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Biomedical subjects

L Y Cheung

Publications and source records attributed to L Y Cheung.

At least 73 records · Page 4Linked to original sources

Microelectrode studies of Necturus antral mucosa: electrical potentials and resistances.

Intracellular microelectrode techniques were applied to Necturus antral mucosa. Stable intracellular impalements were obtained with 15-50 M omega microelectrodes filled with 3M KCl. It was possible to change rapidly the mucosal bathing solution while maintaining the microelectrode in the cell. With these techniques, we were able to measure the electrical potentials and resistances of the cell membranes and the shunt pathway. The transepithelial potential was -4.9 +/- 1.3 mV, serosal solution reference. Apical cell membrane potential was -43.9 +/- 0.6 mV, cell negative to the mucosal solution. Basolateral cell membrane potential was -48.8 +/- 1.3 mV, cell negative to serosal solution. Transepithelial resistance was 427 +/- 66 omega . cm2. The ratio of apical to basolateral membrane resistances was 3.4 +/- 0.3. The electrical resistances of the transcellular and paracellular pathway were determined by the measurement of the total transepithelial resistance and the ratio of apical to basolateral cell membrane resistances before and after blocking apical membrane sodium permeability with amiloride. The resistances of the apical cell membrane, basolateral cell membrane, and the shunt were 2,203 +/- 585, 1,296 +/- 384, and 604 +/- 81 omega . cm2, respectively (mean +/- SE). Calculations from these measurements indicate that the shunt contribution to transepithelial conductance was approximately 85%.

Amiloride↗

Acidification of arterial blood enhances gastric mucosal injury induced by bile salts in dogs.

The influence of intraarterial infusion of hydrochloric acid on gastric mucosal injury induced by topical bile salts was assessed in a canine ex vivo model. Exposure of the gastric mucosa to 5.0 mM sodium taurocholate in acid bathing solution alone resulted in a slight but not significant reduction in intramural pH of gastric mucosa and mild mucosal damage. When hydrochloric acid (0.1 N) was infused directly into the artery perfusing the stomach of the dogs, the intramural pH of gastric mucosa markedly decreased. The mucosal acidification was associated with severe ulcers in all test dogs that received intraarterial infusion of hydrochloric acid. The deleterious effect of intraarterial infusion of hydrochloric acid was not due to ischemia since the gastric blood flow remained relatively unchanged. The severe mucosal ulcerations were perhaps caused by the decrease in the ability of gastric blood to buffer the incoming luminal acid induced by topical bile salts. These results suggest that (1) the pH of arterial blood perfusing the stomach may also be an important determinant in the ability of the gastric mucosa to protect itself against acid injury, and (2) better management of systemic acid-base balance may contribute to a lower incidence of stress ulcers in critically ill patients.

Animals↗

Mechanisms of cation permeation across apical cell membrane of Necturus gallbladder: effects of luminal pH and divalent cations on K+ and Na+ permeability.

Conventional microelectrode techniques were combined with unilateral mucosal ionic substitutions to determine the effects of luminal pH and luminal alkali-earth cation concentrations on apical membrane cation permeability in Necturus gallbladder epithelium. Acidification of the mucosal solution caused reversible depolarization of both cell membranes and increase of transepithelial resistance. Low pH media also caused: (a) reduction of the apical membrane depolarization induced by high K, and (b) increase of the apical membrane hyperpolarization produced by Na replacement with Li or N-Methyl-D-glucamine. These results, in conjunction with estimates of cell membrane conductances, indicate that acidification of the luminal solution produces a reduction of apical membrane K permeability (PK). Addition of alkali earth cations (Mg2+, Ca2+, Sr2+, or Ba2+) produced cell membrane depolarization, increase of relative resistance of the luminal membrane and reduction of the apical membrane potential change produced by a high-K mucosal medium. These results, as those produced by low pH, can be explained by a reduction of apical membrane PK. The effects of Ba2+ on membrane potential and relative apical membrane PK were larger than those of all other four cations at all concentrations tested (1-10 mM). The effect of Sr2+ was significantly larger than those of Mg2+ and Ca2+ at 10 mM, but not different at 5 mM. The reduction of PK produced by mucosal acidification appears to be mediated by: (a) nonspecific titration of membrane fixed negative charges, and (b) an effect of luminal proton activity on the apical K channel. Divalent cations reduce apical membrane PK probably by screening negative surface charges. The larger magnitude of the effects of Ba2+ and Sr2+ can be explained by binding to membrane sites, in the surface or in the K channel, in addition to their screening effect. We suggest that the action of luminal pH on K secretion in some segments of the renal tubule could be mediated in part by this pH-dependent K permeability of the luminal membrane.

Animals↗

Effect of topical 16,16-dimethyl prostaglandin E2 on aspirin-induced disruption of gastric permeability barrier in dogs.

This study was designed to evaluate whether stimulation of mucus and alkaline secretion by topical 16,16-dimethyl prostaglandin E2 (dmPGE2) would protect gastric mucosa against aspirin-induced disruption of permeability barrier to lumina acid. A chambered segment of canine fundic stomach with intact vascular supply was partitioned into two compartments. One was pretreated with topical dmPGE2 (25 micrograms/15 ml isotonic acid) and the other served as control. Topical dmPGE2 resulted in 1) mucus release as evidenced by gross and microscopic examinations, 2) luminal volume gain from 0.05 +/- 0.01 to 1.05 +/- 0.30 ml/15 min (p less than 0.01) and 3) an increase in Na+ efflux from 9 +/- 4 to 165 +/- 20 muEq/15 min (p less than 0.001). These effects of dmPGE2 did not protect the gastric mucosa against disruption of permeability barrier induced by 20 mM aspirin, which resulted in a similar amount of H+ back-diffusion in dmPGE2-treated mucosa (8 +/- 7 to 129 +/- 8 muEq/15 min, p less than 0.001) and in control mucosa (from 5 +/- 7 to 118 +/- 24 muEq/15 min, p less than 0.001). Also there was no significant difference in the degree of reduction in mucosal potential difference between dmPGE2-treated mucosa (from 60 +/- 4 to 34 +/- 2 -mV p less than 0.01) and control mucosa (from 58 +/- 4 to 36 +/- 3 -mV p less than 0.001).

Administration, Topical↗

Local effects of 16, 16-dimethyl prostaglandin E2 on gastric blood flow and acid secretion.

The effects of luminal administration of 16, 16-dimethyl PGE2 on gastric blood flow and histamine-stimulated acid secretion were determined in a double-chambered preparation of canine fundic stomach. This model permitted simultaneous assessment of two segments of mucosa (17 cm2 each), one control and the other test, supplied by the same vascular pedicle. Topical application of 25 microgram 16, 16-dimethyl PGE2 in 15 ml HCl to the test chamber significantly increased mucosal blood flow of the test chamber from 1.2 +/- 0.1 to 2.5 +/- 0.5 ml/min (P less than 0.05) whereas no significant change in mucosal blood flow was noted in the control mucosa. Intravenous infusion of histamine at 1.0 microgram/kg/min stimulated comparable amounts of acid secretion in both segments of mucosa. The addition of 16, 16-dimethyl PGE2 (25 microgram in 15 ml of HCl) in the bathing solution of the test chamber significantly reduced histamine-stimulated acid secretion from 22.5 +/- 3.1 to 8.4 +/- 1.2 microEq/min (P less than 0.01) in the test mucosa whereas the control mucosa showed no evidence of secretory inhibition throughout the experiment. Since the control mucosa was supplied by the same vascular pedicle as the test mucosa, we concluded that the observed vasodilating and antisecretory effects of luminal administration of 16, 16-dimethyl PGE2 were local rather than systemic effects following its absorption from the stomach.

16,16-Dimethylprostaglandin E2↗

Controlled intragastric pH and cimetidine inhibition of histamine-stimulated gastric acid secretion in the dog.

This study tested a circulating intragastric titration system with an examination of the kinetics of cimetidine inhibition of histamine-stimulated gastric acid secretion of pH 7.0. Dogs were anesthetized, intubated with a biluminal nasogastric device, and connected to the titrating system. The dogs were stimulated with histamine at 0.0, 0.25, 0.50, 1.0, 2.0, and 4.0 microgram/kg/min IV. The dose variations were repeated on separate days with cimetidine infusion at 0.0, 20, and 40 microgram/kg/min IV. Calculated maximal response was 4.52 mEq/kg/hr. Histamine D50 was 0.60 microgram/kg/min. Cimetidine ID50 was 22.6 microgram/kg/min when histamine was given at 1.0 microgram/kg/min. Although acid secretion was higher than other published values, cimetidine inhibition kinetics were not significantly different from published values. A positive correlation was found between cimetidine ID50 and the logarithm of the histamine infusion rate. Our data suggest that (1) a simple circulating intragastric titration system can give accurate results in acid secretion studies, (2) increased gastric pH may enhance histamine-stimulated acid secretion, (3) neutralization of gastric contents does not interfere with cimetidine inhibition kinetics which is competitive, and (4) at artifically high rates of histamine infusion, cimetidine can actually increase acid secretion. We suggest that a circulating intragastric system may be tested in a surgical intensive care unit to evaluate potential clinical value in antiulcer therapy.

Animals↗

Topical effects of 16,16-dimethyl prostaglandin E2 on gastric blood flow in dogs.

The effects of luminal instillation of 16,16-dimethyl prostaglandin E2 (dmPGE2) on total gastric blood flow and its fractional distribution between the layers of gastric tissue were determined in exteriorized segments of the greater curvature of dog stomach. Total gastric blood flow was measured simultaneously by venous outflow and alpha-labeled microspheres; both methods correlated well with each other (r = 0.88, P less than 0.01). In the nonstimulated stomach, dmPGE2 caused an increase in total gastric blood flow from 4.2 +/- 0.8 to 7.4 +/- 1.2 ml/min (P less than 0.05). In contrast, dmPGE2 significantly reduced gastric blood flow in histamine-stimulated stomach (from 14.6 +/- 1.2 to 9.2 +/- 1.0 ml/min; P less than 0.01). The changes in mucosal blood flow ere proportional to the alterations in total blood flow because the fractional distribution of blood flow to the mucosa remained relatively unchanged during dmPGE2 administration. These observations suggest that dmPGE2, a known vasodilator, induces an increase in gastric blood flow in the resting stomach, whereas it reduces gastric blood flow in the actively secreting stomach as a result of secretory inhibition.

Animals↗

Significance of retained barium in the appendix.

Barium is occasionally retained in the appendix after radiographic examinations of the gastrointestinal tract, and its significance has been debated for many years. This report details three cases in which barium was present in the appendix at the time of acute appendicitis. Review of these three cases and 13 cases previously reported suggests that retained appendiceal barium may be significant when it exists in either of two patterns. In patients with appropriate symptoms, a barium appendicolith has the same significance as a calcified appendicolith, strongly suggesting a diagnosis of appendicitis. Barium outlining a dilated appendical lumen also suggests appendicitis in the appropriate clinical setting. The significance of retained barium in the appendix in asymptomatic patients remains uncertain.

Appendicitis↗

The psychosocial needs of the Chinese elderly.

Changing Chinese family patterns caused by immigration have contributed to the breakdown of traditional community and familial control in Chinese-American families. As a result, the Chinese-American elderly are faced with unique psychosocial problems that workers must consider when providing services to this population.

Aged↗

Protection of gastric mucosa against acute ulceration by intravenous infusion of sodium bicarbonate.

The influence of intravenous infusion of sodium bicarbonate on gastric mucosal injury induced by topical sodium taurocholate and hemorrhagic shock was assessed in a canine ex vivo model. As expected, exposure of the gastric mucosa to sodium taurocholate and acid resulted in excessive back diffusion of hydrogen ions (H+) and mild mucosal damage. This mucosal injury was enhanced by hemorrhagic shock in the control dogs. The degree of mucosal injury was significantly less in the test dogs that received intravenous infusions of sodium bicarbonate. The protection afforded by intravenous bicarbonate was not due to a reduction in the amount of H+ entering the tissue, since the net H+ loss from the lumen was not significantly different between the control and the test dogs. The protection effect of intravenous infusion of sodium bicarbonate is probably secondary to an enhancement of mucosal tolerance to H+. These results support the hypothesis that the enhancement of mucosal injury during hemorrhagic shock may be a result of a decrease in the ability of the gastric mucosa to buffer the influxing H+.

Animals↗

Intravenous cholangiography in the diagnosis of acute cholecystitis.

We reviewed our experience with intravenous cholangiography in the evaluation of 70 patients with suspected acute cholecystitis. Twenty-one of these patients had visualization of the biliary ducts without opacification of the gallbladder, a roentgenographic finding that was considered diagnostic of acute cholecystitis. Twenty of the 21 patients were noted to have acute cholecystitis during exploratory laparotomy. The remaining patient had a normal gallbladder, but was found to have a liver abscess. Opacification of the gallbladder with evidence of gallstones was found in eight patients; all had acute cholecystitis. Visualization of the gallbladder without gallstones was found in 22 patients, revealing no acute cholecystitis in this group. Many of these patients were admitted to the hospital with a primary diagnosis of acute cholecystitis and were spared an unnecessary surgical exploration. Nineteen patients had nonvisualization of the gallbladder and biliary ducts. This roentgenographic finding may be caused by acute intra-abdominal conditions other than cholecystitis and caution is warranted in its interpretation. This test has been found to be a reliable adjunct in the work-up of patients with suspected acute cholecystitis.

Acute Disease↗

Secretory state of gastric mucosa and its resistance to aspirin injury.

The influence of the secretory status on gastric mucosal tolerance to aspirin injury was assessed in a canine ex vivo model, which provided two segments of mucosa supplied by a single vascular pedicle in the same dog. Acid secretion was stimulated by intravenous infusion of histamine in one mucosa, whereas the secretory response to histamine was significantly impaired by topical treatment with 16,16-dimethyl prostaglandin E2 in the other. As expected, the secreting mucosa exhibited a twofold greater blood flow than the inhibited mucosa. Exposure of both mucosae to 20 mM aspirin for 30 minutes resulted in the appearance of small multiple superficial erosions. The degree of mucosal injury was not significantly different between the secreting and inhibited mucosae. The extent of mucosal damage was similar to that seen when aspirin in acid was placed on resting mucosa in the same model. These data do not support the hypothesis that histamine-stimulated acid secretion and accompanying increase in gastric mucosal blood flow protects the stomach against aspirin injury.

Animals↗