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Biomedical subjects

S J Hong

Publications and source records attributed to S J Hong.

At least 163 records · Page 9Linked to original sources
PubMed1989

Antagonism by tubocurarine and verapamil of the regenerative acetylcholine release from mouse motor nerve.

The role of presynaptic acetylcholine receptors and Ca2+ channels in the regenerative acetylcholine release was studied in the cut muscle preparation of mouse phrenic nerve hemidiaphragm. The regenerative release shown as a prolonged endplate depolarization was evoked by stimulation of the nerve with a train of pulse at 75-300 Hz when acetylcholinesterase activity was depressed with neostigmine or by lowering temperature. Tubocurarine, cobratoxin, verapamil, diltiazem and nifedipine at low concentrations, which had a negligible effect on the endplate potential, shortened the duration of regenerative depolarization while leaving the amplitude unaffected. In contrast, Mn2+ at concentrations that markedly reduced the amplitude of single endplate potentials caused little suppression of the regenerative depolarization though intensive stimulation was needed to trigger the response. On the other hand, atropine inhibited the regenerative depolarization only at high concentrations which also depressed endplate potentials. These results indicate that the mechanism for evoking the regenerative release involves the activation of acetylcholine receptors and Ca2+ channels which are sensitive to tubocurarine and Ca2+ channel blockers. The Ca2+ channel concerned, however, appears to differ from that involved in the normal quantal release of acetylcholine.

Acetylcholine↗
PubMed1989

Use of geographutoxin II (mu-conotoxin) for the study of neuromuscular transmission in mouse.

1. Endplate potentials (e.p.ps) were investigated in the presence of geographutoxin II (GTXII) in the mouse phrenic nerve diaphragm preparation. This toxin preferentially blocks muscle Na+ channels which allows the study of e.p.ps in the absence of nicotinic receptor antagonists or substances to depress acetylcholine release. 2. GTXII abolished muscle action potentials and antagonized the depolarization of the muscle membrane produced by the crotamine-induced opening of Na+ channels. 3. E.p.ps as large as 19-25 mV were observed after 2-4 micrograms ml-1 GTXII. These concentrations of GTXII did not cause discernible changes of resting membrane potential and frequency and amplitude of miniature e.p.ps. 4. Lower concentrations (1-2 micrograms ml-1) of GTXII caused incomplete blockade of the muscle Na+ channel resulting in exaggerated 'e.p.ps', while higher concentrations of GTXII (8 micrograms ml-1) abolished e.p.ps by a prejunctional effect. 5. Trains of e.p.ps on repetitive stimulation after GTXII neither ran down, as in tubocurarine-treated preparations, nor facilitated, as in low Ca2+ and/or high Mg2+-treated preparations, and were indistinguishable from those of untreated cut muscle preparation. 6. In cut muscle preparations, GTXII did not affect the rise and decay times, amplitude or rundown of e.p.ps. 7. It is concluded that GTXII is a useful agent for studying neuromuscular transmission. This method provides e.p.ps which are neither attenuated nor modified because manipulations that alter transmitter release and postjunctional receptor responses are avoided.

Animals↗
PubMed1989

Nicardipine inhibits axon conduction but causes dual changes of acetylcholine release in the mouse motor nerve.

The effects of nicardipine, a dihydropyridine Ca2(+)-channel antagonist, on neuromuscular transmission and impulse-evoked release of acetylcholine were compared with those of nifedipine. In the isolated mouse phrenic nerve diaphragm, nicardipine (50 microM), but not nifedipine (100 microM), induced neuromuscular block, fade of tetanic contraction, and dropout or all-or-none block of end-plate potentials. Nicardipine had no significant effect on the resting membrane potential and the amplitude of miniature end-plate potentials but increased the frequency and caused the appearance of large size miniature potentials. The quantal contents of evoked end-plate potentials were increased. In the presence of tubocurarine, however, nicardipine depressed the amplitude of end-plate potentials. The compound nerve action potential was also decreased. It is concluded that nicardipine blocks neuromuscular transmission by acting on Na+ channels and inhibits axonal conduction. Nicardipine appeared to affect the evoked release of acetylcholine by dual mechanisms, i.e., an enhancement presumably by an agonist action on Ca2+ channels, like Bay K 8644 and nifedipine, and inhibition by an effect on Na+ channels, like verapamil and diltiazem. In contrast with its inactivity on the amplitude of miniature end-plate potentials, depolarization of the end plate in response to succinylcholine was greatly depressed. The contractile response of baby chick biventer cervicis muscle to exogenous acetylcholine was noncompetitively antagonized by nicardipine (10 microM), but was unaffected by nifedipine (30 microM). These results may implicate that nicardipine blocks the postsynaptic acetylcholine receptor channel by enhancing receptor desensitization or by a use-dependent effect.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1989

[Study on Centrocestus armatus in Korea. I. Infection status of Zacco platypus and Z. temminckii with the metacercariae of C. armatus].

This study was performed to observe the infection rate and infection intensity of fresh water fish such as pale chub (Z. platypus) and dark chub (Z. temminckii) with the metacercariae of C. armatus. The fish were caught in several rivers and streams from June to September, 1988 and examined by artificial digestion technique. Total 370 fish were caught at 19 rivers. The metacercarial (C. armatus) infection rate and average burden in Z. platypus were 86.8% and 224, and those in Z. temminckii were 78.5% and 131. The infection rate and burden per fish were 73.4% and 32 in the fish caught from the Han river, and 88.0% and 44 from the Youngsan river. All fish caught from the Keum and the Tamjin river were infected and their mean metacercarial density was 45 and 59 respectively. The infection rate and density in fish caught from the Seomjin and Nagdong rivers were 100% and 119, and 81.0% and 348 respectively. From this study, it is confirmed that C. armatus is widely distributed along 5 major rivers in Korea.

Animals↗
PubMed1989

Study on Centrocestus armatus in Korea. II. Recovery rate, growth and development of worms in albino rats.

Some biological characteristics of Centrocestus armatus were studied using albino rats as its experimental host. The metacercariae were collected from Zacco platypus by artificial digestion method. Laboratory rats (Wistar) were fed each 100 or 200 metacercariae and sacrificed on 1, 2, 3, 4, 5, 6, 8, 14 and 28 days after infection to recover worms of various ages. The average recovery rate was 10.7% from 82 rats. The rate decreased rather slowly for the first 8 days but showed a steep decrease thereafter. Of the worms, 35.5% were recovered from the duodenum and 62.5% from the jejunum. At metacercarial stage, body length was 293 microns and body width 144 microns. At adult stage, the length and width reached 382 microns and 214 microns respectively at 14 days after infection. The testes and Mehlis' gland were recognized at metacercarial stage, whereas the ovarian analage appeared on the 1st day of infection, seminal vesicle and vitellaria on the 2nd day, and seminal receptacle and uterine eggs on the 3rd day. Until 8 days after infection the genital organs developed continuously and the number of uterine eggs increased. The above results show that albino rats are one of useful experimental hosts for C. armatus and the worms can develop to adults in 3 days after infection.

Animals↗
PubMed1989

[A human case of tick bite by Ixodes nipponensis on the scalp].

A human case of tick bite on the scalp was found at a local hospital on June, 1984. The patient, 63-year old female, was attacked by a tick while working in a farm forest which located in the suburbs of Seoul. The clinical complaint was a (worm) mass on the scalp which she thought as a tumor. On admission the patient complained of facial edema and general malaise. After removal of the mass (tick), small bleeding and discoloration were observed around the biting site. The tick was morphologically examined and identified as Ixodes nipponensis. This is the 4th human case of tick bite reported in the literature of Korea.

Animals↗
PubMed1989

Identification of Stictodora lari (Heterophyidae) metacercariae encysted in the brackish water fish, Acanthogobius flavimanus.

Metacercariae of the genus Stictodora encysted in the head tissue of Acanthogobius flavimanus (the gobies) caught at Sachun-gun, Kyongnam Province, were identified to be Stictodora lari Yamaguti, 1939 (Trematoda: Heterophyidae), a new parasite fauna in Korea. The metacercariae were 0.39-0.43 mm by 0.32-0.35 mm in size, long elliptical, and with a thin and transparent cyst wall. Total 200 metacercariae were collected from 50 gobies. In order to obtain adult worms two kittens and a puppy were infected each with 34-100 metacercariae, and total 33 adults were recovered between the day 4 and day 8 post-infection. The S. lari adults measured 0.95-1.18 mm long and 0.26-0.32 mm wide and the eggs in uteri 0.028-0.033 mm by 0.017-0.020 mm. The most characteristic morphological feature of these flukes was the presence of a gonotyl and gonotyl spines arranged in two groups; densely crowded group of 30-40 spines and linearly-arranged one of 30-40 spines, together of which made a comma (or reversed comma) shape along the lateral margin of the gonotyl. It has been proved by this study that S. lari is distributed in southern coasts of Korea.

Animals↗
PubMed1989

[Cultivation of horseshoe crab amebocytes].

The in vitro and in vivo cultivation of horseshoe crab amebocytes is studied. Partial bleeding promotes the proliferation of horseshoe crab amebocytes, and could be a useful method for amebocyte production in vivo. The optimal conditions of in vitro cultivation of amebocytes were incubation at 15 degrees C and pH delta 6.8-7.2. The best medium was the hemolymph of the horseshoe crab. Measuring DNA synthesis of amebocytes by 3H-thymidine uptake showed that no proliferation of amebocytes occurs during in vitro cultivation. Because some protozoa were found in the hemolymph, primaquine, quinine, pyrimethamine and metronidazole were used in the culture medium. Primaquine and metronidazole have a protozoacidal effect on the protozoa parasitising in the horseshoe crab.

Animals↗
PubMed1988

Neuromuscular block by verapamil and diltiazem and inhibition of acetylcholine release.

The effects of Ca2+-channel antagonists, verapamil, diltiazem and nifedipine, on the neuromuscular transmission were studied in the isolated mouse phrenic nerve-diaphragm preparations. All 3 drugs increased the twitch response evoked by direct single stimulation at 10-100 microM. The neuromuscular transmission at 0.1 Hz was blocked by verapamil and diltiazem, but not by nifedipine, only at very high concentrations (greater than or equal to 100 microM). In the time course of block, no endplate potential (e.p.p.) could be recorded, whenever the junction failed to elicit an action potential, suggesting that the block is due to an axonal conduction failure. Conduction block became apparent in both axon and muscle at low concentrations (greater than 10 microM) of verapamil and diltiazem at 100 Hz. When the safety margin of neuromuscular transmission was reduced by tubocurarine or low Ca2+ plus high Mg2+, verapamil and diltiazem, but not nifedipine, reduced the single twitch response to nerve stimulation at concentrations that did not cause axon conduction block. The inhibition was dependent on the frequency of nerve stimulation, enhanced by low-Ca2+ and antagonized by high-Ca2+. Verapamil (50 microM) inhibited the mean amplitude of the median size miniature e.p.p. by only 8%, whereas it increased the frequency by 4-5-fold and the proportion of both small and giant miniature e.p.p.s. The e.p.p. amplitude was inhibited by verapamil by about 67% in low-Ca2+ media and by about 38% in normal Tyrode. Similar but somewhat lesser effect was obtained with diltiazem. It is concluded that verapamil and diltiazem, but not nifedipine, inhibit the transmitter release.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1988

Somatostatin modulation of neurally mediated pepsinogen secretion from frog esophageal mucosa.

Frog esophageal mucosa contains peptic glands which are innervated by cholinergic neurons. When incubated in a medium containing 1.5 mM CaCl2, pepsinogen release from esophageal mucosa was increased by a high potassium concentration (55 mM KCl), 1,1-dimethyl-4-phenylpiperazinium (DMPP) or bethanechol. Whereas the response to bethanechol remained little changed, the response to high KCl concentrations or DMPP was abolished in the absence of Ca2+. The stimulatory effects of high KCl concentrations and DMPP were also eliminated by the presence of atropine or somatostatin. Furthermore, pepsinogen release in response to bethanechol was dose-dependently inhibited by somatostatin. Frog esophagus was found to contain somatostatin-like immunoreactivity, with a higher density at the end adjacent to the stomach. Chromatography of mucosa extract on Sephadex G-50 revealed a single peak of somatostatin-like immunoreactivity that coeluted with somatostatin-14. Immunohistochemical staining of the mucosa with peroxidase antiperoxidase technique demonstrated the presence of two varieties of somatostatin-like immunoreactivity-containing cells, one individually dispersed within the intercalated septa and the other in groups within the interlobular septa of the peptic glands. These results seem to indicate that somatostatin or somatostatin-like immunoreactivity may play a modulatory role in neurally mediated pepsinogen secretion in the frog esophagus.

Animals↗
PubMed1988

Reversals of the neostigmine-induced tetanic fade and endplate potential run-down with respect to the autoregulation of transmitter release.

1. In order to shed more light on the role of presynaptic cholinoceptors in the modulation of transmitter release, the effects of tubocurarine, choline and hexamethonium on neostigmine-induced tetanic fade and run-down of endplate potentials (e.p.ps) in response to indirect stimulation with trains of pulses were studied in the intact and cut isolated phrenic nerve-diaphragm preparation of the mouse, respectively. 2. Tubocurarine, choline and hexamethonium reduced both the tetanic fade and e.p.p. run-down caused by neostigmine, despite the fact that they themselves also induced these two effects. 3. At a given degree of postsynaptic inhibition, choline and hexamethonium caused less e.p.p. run-down and reversed the neostigmine-induced tetanic fade and e.p.p. run-down better than tubocurarine. Moreover, the e.p.p. run-down caused by choline or hexamethonium, but not that induced by tubocurarine, was reciprocally reversed by neostigmine. 4. Tubocurarine, choline and hexamethonium significantly decreased the endplate depolarization induced by repetitive nerve stimulation in the presence of neostigmine. The remaining depolarization continued to grow during repetitive stimulation in the presence of choline or hexamethonium, but not, however, in the presence of tubocurarine; a finding which suggests that choline and hexamethonium but not tubocurarine may be displaced from the receptor by the accumulated acetylcholine. 5. The mutual reversal by neostigmine and cholinoceptor antagonists of e.p.p. run-down may implicate the presence of a positive (physiological) and a negative (pharmacological) feedback regulation for evoked transmitter release via nicotinic cholinoceptors in the mammalian motor nerve, depending on the concentration of acetylcholine within the synaptic cleft.

Animals↗
PubMed1987

Dissociation of the end-plate potential run-down and the tetanic fade from the postsynaptic inhibition of acetylcholine receptor by alpha-neurotoxins.

The effects of so-called postsynaptic snake alpha-neurotoxins (alpha-bungarotoxin, cobratoxin, erabutoxin b) on the wanings of tetanic contraction (tetanic fade) and the run-down of end-plate potentials during stimulation at 100 Hz were studied, respectively, in intact and cut mouse phrenic nerve-diaphragm preparations. No tetanic fade was evident with high concentrations of toxins until the complete failure of contractile response whereas the tetanic fade was evident after prolonged incubation with lower concentrations of toxins. The proportion of junctions exhibiting end-plate potential run-down increased progressively during toxin incubation. However, depression of end-plate potential amplitude by the toxins was not necessarily accompanied by run-down. The tetanic fade and the run-down became more pronounced for a time shortly after washout of toxins despite the restoration of single twitches and end-plate potential amplitudes, indicating the presynaptic origin of these effects induced by alpha-neurotoxins. We demonstrated that the functions of the pre- and postsynaptic acetylcholine receptors can be dissociated by using the different kinetics of toxin-receptor interactions. The results also implicate that a positive feedback enhancement of transmitter release operates via the presynaptic acetylcholine receptor in the neuromuscular junction in normal physiological conditions during repetitive pulses.

Action Potentials↗
PubMed1987

Does endogenous adenosine modulate the release of acetylcholine from motor nerve during single and repetitive stimulations in the mouse diaphragm?

In order to elucidate the physiological role of endogenous adenosine in regulating the release of acetylcholine, the effects of 8-phenyltheophylline, an antagonist of adenosine receptors and dipyridamole, an uptake inhibitor of adenosine, on the contractile response and quantal release of acetylcholine during single and repetitive stimulations of isolated mouse phrenic nerve-diaphragm preparations were studied. The curves relating the concentration vs. inhibition of contractile response to added adenosine and ATP were shifted parallel to the left by dipyridamole, but were shifted to the right by 8-phenyltheophylline at concentrations with little Ca2+-mobilization or phosphodiesterase inhibition. In the absence of exogenously added adenosine, 8-phenyltheophylline increased the quantal content of end-plate potentials (1 Hz), whereas dipyridamole decreased the quantal content. Successive decrease of the amplitude of end-plate potentials (e.p.p. run-down) evoked at 50 Hz was not changed either by 8-phenyltheophylline or by dipyridamole, suggesting that adenosine or ATP released from the motor nerve does not accumulate to an effective concentration even after repetitive stimulation for a feed-back regulation of the transmitter release. It is concluded that endogenous adenosine does inhibit the release of acetylcholine from motor nerve. However, the source of adenosine may be mostly from the muscle and is probably not involved in the feedback autoregulation.

Acetylcholine↗
PubMed1987

The frequency distribution of cardiovascular diseases in 13 hospital admitted patients in Korea. Korean Society of Circulation.

The frequency distribution of cardiovascular disease are changing recently due to the development of living environment. Unfortunately there are few epidemiological studies of cardiovascular diseases in general population, we tried to estimate the recent trend of cardiovascular diseases studying hospitalized patients in nationwide 13 large hospitals during a year of 1985. The hypertensive disease (24.1%) was the most common cardiovascular disease and the next were cerebrovascular disease (15.8%), arrhythmias (12.2%), ischemic heart disease (9.7%), congenital heart disease (9.1%), and rheumatic heart disease (5.4%) in order. This results showed that hypertensive disease and cerebrovascular disease are still the major cardiovascular disease and ischemic heart disease and arrhythmias are increased. But chronic rheumatic heart disease is declined compared with previous studies in hospitalized patients.

Adolescent↗