AIM: To study the changes of portal blood flow in congestive heart failure. METHODS: We studied the congestion index (CI) and portal vein pulsatility index (PI) in patients with varied degrees of congestive hear...AIM: To study the changes of portal blood flow in congestive heart failure. METHODS: We studied the congestion index (CI) and portal vein pulsatility index (PI) in patients with varied degrees of congestive heart failure using ultrasonic Doppler. Ten patients with mean right atrial pressure (RA) 〈10 mmHg were classified as group 1 and the remaining 10 patients with RA〉 10 mmHg as group 2. RESULTS: There were no difference on cardiac index (HI, P= 0.28), aortic pressure (AO, P= 0.78), left ventricular end-diastolic pressure (LVED, P=0.06), maximum portal blood velocity (Vmax, P= 0.17), mean portal blood velocity (Vmean, P=0.15) and portal blood flow volume (PBF, P= 0.95) between the two groups. Group 2 patients had higher pulmonary wedge pressure (PW, 29.9 ± 9.3 mmHg vs 14.6±7.3 mmHg, P=0.002), pulmonary arterial pressure (PA, 46.3± 13.2 mmHg vs 25.0±8.2 mmHg, P=0.004), RA (17.5±5.7 mmHg vs 4.7±2.4 mmHg, P〈 0.001), right ventricular end-diastolic pressure (RVED, 18.3±5.6 mmHg vs 6.4±2.7 mmHg, P〈0.001), CI (8.7±2.4 vs 5.8± 1.2, P=0.03), and PI (87.8±32.3% vs 27.0±7.4%, P〈0.001) than Group 1. CI was correlated with PI (P〈0.001), PW (P〈0.001), PA (P〈0.001), RA (P=0.043), RVED (P=0.005), HI (P〈0.001), AO (P〈0.001), CO (P〈0.001), LVED (P〈0.001), Vmax (P〈0.001), Vmax (P〈0.001), cross-sectional area of the main portal vein (P〈0.001) and PBF (P〈0.001). CI could be as high as 8.3 in patients with RA〈 10 mmHg and as low as 5.9 in those with RA≥10 mmHg.CONCLUSION: Our data show that RI is a more significant indicator than CI in the clinical evaluation of high RA≥ 10 mmHg, whereas CI is better than PI in the assessment of left heart function.展开更多
AIM:To explore the role of prostaglandin F2α(PGF2α) on pacemaker activity in interstitial cells of Cajal(ICC)from mouse small intestine. METHODS:In this study,effects of PGF2αin the cultured ICC cells were in...AIM:To explore the role of prostaglandin F2α(PGF2α) on pacemaker activity in interstitial cells of Cajal(ICC)from mouse small intestine. METHODS:In this study,effects of PGF2αin the cultured ICC cells were investigated with patch clamp technology combined with Ca 2+ image analysis. RESULTS:Externally applied PGF2α(10μmol/L)produced membrane depolarization in current-clamp mode and increased tonic inward pacemaker currents in voltage-clamp mode.The application of flufenamic acid(a non-selective cation channel inhibitor)or niflumic acid(aCl channel inhibitor)abolished the generation of pacemaker currents but only flufenamic acid inhibited the PGF2α-induced tonic inward currents.In addition,the tonic inward currents induced by PGF2αwere not inhibited by intracellular application of 5’-[-thio]diphosphate trilithium salt.Pretreatment with Ca 2+ free solution, U-73122,an active phospholipase C inhibitor,and thapsigargin,a Ca 2+ -ATPase inhibitor in endoplasmic reticulum,abolished the generation of pacemaker currents and suppressed the PGF2α-induced tonic inward currents.However,chelerythrine or calphostin C,protein kinase C inhibitors,did not block the PGF2α-induced effects on pacemaker currents.When recording intracellular Ca 2+ ([Ca 2+ ]i)concentration using fluo-3/AM,PGF2α broadly increased the spontaneous[Ca 2+ ]i oscillations. CONCLUSION:These results suggest that PGF2αcan modulate pacemaker activity of ICC by acting non-selective action channels through phospholipase C-dependent pathway via[Ca2+]i regulation展开更多
基金Supported by the grant from the Cathay Groups,Taipei,Taiwan,China
文摘AIM: To study the changes of portal blood flow in congestive heart failure. METHODS: We studied the congestion index (CI) and portal vein pulsatility index (PI) in patients with varied degrees of congestive heart failure using ultrasonic Doppler. Ten patients with mean right atrial pressure (RA) 〈10 mmHg were classified as group 1 and the remaining 10 patients with RA〉 10 mmHg as group 2. RESULTS: There were no difference on cardiac index (HI, P= 0.28), aortic pressure (AO, P= 0.78), left ventricular end-diastolic pressure (LVED, P=0.06), maximum portal blood velocity (Vmax, P= 0.17), mean portal blood velocity (Vmean, P=0.15) and portal blood flow volume (PBF, P= 0.95) between the two groups. Group 2 patients had higher pulmonary wedge pressure (PW, 29.9 ± 9.3 mmHg vs 14.6±7.3 mmHg, P=0.002), pulmonary arterial pressure (PA, 46.3± 13.2 mmHg vs 25.0±8.2 mmHg, P=0.004), RA (17.5±5.7 mmHg vs 4.7±2.4 mmHg, P〈 0.001), right ventricular end-diastolic pressure (RVED, 18.3±5.6 mmHg vs 6.4±2.7 mmHg, P〈0.001), CI (8.7±2.4 vs 5.8± 1.2, P=0.03), and PI (87.8±32.3% vs 27.0±7.4%, P〈0.001) than Group 1. CI was correlated with PI (P〈0.001), PW (P〈0.001), PA (P〈0.001), RA (P=0.043), RVED (P=0.005), HI (P〈0.001), AO (P〈0.001), CO (P〈0.001), LVED (P〈0.001), Vmax (P〈0.001), Vmax (P〈0.001), cross-sectional area of the main portal vein (P〈0.001) and PBF (P〈0.001). CI could be as high as 8.3 in patients with RA〈 10 mmHg and as low as 5.9 in those with RA≥10 mmHg.CONCLUSION: Our data show that RI is a more significant indicator than CI in the clinical evaluation of high RA≥ 10 mmHg, whereas CI is better than PI in the assessment of left heart function.
基金Supported by Research Fund from Chosun Hospital 2008
文摘AIM:To explore the role of prostaglandin F2α(PGF2α) on pacemaker activity in interstitial cells of Cajal(ICC)from mouse small intestine. METHODS:In this study,effects of PGF2αin the cultured ICC cells were investigated with patch clamp technology combined with Ca 2+ image analysis. RESULTS:Externally applied PGF2α(10μmol/L)produced membrane depolarization in current-clamp mode and increased tonic inward pacemaker currents in voltage-clamp mode.The application of flufenamic acid(a non-selective cation channel inhibitor)or niflumic acid(aCl channel inhibitor)abolished the generation of pacemaker currents but only flufenamic acid inhibited the PGF2α-induced tonic inward currents.In addition,the tonic inward currents induced by PGF2αwere not inhibited by intracellular application of 5’-[-thio]diphosphate trilithium salt.Pretreatment with Ca 2+ free solution, U-73122,an active phospholipase C inhibitor,and thapsigargin,a Ca 2+ -ATPase inhibitor in endoplasmic reticulum,abolished the generation of pacemaker currents and suppressed the PGF2α-induced tonic inward currents.However,chelerythrine or calphostin C,protein kinase C inhibitors,did not block the PGF2α-induced effects on pacemaker currents.When recording intracellular Ca 2+ ([Ca 2+ ]i)concentration using fluo-3/AM,PGF2α broadly increased the spontaneous[Ca 2+ ]i oscillations. CONCLUSION:These results suggest that PGF2αcan modulate pacemaker activity of ICC by acting non-selective action channels through phospholipase C-dependent pathway via[Ca2+]i regulation