Changes of serum soluble P-selectin and tumor necrotic factor-alpha in patients with CMV induced acute coronary syndrome / 中华实验和临床病毒学杂志

<p><b>OBJECTIVE</b>To explore the changes and relationship between serum soluble P-selectin, tumor necrosis factor-alpha (TNF-alpha) in coronary heart disease patients with acute coronary syndrome (ACS) and human cytomegalovirus (HCMV) infection.</p><p><b>METHODS</b>The levels of circulating soluble P-selectin, TNF-alpha, HCMV-IgM and HCMV-IgG were determined by enzyme-linked immunosorbent assay (ELISA) in 79 cases for ACS group, 30 cases for stable angina (SA) group and 30 healthy control cases.</p><p><b>RESULTS</b>(1) The serum positive rate of HCMV-IgM and HCMV-IgG in the ACS, SA and healthy control groups were 30.4% (24/79), 10.0% (3/30) and 6.7% (2/30); 86.1% (68/79), 80.0% (24/30) and 53.3% (16/30), respectively. Positive rate of HCMV-IgM in the ACS was higher than those in SA and healthy control groups (P < 0.01), positive rate of HCMV-IgG in the ACS and SA groups were higher than that of the healthy control group (P < 0.01). (2) Compared with the SA group and healthy control group, the levels of the serum soluble P-selectin and TNF-alpha were significantly higher in patients with ACS [(6437.3 +/- 666.9) pg/ml vs. (1520.0 +/- 112.7) pg/ml and (1481.0 +/- 109.1) pg/ml, (56.2 +/- 18.4) pg/ml vs. (27.3 +/- 13.7) pg/ml and (28.1 +/- 11.3) pg/ml], respectively, P < 0.01). The AMI group, compared with the UA group in the ACS group, had significantly higher levels of the serum soluble P-selectin and TNF-alpha (P < 0.01). Compared with the SA group, the levels of the serum soluble P-selectin and TNF-alpha were not significantly different in healthy control group. (3) The levels of the serum soluble P-selectin and TNF-alpha in HCMV-IgM positive patients were significantly higher than the HCMV-IgM negative patients in the ACS group (P < 0.01).</p><p><b>CONCLUSION</b>The chronic infection with HCMV might injure endothelial cells that subsequently contribute to the formation and progression of atherosclerosis, the acute infection with HCMV may induce increased serum levels of soluble P-selectin and TNF-alpha that might participate in acute coronary events.</p>

Vasonatrin peptide attenuates the enhancement of electrically-induced intracellular calcium transient by isoproterenol in rat cardiac myocytes / 生理学报

The purpose of this study was to investigate the effects of vasonatrin peptide (VNP) on electrically-induced intracellular calcium ([Ca(2+)](i)) transient and mechanism of the effects in the cardiac myocytes. The [Ca(2+)](i) transient was measured with a fluoremetric method. The effects of HS-142-1, 8-Br-cGMP and methylene blue (MB) on [Ca(2+)](i) transient in cardiac myocytes were also determined. Isoproterenol (Iso) at 10(-10)~10(-6) mol/L augmented electrically-induced [Ca(2+)](i) transient dose-dependently, which was (13+/-8)% (P>0.05), (26+/-13)% (P< 0.05), (66+/-10)% (P<0.01), (150+/-10)% (P<0.01) and (300+/-25)% (P<0.01), respectively. These effects were blocked by an beta-adrenergic bloker propranolol (10(-6) mol/L). The effect of Iso (10(-8) mol/L) on [Ca(2+)](i) transient was attenuated in a dose-dependent manner by VNP at 10(-10)~10(-6) mol/L, which was (99+/-3)% (P>0.05), (96+/-2)% (P<0.05), (84+/-6)% (P<0.01), (66+/-3)% (P<0.01) and (62+/-3)% (P<0.01), respectively. 8-Br-cGMP (10(-7)~10(-3) mol/L) aslo attenuated 10(-8) mol/L Iso-induced [Ca(2+)](i) transient dose-dependent. The effect of VNP on [Ca(2+)](i) transient was almost abolished in the presence of HS-142-1 (2x10(-5) mol/L), an antagonist of the natriuretic peptide guanylate cyclase (GC) receptors. MB (10(-5) mol/L), an inhibitor of GC, not only blocked the effect of VNP in myocytes, but also augmented electrically-induced [Ca(2+)](i) transient. VNP and HS-142-1 themselves did not change the [Ca(2+)](i) transient in the cardiac myocytes significantly. But MB augmented the [Ca(2+)](i) transient in the cardiac myocytes significantly. These results suggest that VNP attenuates [Ca(2+)](i) transient induced by Iso. This effect is possibly achieved by binding VNP with the natriuretic peptide GC receptors in the myocytes, leading to an increase in intracellular cGMP.