tiffness of large arteries has been related to cardiovascular mortality, but the mechanisms underlying this relationship have not been established. 1 Methods are used to estimate this stiffness include carotid ultrasound (CU) and pulse-wave-velocity (PWV). 2 Carotid artery stiffness detected by CU is known to representative of systemic arteriosclerosis. The measurement of PWV is very useful for diagnosing arteriosclerosis in any part of the body 3-7 and a new method for measuring PWV has been proposed in Japan. Brachial -ankle PWV (baPWV) measures the PWV in the arm and leg by applying air pressure using the volume plethysmographic method. However, baPWV is reportedly influenced by several factors such as blood pressure (BP), autonomic nerve function etc and therefore does not reflect arteriosclerosis in some cases.The stiffness parameter is reported to be independent of BP. 8 Beta of the thoracic descending aorta (TDA) has been obtained previously only by transesophageal echocardiography (TEE), 9 but recently this problem has been solved with the advent of the cardio-ankle vascular index (CAVI). CAVI is a new parameter that is also independent of BP 10-12 and in the present study, we examined the accuracy and usefulness of CAVI and compared it with other parameters of arteriosclerosis, using CU and serum lipids measurement in patients with chest pain syndrome. Methods Principle of CAVI and Method of MeasurementCAVI was obtained by substituting the stiffness parameter in the following equation for determining vascular elasticity and PWV. The stiffness parameter indicates BPindependent patient-specific vascular stiffness measured by arterial US. The stiffness parameter is calculated as: (1) where Ps and Pd are respectively the systolic and diastolic BP in mmHg. D is the diameter of the blood vessel and ∆D is the change of D.Bramwell-Hill's formula expresses the relationship between volume elastic modulus and PWV as follows:where ∆P is pulse pressure, is blood density, V is the volume of the blood vessel and ∆V is the change of V.From equation (2), the following formula is derived:where D is the diameter of the blood vessel and ∆D is the change of D. If we substitute equation (3) for equation (1), we obtain the stiffness parameter:CAVI is measured as follows. PWV is obtained by dividing vascular length (L) by the time (T) taken for the pulse wave to propagate from the aortic valve to the ankle Circ J 2007; 71: 1710 -1714 (Received February 15, 2007 revised manuscript received June 20, 2007; accepted July 4, 2007) Division of Cardiology, Tokuyama Central Hospital, Shunan, *Division Methods and ResultsThe purpose of this study was to evaluate the accuracy and usefulness of CAVI and to compare it with other parameters of arteriosclerosis by carotid ultrasound (CU). The instantaneous dimensional change of the TDA on TEE was measured simultaneously with systemic pressure of the brachial artery in 70 patients in sinus rhythm. There were significant correlations between CAVI and age (r=0.65, p<0.01), and CAVI and...
Extracellular signal-regulated kinase 1/2 (ERK1/2) is known to function in cell survival in response to various stresses; however, the mechanism of cell survival by ERK1/2 remains poorly elucidated in ischemic heart. Here we applied functional proteomics by two-dimensional electrophoresis to identify a cellular target of ERK1/2 in response to ischemic hypoxia. Approximately 1500 spots were detected by Coomassie Brilliant Blue staining of a sample from unstimulated cells. The staining intensities of at least 50 spots increased at 6-h reoxygenation after 2-h ischemic hypoxia. Of the 50 spots that increased, at least 4 spots were inhibited in the presence of PD98059, a MEK inhibitor. A protein with a molecular mass of 52 kDa that is strongly induced by ERK1/2 activation in response to ischemic hypoxia and reoxygenation was identified as ␣-enolase, a rate-limiting enzyme in the glycolytic pathway, by liquid chromatographymass spectrometry and amino acid sequencing. The expressions of the ␣-enolase mRNA and protein are inhibited during reoxygenation after ischemic hypoxia in the cells containing a dominant negative mutant of MEK1 and treated with a MEK inhibitor, PD98059, leading to a decrease in ATP levels. ␣-Enolase expression is also observed in rat heart subjected to ischemia-reperfusion. The induction of ␣-enolase by ERK1/2 appears to be mediated by c-Myc. The introduction of the ␣-enolase protein into the cells restores ATP levels and prevents cell death during ischemic hypoxia and reoxygenation in these cells. These results show that ␣-enolase expression by ERK1/2 participates in the production of ATP during reoxygenation after ischemic hypoxia, and a decrease in ATP induces apoptotic cell death. Furthermore, ␣-enolase improves the contractility of cardiomyocytes impaired by ischemic hypoxia. Our results reveal that ERK1/2 plays a role in the contractility of cardiomyocytes and cell survival through ␣-enolase expression during ischemic hypoxia and reoxygenation.
A water extract of licorice root inhibits granuloma angiogenesis in adjuvant-induced chronic inflammation (Phytother. Res., 5, 195. 1991). The present study has investigated the effects of licorice-derived compounds on granuloma angiogenesis. Isoliquiritin (0.31-3.1 mg/kg), a licorice-derived flavonoid, inhibited the carmine content of granuloma tissue 50-fold greater than licorice extract. Glyeyrrhizin (20-80 mg/kg), a licorice-derived saponin, inhibited carmine content with a weak potency. The licorice extract (0.01-1 mg/ml) also inhibited tube formation from vascular endothelial cells in a concentration-dependent manner. From the chemical structure-activities of used licorice-derived flavonoids (0.1-100 microM), their potencies for anti-tube formation were in the order isoliquiritigenin > isoliquiritin > liquiritigenin >> isoliquiritin-apioside. Glycyrrhizin (0.1-100 microM) and glycyrrhetinic acid (0.1-10 microM) increased tube formation. A glycyrrhizin (82 micrograms/ml)-induced increase in tube formation was inhibited by isoliquiritin. The combined effect of a mixture of 82 micrograms/ml glycyrrhizin and 4.2 micrograms/ml isoliquiritin, a similar concentration ratio to their yield ratio in the licorice extract, corresponded to the effect of 100 micrograms/ml extract. In conclusion, the anti-angiogenic effect of licorice extract depended on the anti-tube formation effect of isoliquiritin.
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