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Biomedical subjects

D Wu

Publications and source records attributed to D Wu.

At least 685 records · Page 38Linked to original sources
PubMed1975

The electrophysiological effects of ouabain on sinus node and atrium in man.

Electrophysiological studies were performed in 16 patients before and 30 min after intravenous administration of ouabain (0.1 mg/kg). P-A interval (mean+/-SEM) was 40+/-2.1 ms before and 44+/- 1.5 ms after ouabain (P less than 0.001). Atrial effective and functional refractory periods (ERP and FRP) were measured in all patients during sinus rhythm and during driving at equivalent paced rates in 12 patients. The mean atrial ERP and FRP during sinus rhythm were, respectively, 244+/-10.5 and 307+/-11.0 ms before and 253+/-9.7 and 318+/-11.4 ms after infusion of ouabain (NS). Mean atrial ERP and FRP during driving were, respectively, 231+/-15.3 and 264+/-14.9 ms before and 266+/-18.6 and 296+/-19.7 ms after ouabain (P less than 0.01 and P less than 0.01). Mean sinus cycle length and sinus recovery times were, respectively, 887+/-31.2 and 1,113+/-38.7 ms before and 905+/-38.2 and 1,008+/-30.7 ms after infusion of ouabain (NS and P less than 0.005). Calculated sinoatrial conduction times before and after ouabain were 90+/-6.8 and 110+/-8.5 ms, respectively (P less than 0.005). In summary, ouabain produced depression of intraatrial conduction as manifested by increase in P-A interval and atrial effective and functional refractory periods. Ouabain significantly increased calculated sinoatrial conduction time without significant effect on spontaneous sinus cycle length.

Adult↗
PubMed1975

P-A interval: lack of clinical, electrocardiographic and electrophysiologic correlations.

P-A interval is measured from the onset of the P wave to the onset of the low right atrial electrogram during His bundle recording. The significance of this interval was evaluated in 214 patients with intact A-V conduction and bundle branch block. One hundred fifty-eight patients had normal P-A (NPA) 27 +/- 9, mean +/- SD, and 56 had prolonged P-A (PPA). The NPA and PPA patients were similar (P greater than .10) in regard to sex, age, cardiac functional class, and P-R. PPA patients had significantly (P less than .05) greater P duration (mean +/- SEM, PPA vs NPA) 106 +/- 2 msec vs 100 +/- 1 msec), slower heart rates (72 +/- 2 vs 79 +/- 1), and longer sinus recovery times (1104 +/- 44 msec vs 980 +/- 38 msec). A-H was slightly shorter in PPA than in NPA patients suggesting that a systematic error in measruement of PA due to a relatively distal recording site may have been responsible for PA prolongation in some patients. Patients were prospectively followed for 16-56 months (mean 21.9 +/- 0.8 months). PPA was associated with only minor increase in P wave duration and decrease in sinus automaticity. PPA did not predict future occurrence of significant atrial dysrhythmia.

Arrhythmias, Cardiac↗
PubMed1975

New manifestations of dual A-V nodal pathways.

Electrophysiological studies with extrastimulus technique demonstrated evidence of dual A-V pathways in two patients with paroxysmal supraventricular tachycardia (PSVT). In case one, the second P of paced Wenckebach sequences was followed by two conducted QRS complexes without an intervening P wave. The A-H of the first and second QRS were consistent with the fast and slow pathway conduction times. The second QRS was followed by an atrial echo and PSVT, suggesting that the first pathway was available for retrograde propagation following the second QRS. In case two, PSVT was induced with atrial extrastimulus, followed by development of A-V dissociation. The two cases suggest the following conclusions: (1) dual A-V nodal pathways may allow the occurrence of double antegrade conduction of one P; (2) the atria are not necessary for A-V nodal circus movements in "dual pathway" A-V nodal reentrant PSVT.

Animals↗
PubMedDate not supplied

Assessment of cerebral blood flow reserve using functional magnetic resonance imaging.

Imaging of activated brain areas based on changes of blood deoxyhemoglobin levels is now possible with MRI. Acetazolamide (ACZ) increases cerebral blood flow (CBF) without changing cerebral oxygen consumption; this results in signal changes observed in gradient echo MR images from the areas with an increase in CBF. We assessed signal changes after ACZ application in seven healthy subjects with a conventional 1.5-T MRI scanner. The susceptibility-sensitized three-dimensional fast low-angle shot (FLASH) sequence was used to visualize signal changes induced by ACZ. We analyzed anatomic localization of different ranges of detected signal changes. ACZ caused significant signal changes in the gray matter and at the edge of the cerebral cortex, the latter corresponding to draining surface veins. No significant differences were seen among different brain areas within the same slice. Using the maximal intensity projection technique, we were able to partially separate signal changes originating in draining veins from signal originating in the gray matter microvasculature. Signal changes from the microvessels reflect cerebrovascular reserve. Blood-oxygen-level-dependent (BOLD) based MRI can evaluate CBF reserve with high spatial and temporal resolution. To assess cerebrovascular reserve, it is necessary to separate signal changes originating in large vessels from signal from brain microvasculature.

Acetazolamide↗
PubMedDate not supplied

CYP2E1-dependent toxicity and up-regulation of antioxidant genes.

Induction of cytochrome P450 2E1 (CYP2E1) by ethanol appears to be one of the central pathways by which ethanol generates a state of oxidative stress. Glutathione (GSH) is critical in preserving the proper cellular redox balance and for its role as a cellular protectant. The goal of the present study was to characterize the GSH homeostasis in human hepatocarcinoma cells (HepG2-E47 cells) that overexpress CYP2E1. Toxicity in the E47 cells was markedly enhanced after GSH depletion by buthionine sulfoximine (BSO) treatment. The antioxidant trolox partially prevented the apoptosis and necrosis, while diallylsulfide, a CYP2E1 inhibitor, was fully protective. Damage to mitochondria appears to play a role in the CYP2E1- and BSO-dependent toxicity. CYP2E1-overexpressing cells showed increases in total GSH levels, GSH synthetic rate and in gamma-glutamylcysteine synthetase (GCS) mRNA. This GCS increase was due to transcriptional activation of the GCS gene and could be blocked by certain antioxidants. Activity, protein and mRNA levels for other antioxidants such as catalase, alpha- and microsomal glutathione transferases were also increased in the E47 cells. Up-regulation of these antioxidant genes may reflect an adaptive mechanism to remove CYP2E1-derived oxidants. These oxidants are diffusable and were able to elevate collagen type I protein in a co-culture system consisting of the E47 cells + rat hepatic stellate cells. Such interactions between CYP2E1, mitochondria and altered GSH homeostasis, and elevation of collagen levels, may play a role in alcohol-induced liver injury.

Animals↗
PubMedDate not supplied

Low-amiloride-affinity Na+ channel in the epithelial cells isolated from the endolymphatic sac of guinea-pigs.

By using the whole-cell patch-clamp technique, an amiloride-sensitive Na+-selective conductance was found in epithelial cells from the endolymphatic sac (ES) epithelia of guinea-pigs. In the current-clamp configuration, the average resting membrane potential was -41.7+/-8.4 mV (n = 22). Application of amiloride at a concentration of 20 microM elicited a decrease in cation conductance that was responsible for a membrane hyperpolarization by 17.9+/-6.0 mV (n = 22). Substitution of N-methyl d-glucamine chloride (NMDG-Cl) for external NaCl led to a more significant membrane hyperpolarization by 28.4+/-8.3 mV (n = 22). At holding potential of -70 mV, amiloride and ethylisopropylamiloride (EIPA) blocked the inward current in a concentration-dependent manner over the range of concentrations of between 0.1 microM and 50 microM, with an inhibitory constant (Ki) of 1.3+/-0.4 microM (n = 7) and 1.5+/-0.3 microM (n = 5), respectively. In the voltage-clamp configuration, substitution of NMDG-Cl for external NaCl significantly reduced the inward current (n = 9), indicating that the whole-cell conductance has a high permeability for Na+. Superfusion with 20 microM amiloride induced a significant reduction of the inward current, shifted the reversal potential from -39.4+/-8.8 mV to -60.4+/-10.5 mV (n = 12), and decreased the inward conductance from 5.0+/-1.3 nS to 3.7+/-1.5 nS (n = 12). The permeability ratio of Na+ over K+, calculated from the difference in reversal potential between the currents before and after application of amiloride, was approximately 5:1. Additionally, the conductance was not activated by application of forskolin, 3-isobutyl-1-methylxanthine (IBMX) and 8-bromo-cAMP (8-Br-cAMP). These findings suggest that a low-amiloride-affinity Na+ channel localized in the ES epithelial cells may be involved in uptake of Na+ in the ES.

Amiloride↗