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B W Wu

Publications and source records attributed to B W Wu.

29 records · Page 2Linked to original sources
PubMed1989

[Effects of arginine aspirin on changes in effective refractory period and ventricular fibrillation threshold of ischemic myocardium in rabbit].

The effects of arginine aspirin (AAs) on the effective refractory period (ERP) and ventricular fibrillation threshold (VFT) of ischemic ventricular muscle were observed in 24 anesthetized open-chest rabbits. that the platelet aggregation rate was shown to be increased by 11 +/- 5%, and VFT decreased by 24 +/- 3 mA at 50 min after coronary occlusion. Compared with values at 10 min postocclusion, ERP of ventricular muscle in border ischemic zone (BIZ) and central ischemic zone (CIZ) was shortened by 20 +/- 10% and prolonged by 35 +/- 22 ms, respectively, and dispersions of ERP between CIZ and BIZ were increased by 52 +/- 17 ms, compared with control values, (p less than 0.01). By giving an intravenous injection of AAs at 0.5 h before coronary occlusion, changes in parameters as mentioned above were obviously relieved as compared with the same parameters in the group of simple coronary occlusion at 50 min postocclusion, (p less than 0.01). These results suggest that AAs may inhibit platelet aggregation, reduce dispersions of ERP and elevate VFT after coronary occlusion.

Animals↗
PubMed1986

Effect of the 17- and 23-kilodalton polypeptides, calcium, and chloride on electron transfer in photosystem II.

Electron paramagnetic resonance (EPR) measurements were performed on photosystem II (PSII) membranes that were treated with 2 M NaCl to release the 17- and 23-kilodalton (kDa) polypeptides. By using 75 microM 3-(3,4-dichlorophenyl)-1,1-dimethylurea to limit the photosystem II samples to one stable charge separation in the temperature range of 77-273 K, we have quantitated the EPR signals of the several electron donors and acceptors of photosystem II. It was found that removal of the 17- and 23-kDa polypeptides caused low potential cytochrome b559 to become fully oxidized during the course of dark adaptation. Following illumination at 77-130 K, one chlorophyll molecule per reaction center was oxidized. Between 130 and 200 K, both a chlorophyll molecule and the S1 state were photooxidized and, together, accounted for one oxidation per reaction center. Above 200 K, the chlorophyll radical was unstable. Oxidation of the S1 state gave rise to the S2-state multiline EPR signal, which arises from the Mn site of the O2-evolving center. The yield of the S2-state multiline EPR signal in NaCl-washed PSII membranes was as high as 93% of the control, untreated PSII membranes, provided that both Ca2+ and Cl- were bound. Furthermore, the 55Mn nuclear hyperfine structure of the S2-state multiline EPR signal was unaltered upon depletion of the 17- and 23-kDa polypeptides. In NaCl-washed PSII samples where Ca2+ and/or Cl- were removed, however, the intensity of the S2-state multiline EPR signal decreased in parallel with the fraction of PSII lacking bound Ca2+ and Cl-.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium↗
PubMedDate not supplied

Effects of dopexamine hydrochloride on calcium channels in isolated guinea pig ventricular myocytes.

The mechanisms responsible for the cardiac positive inotropic effects of dopexamine hydrochloride, a combined dopamine receptor agonist at both D1-receptors and beta 2-adrenoceptors, were studied. The calcium channel currents were recorded using whole-cell patch clamp technique in isolated guinea pig ventricular myocytes. At a holding potential of -40 mV, cells were depolarized to 0 mV for 400 ms at a frequency of 0.2 Hz. Dopexamine hydrochloride at doses of 5, 50 and 100 microM increased the verapamil-sensitive Ca2+ inward current by 109, 147 and 194%, respectively. The effects of dopexamine hydrochloride on Ca2+ current reached its maximum at 5 min and partially recovered after washout of the drugs. The increased Ca2+ current induced by dopexamine hydrochloride was completely inhibited by 20 microM propranolol, a beta-adrenoceptor antagonist, and was not antagonized by 20 microM of SCH23390, a highly selective D1-receptor antagonist. These results suggest that the cardiac positive inotropic effects of dopexamine hydrochloride are brought about by the increase of Ca2+ current via stimulation of beta 2-adrenoceptors.

Adrenergic beta-Agonists↗