Hepatic venous outflow obstruction during hepatic resection diagnosed by transesophageal echocardiography.
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Aged↗
Biomedical subjects
Y Kang
Publications and source records attributed to Y Kang.
Spatiotemporally differential inhibition of pyramidal cells in the cat motor cortex.
1. The spatiotemporal pattern of inhibition in the cat motor cortex was studied in in vitro slice preparations in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and 2-amino-5-phosphonovaleric acid (APV). 2. After intracortical microstimulation (0.5-6 microA), fast and slow inhibitory postsynaptic potentials (IPSPs) were produced in layers II-VI pyramidal cells and selectively reduced with bicuculline methiodide and phaclofen, respectively. 3. Fast IPSPs were maximally produced by stimulation of the same layer where their cell bodies were located, and they decreased in amplitude as the more superficial layer was stimulated. In contrast, slow IPSPs were maximally produced by stimulation of layer II regardless of the location of the recorded pyramidal cell and decreased in amplitude as the deeper layer was stimulated. 4. The reduction of amplitude of fast IPSPs, in response to a vertical shift of the stimulation site toward more superficial layers, was always correlated with an increase in rise time and with a shift of the reversal potential to a more hyperpolarized level. 5. When the stimulation site was moved horizontally to the more lateral site, fast IPSPs increased in latency and decreased in amplitude gradually without appreciable changes in rise time. Fast IPSPs could be evoked from horizontally remote sites of up to 800-1,200 microns. 6. Inhibitory interneurons, which are responsible for evoking fast IPSPs, appear to be distributed through almost all layers to send horizontally spreading parallel axons making synaptic contacts at different electrotonic distances along apical dendrites of single pyramidal cells. 7. Horizontal spreads were much less in slow IPSPs (< 340-680 microns). The time-to-peak of slow IPSPs produced in layer V pyramidal cells (159.5 +/- 6.8 ms, mean +/- SD, n = 10) was significantly (P < 0.0001) longer than that in layers II and III pyramidal cells (128.5 +/- 7.5 ms, n = 7). Asymmetric reversal properties of slow IPSPs were seen, suggesting the spatial dispersion of synaptic inputs along apical dendrites of pyramidal cells. 8. In layer V pyramidal cells, the time-to-peak of slow IPSPs decreased with increasing membrane hyperpolarization, indicating that the later portion of slow IPSPs was more sensitive to the membrane-potential change than the early portion. This further indicates that the late portion of slow IPSPs is generated at synapses on the more proximal dendrite of pyramidal cells than the early portion, contrary to that expected from the Rall's model of passive dendrite under the condition of synchronous inputs.(ABSTRACT TRUNCATED AT 400 WORDS)
2-Amino-5-phosphonovalerate↗
Electrophysiological and morphological characteristics of layer VI pyramidal cells in the cat motor cortex.
1. Intracellular recordings were made from layer VI pyramidal cells in in vitro slice preparations of the cat motor cortex (area 4 gamma). Layer VI pyramidal cells were identified morphologically by intracellular injection of biocytin. 2. Of 22 layer VI pyramidal cells examined, single action potentials were followed by depolarizing afterpotentials (DAP) in 9 cells, but were not followed by DAP in the remaining 13 cells. The amplitude of DAP was 3.4 +/- 1.4 mV (mean +/- SD, n = 9) when measured from the negative peak of fast afterhyperpolarization to the peak of DAP. 3. In response to depolarizing current pulses with a duration of 300-400 ms, pyramidal cells showing DAP displayed a train of action potentials in a phasic-tonic pattern without any appreciable adaptation in the tonic firing, whereas pyramidal cells lacking DAP exhibited a weak adaptation after phasic firing. Anomalous rectification was seen in both pyramidal cells showing DAP and those lacking DAP. 4. Repetitive doublet or triplet spiking was induced in DAP-showing pyramidal cells in response to a depolarizing current pulse after injecting strong depolarizing current pulses of 400 ms duration at 1 Hz for 30-60 s, but was never induced in DAP-lacking pyramidal cells. Doublet/triplet spiking lasted 5-10 min and returned to the original single spiking. An application of CsCl induced a burst firing in DAP-showing pyramidal cells. 5. In the nine pyramidal cells showing DAP, seven cells had shorter apical dendrites that arborized extensively at layer V and terminated in the middle part of layer III. In the 13 pyramidal cells lacking DAP, 11 cells had longer apical dendrites that arborized less frequently and extended into layer II or I. Main axons could be traced into the deep white matter in 17 of the 22 layer VI pyramidal cells examined. 6. Ascending recurrent axon collaterals were more prominent in pyramidal cells with longer apical dendrites than in pyramidal cells with shorter apical dendrites. The terminal bouton-like swelling observed along the recurrent axon collaterals arising from the pyramidal cells with longer apical dendrite were distributed most densely at the level between the bottom part of layer III and the top part of layer V. In contrast, those arising from the pyramidal cells with shorter apical dendrite were distributed mainly at the levels of layers V and VI.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Cerebral hemodynamic and metabolic changes in fulminant hepatic failure: a retrospective study.
The purpose of this retrospective study was to determine cerebral hemodynamic and metabolic changes in comatose patients with fulminant hepatic failure. Computerized tomography of the brain and cerebral blood flow measurements by the xenon-computerized tomography scan or intravenous xenon-133 methods were obtained in 33 patients with fulminant hepatic failure. In a subgroup of 22 patients, arteriojugular venous oxygen content difference and cerebral metabolic rate for oxygen were determined. Carbon dioxide reactivity was tested in 17 patients, and intracranial pressure was recorded by an epidural monitor in 8 patients. Cerebral blood flow and arteriojugular venous oxygen content difference were adjusted to the average arterial carbon dioxide pressure of the sample (32 mm Hg). Adjusted cerebral blood flow varied from 16.5 to 94.7 ml/100 gm/min; 52% of the patients had reduced adjusted cerebral blood flows (less than 33 ml/100 gm/min), whereas 24% had hyperemic values (greater than 50 ml/100 gm/min). Patients with higher adjusted cerebral blood flows showed cerebral swelling on computerized tomography scan (p < 0.002), were in deeper coma (p < 0.05) and had greater mortality (p < 0.002). The adjusted arteriojugular venous oxygen content difference was negatively correlated with adjusted cerebral blood flow (r = -0.61, p < 0.002). The majority of patients with reduced adjusted cerebral blood flows had low adjusted arteriojugular venous oxygen content differences (less than 5 vol%), indicating hyperemia rather than ischemia. The average cerebral metabolic rate for oxygen was 50% of normal (1.6 +/- 0.4 ml/100 gm/min); even patients with low cerebral metabolic rates for oxygen recovered neurologically.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Biochemical characterization of a mitomycin C resistant colon cancer cell line variant.
Resistance may limit the clinical usefulness of a variety of chemotherapeutic drugs including mitomycin C (MMC). The MMC-sensitive HT-29 colon cancer cell line and its MMC-resistant subline, HT-29R13, were studied in vitro under aerobic conditions to help characterize the mechanisms associated with MMC resistance. HT-29R13 cells exhibit approximately 2-fold resistance to MMC compared with HT-29 cells and lack the typical multidrug-resistance pattern; resistance is stable in the absence of drug exposure. Levels of glutathione (GSH) and total glutathione-S-transferase (GST) activity were not different between the two cell lines; however, levels of GSH reductase and GSH peroxidase were increased significantly in HT-29R13. Although total GST activity was unchanged, GST-pi and GST-alpha isoenzyme expression as measured using western blot were increased significantly in HT-29R13 compared with HT-29. DT-diaphorase levels and topoisomerase II activity were decreased significantly in HT-29R13. Both cell lines had equal P-glycoprotein expression. Multiple drug resistance mechanisms are present in HT-29R13 including decreased drug activation (decreased DT-diaphorase), increased drug detoxification (increased GST-pi and GST-alpha, GSH reductase, GSH peroxidase), and decreased accessibility of DNA targets (decreased topoisomerase II). Further work will be necessary to determine the degree to which each of these mechanisms contribute to MMC resistance in this model.
ATP Binding Cassette Transporter, Subfamily B, Mem↗
Perimeter-maximum-diameter method for measuring the fractal dimension of a fractured surface.
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Journal Article↗
Modulatory effects of tamoxifen and recombinant human alpha-interferon on doxorubicin resistance.
Doxorubicin (DOX) resistance is frequently due to the multidrug resistance gene product P-glycoprotein. This study examined the effects of two biochemical modulators, recombinant human alpha-interferon (IFN-alpha) and tamoxifen (TAM), on the DOX sensitivity, DOX retention, and P-glycoprotein expression of the multidrug-resistant Chinese hamster ovary cell line ChR C5 and the parent AuX B1 cell line. In the absence of either modulator, the 50% inhibitory concentration for DOX after 1-h incubation as determined using a microculture tetrazolium assay was 8.3 microM in ChR C5 cells and 0.4 microM in AuX B1 cells. In ChR C5 cells, IFN-alpha (500 units/ml) for 24 h had no affect on DOX cytotoxicity, but tamoxifen (1.0 microM) for 24 h enhanced DOX cytotoxicity with the 50% inhibitory concentration decreased by 2-fold to 4.2 microM. A combination of IFN-alpha (500 units/ml) for the initial 24 h followed by TAM (1.0 microM) for another 24 h was even more effective in ChR C5 cells with the DOX 50% inhibitory concentration decreased by 4-fold to 2.1 microM. The combination IFN-alpha and TAM dramatically increased DOX accumulation in the resistant ChR C5 cells without significantly affecting P-glycoprotein expression as measured using flow cytometric analysis. IFN-alpha and/or TAM had no effect on DOX cytotoxicity or accumulation in parent DOX-sensitive AuX B1 cells. Both cell lines were estrogen and progesterone receptor negative. These data indicate that synergism between IFN-alpha and TAM may partially reverse DOX resistance and may potentially be useful in enhancing the clinical effectiveness of DOX.
ATP Binding Cassette Transporter, Subfamily B, Mem↗
Development of a recombinant RNA technique for the construction of chimeric RNA with a long poly(C) tract.
The murine cardioviruses and bovine aphthoviruses are distinguished from other (+) strand RNA viruses by their long poly(C) tract in the 5'-noncoding region. The presence of this poly(C) tract has long hampered the construction of full-length cDNA with the complete poly(C) tract, because long poly(dC-dG) homopolymer-containing plasmids are difficult to amplify in bacterial systems. To overcome this problem, we constructed a chimeric RNA by joining the poly(C) region of the viral RNA to the 5'-truncated RNA transcript of the encephalomyocarditis (EMC) virus cDNA. The non-chimeric, recombinant EMC virus with a short poly(C) tract produces recombinant progeny virus, but this is not pathogenic in vivo. On the other hand, the EMC viral RNA chimera with the complete poly(C) tract produces recombinant progeny virus that is pathogenic in vivo. This method of viral RNA construction will be invaluable for functional studies of other cardioviruses and aphthoviruses, as well as for recombinant RNA manipulations.
Animals↗
The relationship of systemic hemodynamics and oxygen consumption to early allograft failure after liver transplantation.
The early postoperative hemodynamic data of 88 patients who underwent primary liver transplantation between July 1989 and October 1990 at the University Health Center of Pittsburgh were analyzed to establish the relationship of systemic hemodynamics and oxygen consumption to perioperative allograft function. The 15 patients whose allografts failed within the 1st month following transplantation were designated as group 1, while 73 patients who retained adequate graft function constituted group 2. Although the cardiac index and oxygen delivery did not differ significantly between the groups, group 1 consistently demonstrated a lower mean arterial pressure, oxygen consumption, arteriovenous oxygen content difference, and arterial ketone body ratio. The etiology of reduced oxygen consumption in group 1 patients is speculative, but the data support the notion that oxygen consumption is a useful, predictive indicator for liver allograft function after transplantation.
Adolescent↗
Development and initial characterization of a mitomycin C-resistant colon cancer cell line variant.
Resistance may limit the clinical usefulness of a variety of chemotherapeutic drugs, including mitomycin C (MMC). In order to study resistance to MMC, a variant of the HT-29 human colon cell line was isolated by exposure to repeated doses of MMC. The 95% inhibitory concentration of MMC for this isolate (HT-29R13) was found to be approximately twice that for the parent line. The level of resistance did not increase with additional drug exposure, and resistance was stable for at least 6 months in the absence of drug exposure. HT-29R13 cells exhibit cross-resistance to melphalan and 5-FU but not to doxorubicin, cis-platinum, or etoposide. HT-29R13 cells are characterized by slightly decreased plating efficiency and slightly increased total protein compared with the parent line. This model of stable, low-level MMC resistance with an unusual cross-resistance pattern may prove useful for the study and characterization of MMC resistance mechanisms.
Cell Cycle↗
Calcium spike underlying rhythmic firing in dopaminergic neurons of the rat substantia nigra.
In order to study a possible mechanism for rhythmic firing of dopaminergic (DA) neurons, intracellular recordings were obtained from 56 rhythmically firing DA neurons in the rat substantia nigra compacta (SNc), using in vitro slice preparations. In the presence of TTX, spontaneous oscillation of the membrane potential was induced in SNc DA neurons when the membrane potential was depolarized more positive from -60 to -40 mV. Each oscillation wave was characterized by a pacemaker-like slow depolarization (PLSD) followed by a relatively prompt repolarization. As the DC depolarization was increased from -60 to -40 mV, the oscillation frequency increased from 0.5 to 5 Hz, but the amplitude of the wave decreased. Of 17 neurons tested in the presence of TTX, the maximum amplitudes of the oscillation varied from 10-15 mV in 8 neurons and were less than 5 mV in 9 neurons. In those 9 neurons, an application of TEA greatly enhanced (up to 15 mV) the amplitude of oscillation. The oscillation ceased when the membrane was hyperpolarized more negative than -60 mV. At the membrane potential more negative than -60 mV in the presence of TTX an injection of a depolarizing current pulse could evoke PLSD which was an all-or-nothing regenerative spike potential. The rate of rise of the PLSD changed depending on the intensity of injected current pulses but their amplitude remained constant. Its time-to-peak was slow (up to 1400 ms), while the decay time was relatively brief (< 500 ms). The threshold membrane potential for evoking PLSD was -53.7 +/- 3.2 mV (n = 10). This was higher than the previously reputed threshold for low threshold Ca2+ spike (LTS) (< -60 mV) and lower than that for high threshold Ca2+ spike (HTS) (> -35 mV) in SNc DA neurons. Even at a holding potential of -45 mV, a depolarizing current pulse could trigger PLSD while LTS was completely inactivated. Cd2+ (0.4 mM) abolished the oscillation and PLSD without marked effects on the LTS (n = 6). A low Ca2+ and high Mg2+ Ringer's solution also abolished the oscillation and PLSD (n = 4). An intracellular injection of EGTA markedly prolonged the decay time course of PLSD characterized by a slow and a relatively fast falling phase (n = 5). This would suggest an involvement of Ca(2+)-dependent K+ conductance and/or Ca2+ dependent inactivation of Ca2+ conductance during repolarization.(ABSTRACT TRUNCATED AT 400 WORDS)
Action Potentials↗
A whole cell patch-clamp study on the pacemaker potential in dopaminergic neurons of rat substantia nigra compacta.
A whole-cell patch-clamp recording was obtained from dopamine (DA) neurons (n = 68) in the substantia nigra compacta (SNc) in in vitro slice preparations in order to study the underlying current for pacemaker-like slow depolarization (PLSD) which was considered as a basis for rhythmic firing of DA neurons. SNc DA neurons were identified immunohistochemically after recording. Results demonstrated that: (1) Under current clamped condition in the presence of TTX, DA neurons (n = 5) displayed the oscillation of membrane potential with high threshold spikes. An application of a hyperpolarizing and depolarizing current pulse (at the membrane potential where oscillation was no longer seen) induced a prominent anomalous rectification and pacemaker-like slow depolarization (PLSD), respectively. (2) Under voltage-clamped conditions in the presence of TTX, a command pulse positive to -50 mV from a holding potential of -80 mV induced a persistent Ca2+ current which was usually preceded by either a transient K+ (n = 7) or a transient Ca2+ (n = 4) current recorded with a patch pipette containing potassium gluconate (145 mM). (3) When outward currents were suppressed by 140 mM CsCl and 10 mM EGTA intercellularly applied through the patch pipette, a command pulse positive to -50 to -40 mV induced either a persistent Ca2+ current alone (n = 4) or a persistent Ca2+ current preceded by a transient Ca2+ current (n = 11). (4) The threshold for activation of the persistent Ca2+ current (Ip) was around -60 to -55 mV. The amplitude of Ip produced by a command pulse stepped to -50 mV from a holding potential of -80 mV was -78 +/- 42 pA (n = 23). (5) The threshold for activation of transient Ca2+ current (IT) was around -70 to -65 mV and inactivated completely at -70 to -65 mV (n = 11). The peak amplitude of IT evoked at -60 to -55 mV from a holding potential of more negative than -80 mV was 489 +/- 170 pA (n = 11). (6) The decay time constant of IT was 28 +/- 12 ms at -60 mV (n = 8) and that of IP was 2.35 +/- 1.37 s at -50 mV (n = 11) when recorded with a pipette containing 10 mM EGTA and 140 mM CsCl. (7) The decay of IP was apparently accelerated by decreasing the concentration of EGTA in the pipette solution from 10 to 1 mM.(ABSTRACT TRUNCATED AT 400 WORDS)
Amplifiers, Electronic↗
Postreperfusion syndrome: hypotension after reperfusion of the transplanted liver.
Sixty-nine patients undergoing liver transplantation were evaluated to elucidate the relationship between hypotension and physiological changes seen on reperfusion of the grafted liver. Measured variables included hemodynamic profiles, core temperature, serum potassium, ionized calcium levels, arterial blood-gas tensions, and acid-base state. Measurements were taken 60 minutes after skin incision (baseline), 5 minutes before reperfusion, and 30 seconds and 5 minutes after reperfusion. On the basis of changes in mean arterial pressure (MAP) patients were divided in two groups. Group 1 (n = 49) maintained MAP greater than 70% and group 2 (n = 20) had MAP less than 70% of the baseline value for at least 1 minute within 5 minutes after reperfusion. On reperfusion, changes common to both groups were 27% increase in cardiac filling pressures, 23% base deficit, and 30% serum potassium level and a decrease of 16% in cardiac output and 9% in temperature. Compared with group 1, group 2 had greater decrease in systemic vascular resistance (SVR) (1097 +/- 868 and 741 +/- 399 dyn.s-1. cm-5, respectively, P < .05) and higher potassium level (4.5 +/- 0.8 and 5.3 +/- 0.8 mmol/L, P < .05). Collectively in both groups, there was no correlation between MAP and physiological variables; however, there was a poor correlation with SVR (r = .32, P < .01). Reperfusion hypotension seen in group 2 patients correlated only with a decrease in systemic vascular resistance (r = .5, P < .05). Acute hyperkalemia, hypothermia, and acidosis do not appear to be major causes of reperfusion hypotension.
Adult↗
Clinical use of synthetic antifibrinolytic agents during liver transplantation.
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Aminocaproic Acid↗
Pulmonary hypertension and liver transplantation.
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Contraindications↗
Insulin decreases the serum potassium concentration during the anhepatic stage of liver transplantation.
BACKGROUND: Severe hyperkalemia is a serious problem during orthotopic liver transplantation. The effectiveness of insulin in decreasing serum potassium concentration during the anhepatic stage of orthotopic liver transplantation was investigated. METHODS: Forty patients with serum potassium concentrations greater than 4.0 mM/L at the onset of the anhepatic stage were randomized into two groups. Control group patients (n = 20) received no treatment, and treatment group patients (n = 20) received an intravenous bolus of regular insulin (20 u) 10 min into the anhepatic stage, followed by a glucose infusion (500 ml 5% dextrose in water) over 15 min. RESULTS: In the control group, the potassium concentration did not change, whereas in the treatment group, it decreased from 4.70 +/- 0.54 to 4.18 +/- 0.63 mM/L (mean +/- SD) within 15 min and to 3.57 +/- 0.55 mM/L 60 min after therapy. The potassium concentration was less in the treatment group than in the control group within 30 min of treatment (3.97 +/- 0.52 vs. 4.49 +/- 0.43 mM/L, respectively; P < 0.05). The potassium concentration increased similarly 30 s after graft reperfusion in both groups of patients, but was less in the treatment group (5.91 +/- 1.63 vs. 7.37 +/- 1.67 mM/L, respectively; P < 0.05). The potassium concentration returned to prereperfusion levels within 5 min after graft reperfusion. CONCLUSIONS: In patients undergoing orthotopic liver transplantation, the administration of insulin rapidly decreases serum potassium concentration, even in the absence of the liver, suggesting an important contribution by extrahepatic tissues in the insulin-stimulated uptake of potassium.
Adult↗
A genetically determined host factor controlling susceptibility to encephalomyocarditis virus-induced diabetes in mice.
Levels of insulin mRNA in pancreata from SJL/J male mice susceptible to encephalomyocarditis (EMC)-D virus-induced diabetes started to decrease rapidly 24 h after injection with EMC-D virus and only a trace remained 72 h after injection. In contrast, insulin mRNA in pancreata from C57BL/6J male mice resistant to EMC-D virus-induced diabetes did not show any significant changes 0 to 96 h after injection. EMC-D viral RNA in pancreata from SJL/J mice started to increase rapidly 24 h after injection, reached its peak at 48 h and then decreased gradually. In contrast, EMC-D viral RNA in pancreata from C57BL/6J mice was undetectable except for the 24 and 48 h points after injection. EMC-D virus could bind readily to freshly isolated beta cells from SJL/J mice but scarcely bound to beta cells from C57BL/6J mice. In contrast, there was no significant difference between SJL/J and C57BL/6J mice in binding of EMC-D virus to their cultured beta cells. The rate of EMC-D viral attachment to beta cells from C57BL/6J mice increased significantly during the first 24 h culture period and reached the same rate of attachment as that seen for beta cells from SJL/J mice. This suggests that viral receptors on the beta cells derived from strains of mice resistant to EMC virus-induced diabetes are not expressed in vivo, but are expressed during cell culture, rendering the beta cells susceptible to EMC viral infection. On the basis of our previous and present observations, we conclude that a genetic factor controlling susceptibility to EMC-D virus-induced diabetes may operate by modulating the expression of viral receptors on the beta cells.
Animals↗
Right ventricular function during orthotopic liver transplantation.
Right ventricular (RV) function was assessed in 20 patients undergoing orthotopic liver transplantation to determine its role in the hemodynamic instability frequently seen during this procedure. A modified pulmonary artery catheter equipped with a fast response thermistor was used to determine RV ejection fraction (EFrv), allowing for calculation of RV end-diastolic volume index (EDVIrv, as the ratio of stroke index [SI] to EFrv) and RV end-systolic volume index (ESVIrv, as the difference between EDVIrv and SI). The above hemodynamic measures were taken during dissection for hepatectomy (stage I), during the anhepatic stage (stage II), and after reperfusion of the grafted liver, the neohepatic stage (stage III). No patient had pulmonary hypertension during the study interval. No correlation was observed between right atrial pressure (Pra) and EDVIrv, indicating that Pra is a less reliable clinical indicator of RV preload. RV function appeared to be well preserved throughout the procedure, as indicated by a relatively constant and supranormal EFrv, although a small and probably clinically unimportant decrease in EFrv was observed during the anhepatic stage (0.52, 0.50, and 0.55 during stages I, II, and III, respectively). There was a strong correlation between SI and EDVIrv for pooled data over a wide range of EDVIrv (60-185 mL.m-2). Although unstable central blood temperature precluded the determination of EFrv within the first 5 min after reperfusion, RV function was unaltered otherwise during uncomplicated orthotopic liver transplantation using venovenous bypass, indicating that orthotopic liver transplantation per se is not associated with significant RV dysfunction.
Adult↗