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L Y Cheung

Publications and source records attributed to L Y Cheung.

At least 55 records · Page 3Linked to original sources
PubMed1987

Effects of luminal salt concentration on electrical pathways in Necturus antrum.

By use of microelectrode techniques the electrical resistances of the cell membranes and paracellular pathways of surface epithelium in Necturus antrum were determined under control conditions (Ringer solutions containing 106.6 mM Na+, 91.4 mM Cl-) and during exposure to mucosal solutions containing high Na+ and Cl- concentrations. Resistances were determined by briefly exposing tissues to mucosal solutions containing 10(-4) M amiloride, a reversible inhibitor of Na+ conductances. Under control conditions in eight tissues, measurements obtained by exposure to amiloride were not significantly different from those obtained by an independent method, intraepithelial cable analysis, thus indicating the validity of the measurements obtained by the amiloride method. In 10 tissues, high luminal NaCl concentrations (Ringer salts + 125 mM NaCl) increased the apical cell membrane resistance from 5,778 +/- 267 to 7,714 +/- 422 omega X cm2 (P less than 0.01) and the basolateral membrane resistance from 2,973 +/- 186 to 3,869 +/- 335 omega X cm2 (P less than 0.01). The resistance of the paracellular pathway decreased from 625 +/- 13 to 505 +/- 13 omega X cm2 (P less than 0.001). Similar alterations in these resistances were observed when Na+ or Cl- were increased individually, when added as salts of isethionate- and N-methyl-D-glucamine+, respectively. These effects were not attributable to increases in luminal osmolarity, since mucosal solutions made equally hyperosmotic with 250 mM sucrose elicited increases in paracellular pathway resistance and decreases in resistances of the cell membranes.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed1987

Intracellular pH (pHi) in gastric surface epithelium is more susceptible to serosal than mucosal acidification.

Intracellular microelectrode techniques were used to examine the effects of mucosal or serosal acidification on intracellular pH (pHi) in gastric surface epithelial cells. Necturus antrum was mounted in a modified Ussing chamber, and pHi was determined from the difference between the potentials recorded by intracellular conventional and pH-sensitive microelectrodes. In tissues bathed with bicarbonate-buffered Ringer's solution (pH 7), acidification of the mucosal solution to pH 4.5 by isotonic replacement of the NaHCO3 with NaCl had no significant effects on pHi. In contrast, acidification of the serosal solution to pH 4.5 by replacing the bicarbonate reduced pHi from 7.32 +/- 0.04 to 6.95 +/- 0.06 (p less than 0.001, n = 8). Similarly, in tissues bathed with HEPES-buffered Ringer's solution (pH 7.0), pHi was unaffected by reducing the mucosal solution pH to 4.5 with HCl but fell 0.21 +/- 0.05 pH units (p less than 0.01, n = 7) during acidification of the serosal solution to pH 6. These results suggest that gastric epithelium is more sensitive to acidification from the serosal than the mucosal side. Such a finding is consistent with the concept of a gastric mucosal barrier to luminal acid. It may also explain the gastric epithelium's greater sensitivity to acute ulceration during systemic acidosis.

Animals↗
PubMed1987

Gastric blood flow and mucosal defense mechanisms.

Recent experimental studies have demonstrated that gastric mucosal blood flow is an essential factor in mucosal defense against acute ulceration. Clinically, most patients who develop stress ulcers have experienced an episode of shock from hemorrhage, sepsis, or cardiac dysfunction. Diminished mucosal blood flow is also a common denominator in animal experiments that employ restraint, hemorrhage, or endotoxemia for the production of acute lesions. The mechanisms by which ischemia produces ulceration have been examined extensively. The leading hypothesis is that gastric mucosal blood flow plays an important role in the disposal, or buffering, of the H+ entering the tissue. Ischemia reduces the capacity of the gastric mucosa to neutralize acid that enters the tissue. This, in turn, leads to accumulation of H+ within the tissue, mucosal acidification, and ulceration. Ischemia may also render the stomach more susceptible to acute ulceration by a severe energy deficit of the gastric mucosa. Using a rat hemorrhagic shock model, a series of experiments demonstrated a profound reduction in mucosal ATP and other high-energy phosphate intermediates that coincided with the development of epithelial cell necrosis. In recent years, many of these experimental observations have been applied clinically in the management of critically ill patients at high risk for development of stress lesions. These include the correction of abnormalities in cardiac output and intravascular volume, careful attention to systemic acid-base balance, adequate nutritional support, and the use of antacids or antisecretory agents. As a result of these preventive measurements, the incidence and prevalence of stress ulcers have decreased significantly in recent years.

Aminopyrine↗
PubMed1986

Measurements of intracellular pH in Necturus antral mucosa by microelectrode technique.

Intracellular pH (pHi) was measured in the surface epithelial cells of Necturus antrum using pH-sensitive intracellular microelectrodes. Electrodes were prepared by filling 10- to 20-M omega resistance glass microelectrodes with a H+ ion-selective exchange resin and calibrated before use in solutions of known pH 4.0-8.0. The electrode response (n = 15) was linear (r = 0.93; P less than 0.001) with a slope of 52.1 +/- 2.3 mV/pH unit. Antral mucosa was mounted in a modified Ussing chamber and pHi was determined from the difference between the potentials recorded by intracellular H+-selective and conventional microelectrodes. These measurements of pHi were validated by examining the response of the intracellular microelectrodes to 1) depolarization of the cell membrane produced by K+ substitution for Na+, and 2) alkalinization and acidification of pHi produced by NH+4 substitution for Na+ in the bathing solutions. In tissues bathed with HCO-3-Ringer solution (pH 7.0), the mean pHi was 7.34 +/- 0.02 with a range from 7.24 to 7.43. In N-2-hydroxymethylpiperazine-N' -ethanesulfonic acid (HEPES)-Ringer solution (pH 7.0), pHi was reduced to 7.02 +/- 0.05 (P less than 0.01). Acidification of the luminal solution to pH 6.8 with CO2 produced a 0.22 +/- 0.04-pH unit fall in pHi (P less than 0.001). In contrast, acidification to pH 4.0 with HCl had no significant effects on pHi. These findings indicate that HCO-3 may play an important role in pHi regulation in this tissue. In addition, they suggest that, in contrast to CO2, the surface epithelial cells of Necturus antrum are relatively resistant to acidification by luminal HCl.

Animals↗
PubMed1986

Regional gastric mucosal blood flow after parietal cell vagotomy in dogs.

In this study we used the recently validated H2 clearance method to perform endoscopic measurements of gastric mucosal blood flow (MBF) in anesthetized dogs before and after parietal cell vagotomy (PCV). Under resting conditions, MBF in the gastric corpus before PCV was 72 +/- 5 ml/min/100 gm. This was not altered significantly at 4, 8, or 16 weeks after PCV, and there were not significant long-term changes in MBF on the greater or lesser curvatures of the corpus individually. Before PCV infusion of pentagastrin (8 micrograms/kg/hr) elicited increases in corpus MBF to 104 +/- 4 ml/min/100 gm, accompanied by increases in gastric acid output from resting levels of 2.1 +/- 0.9 to 38.6 +/- 2.4 mEq/hr (p less than 0.001). PCV significantly reduced pentagastrin-stimulated acid secretion by 50%, and secretory inhibition was accompanied by significant reductions in pentagastrin-stimulated MBF in the corpus. Pentagastrin did not alter antral MBFs before or after PCV. In summary PCV does not elicit significant long-term changes in resting MBF in different regions of the gastric corpus, and PCV significantly diminishes increases in acid output and corpus MBF that are normally stimulated by pentagastrin. These observations suggest that alterations in gastric MBF after PCV may be attributable to alterations in acid secretion.

Animals↗
PubMed1985

Endoscopic measurements of gastric mucosal blood flow in dogs.

The feasibility and validity of endoscopic measurements of gastric mucosal blood flow (GMBF) using 3% H2 gas clearance were investigated in the intact stomach of anesthetized dogs. Platinum electrodes were lengthened and modified to permit passage through the instrument channel of a standard gastroscope. In five anesthetized dogs, antral mucosal blood flow (103.2 +/- 5.3 ml/min/100 g tissue) was significantly higher (P less than 0.05) than that in the corpus (66.9 +/- 7.1 ml/min/100 g tissue). Histamine stimulation selectively increased flow in the corpus to 134.5 +/- 7.5 ml/min/100 g tissue. Comparison of endoscopic GMBF measurements in these five dogs on 2 different days revealed a close correlation (r = 0.87, P less than 0.001). Endoscopic H2 clearance measurements obtained in five awake dogs were not significantly different from those obtained during pentobarbitol anesthesia. In 12 dogs, GMBF determined by endoscopic H2 gas clearance showed a good agreement (r = 0.91, P less than 0.001) with that measured by radioactive microspheres. These two methods also demonstrated comparable changes in GMBF induced by intravenous infusion of histamine and vasopressin. It was concluded that 3% H2 gas clearance can be used to accurately and reproducibly measure GMBF through the endoscope, a unique advantage of this method for potential clinical use.

Anesthesia↗
PubMed1985

Focal gastric mucosal blood flow at the site of aspirin-induced ulceration.

Focal gastric mucosal blood flow as measured by the hydrogen gas clearance method was compared with total gastric blood flow as determined by venous outflow in an isolated segment of canine stomach before, during, and after exposure to aspirin. Despite an increase in total gastric blood flow from 10.8 +/- 1.6 ml/min per chamber to 17.4 +/- 1.9 ml/min per chamber and mucosal blood flow at nonulcerated sites from 29.5 +/- 4.3 ml/min per 100 g to 83 +/- 14.4 ml/min per 100 g, mucosal blood flow at the site of aspirin-induced ulceration was significantly reduced from 29.5 +/- 4.3 ml/min per 100 g to 12.5 +/- 2.5 ml/min per 100 g. After the removal of aspirin, mucosal blood flow returned to control levels. Such a redistribution of mucosal blood flow in response to aspirin is consistent with the localized nature of acute aspirin-induced injury. The findings also explain the inability of previous methods measuring blood flow of the entire stomach to demonstrate mucosal ischemia during such injury.

Animals↗
PubMed1985

Intracellular microelectrode studies of Necturus antral mucosa. Effect of aspirin on cell membrane potentials.

Intracellular microelectrode techniques were used to determine the effects of luminal aspirin on epithelial cell membrane potentials of Necturus antral mucosa. In this tissue, prolonged stable intracellular impalements were obtained with 15-50-M omega microelectrodes filled with 3 M KCl. In acidic mucosal solution (pH 4.0) the addition of aspirin at 5.0 mM resulted in a significant decrease of apical cell membrane potential (Vmc) from -36.8 +/- 2.2 to -22.2 +/- 2.1 mV (p less than 0.001) and basolateral cell membrane potentials (Vcs) from -38.8 +/- 1.7 to -25.3 +/- 2.1 mV (p less than 0.001). Upon removal of aspirin from the mucosal solution, both cell membranes hyperpolarized for a brief period before returning to their original potentials. In neutral mucosal solutions (pH 7.0), addition of aspirin (5.0 mM) resulted in a significant increase in apical cell membrane potential (Vmc) from -40.0 +/- 2.4 to -46.8 +/- 3.3 mV (p less than 0.001) and basolateral cell membrane potential (Vcs) from -41.5 +/- 2.0 to -49.7 +/- 2.5 mV (p less than 0.001). This hyperpolarization of the cell was associated with an increase in transmucosal potential from -1.5 +/- 1.8 to -2.9 +/- 1.8 mV (p less than 0.001) and an increase in the ratio of apical to basolateral membrane resistances from 2.2 +/- 0.4 to 3.1 +/- 0.7 (p less than 0.05). These changes in membrane potentials and the ratio of membrane resistances may be caused by a change in ionic conductance of the cell membranes induced by aspirin.

Animals↗
PubMed1985

Microelectrode studies of Necturus antral mucosa. II. Equivalent circuit analysis.

Intracellular microelectrode techniques were employed to determine the equivalent circuit parameters in Necturus antral mucosa. Stable intracellular impalements were obtained using 15- to 50-M omega microelectrodes. Measured transepithelial and cellular potentials and voltage deflections produced by transepithelial current pulses were used to calculate the electrical resistances of the cell membranes and the equivalent electromotive forces (EMF) at both cell borders. The measured potentials were -4.1 +/- 0.8 mV for the entire epithelia, -41.8 +/- 5.1 mV for the apical membrane, and -45.9 +/- 5.0 mV for the basolateral membrane. Values for the resistances were 7,300 +/- 1,900 omega X cm2 for the apical, 3,990 +/- 1,170 omega X cm2 for the basolateral, and 710 +/- 40 omega X cm2 for the shunt. Assuming that the shunt EMF is zero with control Ringer solution on both sides of the tissue, the effect of this relatively low-resistance shunt on electrical parameters can be determined. The cell membrane EMFs are both oriented with the interior negative and are -1.2 +/- 9.7 mV (apical) and -69.7 +/- 11.3 mV (basolateral). The difference between these values and the measured potentials is the result of a flow of current through the shunt from serosa to mucosa, hyperpolarizing the apical and depolarizing the basolateral membranes.

Amiloride↗
PubMed1985

New diagnostic techniques in hepatobiliary disease.

The liver and biliary tree have become increasingly accessible to the clinician through the new diagnostic techniques described in this chapter. There will undoubtedly be more developments and refinements in the years ahead. Already the new techniques of positron-emission tomography and nuclear magnetic resonance hint at a greater potential for improving our capacity to visualize hepatobiliary disease. It would be unrealistic, however, to expect any one of these techniques to become the single procedure of choice for diagnosis in all types of hepatobiliary disease. It will continue to be the clinician's task to pick the proper sequence of available tests to arrive at a diagnosis in the most rapid and efficient manner. It is unlikely that any busy surgeon can keep totally abreast of the subtleties of all new diagnostic techniques. It is clear that in many instances no single test is really the best, and choices should be made on the basis of the resources available. If the clinician is able to make an accurate assessment of the diagnostic capabilities of his or her institution and approaches each individual problem with a logical progression from first-line screening techniques to second-line invasive procedures, few mistakes will be made. The challenge is to minimize the risk, expense, and time involved in obtaining maximum information for definitive diagnosis and treatment.

Biliary Tract↗
PubMed1985

Effect of 16,16-dimethyl prostaglandin E2 on gastric epithelial cell membrane potentials and resistances.

Intracellular microelectrode techniques were employed to examine the effects of 16,16-dimethyl prostaglandin E2 (dmPGE2) on Necturus antral mucosa epithelial cell membrane potentials and resistances. Necturus antral mucosa was mounted in a modified Ussing chamber and stable intracellular impalements were obtained. Addition of 0.01 microgram/ml dmPGE2 to the mucosal solution produced an increase of the apical cell membrane potential (Vmc) from -44.3 +/- 3.1 to -53.5 +/- 3.8 mV (p less than 0.001) and of the basolateral cell membrane potential (Vcs) from -48.8 +/- 2.8 to -57.7 +/- 3.2 mV (p less than 0.001). This reversible, dose-dependent hyperpolarization of both cell membranes was accompanied by a decrease in the electrical resistance of the apical membranes (Ra) from 2550 +/- 250 omega/cm2 to 1870 +/- 210 omega/cm2 (p less than 0.05) and a decrease in the resistance of the basolateral membrane (Rb) from 1020 +/- 250 omega/cm2 to 630 +/- 80 omega/cm2 (p less than 0.05). In addition, there was an increase in the resistance of the shunt (intercellular junction, Rs), the major route of transepithelial ion flow, from 710 +/- 60 omega/cm2 to 750 +/- 80 omega/cm2 (p less than 0.05). Thus dmPGE2 increased the cell membrane potentials and reduced the ionic permeability of the intercellular junction.

16,16-Dimethylprostaglandin E2↗
PubMed1985

Comparison of gastric mucosal blood flow as measured by H2 gas clearance and microspheres during secretory stimulation and inhibition.

H2 clearance is a recently described method of measuring gastric mucosal blood flow that has great potential for clinical use. However, the effects of luminal pH and of secretory activity of the gastric mucosa on the accuracy of H2 clearance measurements have not been systematically examined. We therefore tested the validity of H2 clearance measurements at different pHs in both in vitro and in vivo systems. In addition, we compared measurements by H2 clearance and radioactive microspheres during stimulation and suppression of acid secretion. In vitro, H2 washout was relatively constant over a range of pHs from 2.0 to 8.0. In chambered segments of canine fundus in vivo, H2 clearance was not significantly affected by pH of the luminal solutions either in the resting state or at lower blood flows induced during infusion of vasopressin. Finally, there was a close correlation (r = 0.85; p less than 0.001) between H2 clearance and microsphere measurements under resting conditions, during intravenous histamine stimulation, and after infusion of cimetidine to suppress acid secretion. In summary, H2 clearance reliably and accurately measures gastric mucosal blood flow at different luminal pHs and under conditions that stimulate or suppress acid secretion.

Animals↗
PubMed1984

Measurement of regional gastric mucosal blood flow by hydrogen gas clearance.

Gastric mucosal blood flow as measured by the hydrogen gas clearance method was compared with total gastric blood flow as determined by venous outflow in an isolated segment of canine stomach. During rest and histamine stimulation, hydrogen gas clearance correlated lineally with total gastric blood flow (p less than 0.001). Correlation analysis revealed a slope of 1.21 and a correlation coefficient of 0.97. The slope of 1.21 indicates that the ratio of mucosal to total gastric blood flow was approximately 82 percent. This fractional distribution of blood flow is in agreement with that previously reported by microsphere technique. In the intact stomach of anesthetized rats and dogs, antral mucosal blood flow was significantly higher than that of the corpus. This finding may, in part, contribute to the observation that acute stress erosion occurs predominantly in the corpus of the stomach. Histamine stimulation selectively increased the mucosal blood flow of the corpus, whereas antral mucosal blood flow remained unchanged. As a result, there was no significant difference in mucosal blood flow between the antrum and the corpus during histamine stimulation.

Animals↗
PubMed1984

Measurements of gastric mucosal blood flow by hydrogen gas clearance.

The validity of the use of H2 gas clearance to measure gastric mucosal blood flow (GMBF) was investigated in the intact stomach of anesthetized dogs. With a modified, more sensitive platinum electrode, we were able to reduce the H2 gas concentration to a nonflammable gas mixture. GMBF was repeatedly measured when the dogs inhaled gas containing 100, 10, and 3-5% H2. GMBF measured using 100% H2 demonstrated close correlation with inhaled gases containing 10% H2 (r = 0.84, slope = 0.89) and 3-5% H2 (r = 0.91, slope = 0.88). At a nonflammable concentration of 3% H2, it was safe to add 20% O2 into the gas mixture. The addition of O2 into the inhaled gas eliminated the transient hypoxia noted otherwise. It was also possible to reduce the gas flow rate from 5-10 to 1-3 l/min. Regression analysis of GMBF determined by inhalation of 5% H2 at these flow rates revealed a significant linear correlation (r = 0.95, slope = 1.13). In 10 dogs GMBF determined by using these low concentrations of H2 at the low flow rates also showed a good agreement (r = 0.93, slope = 0.65) with that measured by radioactive microspheres. These two methods also demonstrated comparable changes in GMBF induced by intravenous infusion of histamine and vasopressin. It was concluded that, with the technique as modified in our laboratory, H2 gas clearance could be a safe and accurate tool for quantitating gastric mucosal blood flow.

Animals↗
PubMed1984

Effect of aspirin on epithelial cell membrane potentials of gastric fundic mucosa.

The effects of aspirin on epithelial cell membrane potentials of Necturus fundic mucosa were examined by in vitro experiments according to intracellular microelectrode techniques. Stable intracellular impalements were obtained with 15 to 50 M-ohm microelectrodes filled with 3M KCl. In neutral mucosal solutions (pH 7.0) aspirin (5.0 mM) resulted in a significant increase in apical cell membrane potential (Vmc) from -36.7 +/- 1.5 mV to -43.3 +/- 2.3 mV (p less than 0.001) and basolateral cell membrane potential (Vcs) from -42.7 +/- 1.8 mV to -50.6 +/- 2.4 (p less than 0.001). This hyperpolarization of the cell was associated with an increase in transmucosal potential from -5.8 +/- 0.7 to -7.4 +/- 0.9 (p less than 0.05) and an increase in the ratio of apical to basolateral membrane resistances from 5.1 +/- 1.2 to 8.8 +/- 1.9 (p less than 0.05). These changes were consistent with an increase in potassium conductance induced by the salicylate anion. In acidic mucosal solutions (pH 4.5) aspirin caused a reduction in Vmc and Vcs. This hypopolarization of the cell membrane is consistent with acidification of the epithelial cells. These observations support the proposed mechanisms of aspirin injury: (1) back diffusion of H+ into the cells and (2) influx of the salicylate anions into the cells, which may interfere with intracellular metabolism.

Animals↗
PubMed1983

Effect of cimetidine on canine gastric mucosal pH and blood flow.

The effects of cimetidine inhibition of acid secretion on gastric mucosal blood flow and the intramural pH of gastric mucosa were assessed in a canine model ex vivo. Intravenous infusion of histamine at 1.0 microgram/kg per minute resulted in brisk acid secretion, which was associated with an increase in total gastric and mucosal blood flow and the intramural pH of gastric mucosa. The increased blood flow and mucosal alkalinity may be compensatory mechanisms of the stomach to enhance its tolerance of luminal acid. Cimetidine inhibition of acid secretion was associated with a reduction in mucosal alkalinity and total gastric and mucosal blood flow. These adverse effects of cimetidine on blood flow and mucosal pH, two important factors in the stomach's self-defense against acid injury, may explain the inefficacy of cimetidine in the prevention of stress ulcers.

Animals↗