis, decreased production of TNF-alpha, and lymphocyte hyporesponsiveness predispose patients with SLE to infections.