Three minute, but not one minute, ischemia and nicorandil have a preconditioning effect in patients with coronary artery disease

AbstractOBJECTIVESThis study focused on 1) the determination of the optimal preconditioning (PC) duration, and 2) the protective effect of nicorandil (NC), a hybrid nitrate with a Katpchannel opening effect, during a percutaneous transluminal coronary angioplasty (PTCA) model in humans.BACKGROUNDThe ischemic PC effect is induced in 180 s ischemia, but not in 120 s ischemia in rabbit hearts. However, the duration of ischemia that induces PC effect and the role of the Katpchannel in the PC effect in humans are still unclear.METHODSForty-six patients with stable angina were randomly allocated to four groups: the duration of the first inflation as PC ischemia was 60 s in the PC60 group (n = 12), and 180 s in the PC180 group (n = 12). In the other groups, NC (80 μg/kg) was intravenously given for 1 min in the NC group (n = 12), and isosorbide dinitrate (ISDN) (40 μg/kg) was given in the ISDN group (n = 10). Five minutes after first inflation or drug administration, a second inflation was conducted for 120 s in each group. In the ECG, the lead with the largest shift in ST segment (deltaST max), and the sum of elevated ST levels in all leads (sigmaST) were determined.RESULTSIn the PC60 group, no significant difference was observed in either deltaST max or sigmaST between the first and second inflation. However, the second inflation in the PC180 group showed significantly lower levels of deltaST max and sigmaST compared with those of the first inflation. In the NC group, both deltaST max and sigmaST measured at 30 s and 60 s after balloon inflation were significantly lower than those of the first inflation in the PC60 and PC180 control groups. In the ISDN group, no significant difference was observed in deltaST max or sigmaST.CONCLUSIONIn human PTCA models, a PC effect is observed in 180 s ischemia, but not in 60 s ischemia. A pharmacological PC effect is induced by NC, a Katpchannel opener with a nitrate-like effect but not ISDN. This suggests that the opening of Katpchannels plays an important role in the protecting effect of NC

Application of coastal acoustic tomography: calibration of open boundary conditions on a numerical ocean model for tidal currents

Coastal acoustic tomography (CAT), which measures path-averaged currents from reciprocal acoustic transmission experiments and reconstructs velocity fields from the multiple path-averaged current data, is useful for monitoring tidal currents in coastal shallow water, especially if data assimilation is employed. Previous CAT data assimilation studies have focused on state estimation problems, i.e., the reconstruction of tidal currents and following dynamical discussion. In this study, we investigate the use of path-averaged currents in a boundary control problem. Specifically, we aim to use the observed path-averaged currents to determine the parameters of a numerical ocean model, which were tidal amplitudes and phases as the open boundary conditions in this study. We investigate two methods: using the ensemble Kalman filter (EnKF) results and a linearization approach called model Green’s function method. Both calibration methods decreased the amplitudes of tidal constituents at the open boundaries. We compare the model performance between the model predictions with and without the calibration of the open boundary conditions. The model predictions with the calibrated open boundary conditions improved the agreement with the observed path-averaged current. We also implemented the sequential updates of EnKF with the two calibrated open boundary conditions. The EnKF results with the independently calibrated two open boundary conditions improved the agreement with the comparison data obtained by acoustic Doppler current profiler measurement compared with the original EnKF result with the initial open boundary conditions

NONINVASIVE ESTIMATION OF CARDIAC PROPERTIES IN PATIENTS WITH HYPERTENSION USING SPECKLE TRACKING ECHOCARDIOGRAPHY: A COMPARATIVE STUDY BETWEEN GOOD AND POOR CONTROLLED HYPERTENSION

info:eu-repo/semantics/publishe

P-selectin inhibition prevents early neutrophil activation but provides only modest protection against myocardial injury in dogs with ischemia and forty-eight hours reperfusion

OBJECTIVES This study was designed to determine whether antibody neutralization of the adhesion protein P-selectin would prevent neutrophil activation and reduce myocardial reperfusion injury. BACKGROUND Although inhibition of P-selectin markedly reduces short-term myocardial injury after ischemia and reperfusion, it is unknown whether it can provide meaningful long-term protection and preserve left ventricular function. METHODS Closed-chest dogs underwent 90 min left anterior descending coronary artery occlusion and 48 h reperfusion, and were randomized to 1) a treatment group (n = 11) receiving 1 mg/kg of the blocking anti–P-selectin antibody PB1.3, or 2) a control group receiving 1 mg/kg PNB1.6 (nonblocking antibody against P-selectin, n = 7) or an equivalent volume of saline (n = 2) 10 min before reperfusion. Infarct size was assessed postmortem by triphenyl tetrazolium chloride staining. Contrast left ventriculography was used to measure left ventricular function. Activation of circulating polymorphonuclear neutrophils (PMNs) was assessed by an increase in surface CD18 expression. RESULTS Neutrophil activation was observed at 30 min after reperfusion in the control group, but was abolished in the treatment group. Infarct size was reduced about 25% in the treatment group after controlling for variations in ischemic blood flow (p = 0.003, by analysis of covariance). However, this protective effect was not associated with preservation of blood flow to the ischemic–reperfused myocardium, nor with any improvement in global or regional left ventricular function. CONCLUSIONS The anti–P-selectin antibody PB1.3 prevented early PMN activation, but had only a modest long-term infarct-limiting effect over 48 h reperfusion. Adhesion molecules other than P-selectin may mediate delayed PMN activation and accumulation in reperfused myocardium