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Biomedical subjects

D S Ahn

Publications and source records attributed to D S Ahn.

At least 37 records · Page 2Linked to original sources
PubMed1996

Apoptosis induced by retinoic acid in Hep 3B cells in vitro.

Human hepatoma Hep 3B cells underwent apoptosis in response to 100 microM all-trans retinoic acid (RA) in full serum (10% fetal calf serum) condition in vitro. Cell death began approximately 24 h following treatment, with more than 80% of the cells dead after 60 h. The dead cells, mainly detached cells, exhibited condensed chromatin and DNA fragmentation, which are indicative of endonuclease activation and are the hallmarks of apoptosis in epithelial cells. Concurrent exposure to 1 microM cycloheximide (CX) prevented approximately 50% of cell death and DNA fragmentation induced by RA. Thus, other toxic injury to the cells as well as apoptosis might be involved in cell death. Sixty hours exposure of RA decreased the percentage of cells in G1 phase (16.3 +/- 0.4% versus 52.4 +/- 2.1%; P < or = 0.01) and in G2/M phase (13.4 +/- 1.2% versus 21.2 +/- 0.7%; P < or = 0.01), but did not change percent of cells in S phase (20.8 +/- 0.2% versus 20.7 +/- 0.5%) of the cell cycle compared with control. RA may have caused accumulation of Hep 3B cells before G1 phase, and that G0/G1 transition is a main check point in the active process of apoptosis. Electron micrographs of the cells treated with RA revealed typical morphologic changes of apoptosis, besides toxic injury to the cells. These data strongly indicate that RA is able to induce apoptosis and the induction of apoptosis may contribute to the antitumor activity of RA against hepatoma cells.

Antineoplastic Agents↗
PubMed1996

Characteristics of Ca2+ release mechanisms from an intracellular Ca2+ store in rabbit coronary artery.

To elucidate the Ca2+ release mechanisms in the rabbit coronary artery, arterial preparations were permeabilized with beta-escin and changes in tension were measured under varying experimental conditions. Additionally, we investigated properties and distribution of two kinds of Ca2+ release mechanisms, Ca2+-induced Ca2+ release (CICR) and IP3-induced Ca2+ release (IICR). The results obtained were summarized as follows; 1. When a rabbit coronary artery was incubated in a relaxing solution containing 30 microM beta-escin for 40 min. sensitivity to externally added Ca2+ was much higher in beta-escin permeabilized muscle than in intact preparations. The contractile effect of IP3 in beta-escin permeabilized muscle was also demonstrated; 2. Caffeine and IP3 contracted coronary arteries were permeabilized with beta-escin, but the amplitude of contraction was much larger in the presence of caffeine than of IP3. 3. Intracellular heparin completely inhibited the contractions induced by IP3, but not those by caffeine. On the other hand, procaine inhibited the responses to caffeine, but not those to IP3. Ryanodine inhibited both the caffeine- and IP3-induced contractions. 4. The amplitude of contractile responses was much larger to the maximal stimulation of CICR by applying caffeine than to the maximal stimulation of IICR by applying IP3. After the maximal CICR stimulation by caffeine, the activation of IICR by IP3 without the reloading of Ca2+ could no longer evoke contraction. On the other hand, after the maximal IICR activation, the activation of CICR could still evoke contraction although the amplitude of the contraction was smaller when compared with the case without the initial IICR stimulation. 5. Acetylcholine contracted coronary artery smooth muscles were permeabilized with beta-escin. However, in the absence of added guanosine triphosphate (GTP), the responses were very small. Acetylcholine-induced contraction was inhibited by heparin, but not by procaine. From the above results, it may be concluded that there are two kinds of mechanisms of Ca2+ release, CICR and IICR, in the rabbit coronary artery smooth muscle cell. Also, whereas the CICR mechanism distributes on the membrane of the whole smooth muscle Ca2+ store, the IICR mechanism distributes only on a part of it.

Animals↗
PubMed1996

Changes in intracellular Ca2+ concentration of rabbit coronary artery smooth muscle cell during ischemic cardioplegic period.

To elucidate the possibility whether an elevation of intracellular Ca2+ concentration ([Ca2+]i) in rabbit coronary artery myocytes during ischemic cardioplegic period may serve as one of the mechanisms of the "no-reflow' phenomenon or not, the changes in [Ca2+]i were measured under ischemic cardioplegia conditions using a fluorescent Ca2+ indicator, fura 2/AM. When single cells were perfused with cardioplegic or ischemic cardioplegic solutions, [Ca2+]i was significantly increased and the degree of [Ca2+]i elevation was further augmented by the ischemic cardioplegic solution. Pretreatment of a sarcoplasmic reticulum emptying agent, 20 mM caffeine, had no effect on ischemic cardioplegia-induced [Ca2+]i changes, but application of a Ca2+ channel blocker, 5 x 10 (-1)M nifedipine, or an antagonist of Na+/Ca2+ exchange, 5 mM Ni2+, significantly inhibited the [Ca2+]i elevation, respectively. The magnitude of ischemic cardioplegia-induced [Ca2+]i elevation was dependent on the Ca2+ concentration of perfusate in the range of 0 and 25 mM. When Ni2+ was added to the reperfusion solution, recovery of ischemic cardioplegia-induced [Ca2+]i elevation was very rapid compared with the controls. It is concluded that ischemic cardioplegia-induced [Ca2+]i elevation may serve as one of the mechanisms of the "no-reflow' phenomenon in rabbit coronary artery smooth muscle cells. We propose that Na+/Ca2+ exchange may serve as a key function in ischemic cardioplegia-induced [Ca2+]i elevation.

Animals↗
PubMed1995

Evaluation of retinal toxicity of acetylcholine in rabbit eyes.

PURPOSE: In vitreoretinal surgery, pupillary constriction may be required at the termination of a procedure especially if mechanical pupillary dilation was used in eyes filled with gas or silicone oil. A miotic agent instilled into the anterior chamber will sink and come into direct contact with retina in the aphakic or pseudophakic vitrectomized eye. Therefore, the retinal toxicity of acetylcholine, a miotic used for pupillary constriction, was studied. METHODS: Eight Dutch pigmented rabbit eyes were vitrectomized, had air-fluid exchange, and were injected with a 20% mixture of SF6. Subsequently eyes were randomly selected to have injections of 0.75 ml of 10 mg/ml acetylcholine (Miochol, Iolab Corp., Claremont CA) versus 0.75 ml of lactated Ringer's solution. Short-term (2 weeks) and long-term (6 weeks) retinal toxicity was assessed by ophthalmoscopy, electroretinogram, and histology by light and electron microscopy at both times. RESULTS: Ophthalmoscopy, electroretinographic tracings, histology, and electron microscopy disclosed no significant abnormalities. CONCLUSIONS: Acetylcholine does not appear to have significant retinal toxicity even when undiluted solutions are in direct contact with the retina. We therefore postulate that intraoperative use of acetylcholine in previously vitrectomized eyes filled with gas or silicone is safe.

Acetylcholine↗
PubMed1995

Activation of Ca(2+)-activated K+ channels by beta agonist in rabbit coronary smooth muscle cells.

Isoproterenol (ISO), a beta agonist, causes hyperpolarization of coronary smooth muscle cells via an increase in K+ conductance. This hyperpolarization may cause the coronary vasorelaxation by decreasing the cytoplasmic Ca2+ concentration. It is well known that the activation of beta adrenoreceptors stimulates the adenylate cyclase activity, and the resulting K+ channel phosphorylation by cAMP-dependent protein kinase may be responsible for ISO-induced increase in K+ channel activity. However, it is not clear whether the increase in K+ channel activity by ISO is exclusively due to the activation of adenylate cyclase or not. In this research, the effect of ISO on the isometric tension and the mechanism of ISO-induced K+ channel activation were investigated in various patch clamp conditions. The summarized results are as follows. ISO- and pinacidil induced vasorelaxation was significantly inhibited by the application of TEA or by increasing the external K+ concentration. In the whole cell clamp mode, application of ISO increased K+ outward current, and this effect was completely eliminated by propranolol. In the cell-attached patch, application of ISO or forskolin increased Ca(2+)-activated K+ channel activity. Application of ISO to the bath in the outside-out patches or GTP in the inside-out patches stimulated Ca(2+)-activated K+ channels. From the above results, both A-kinase dependent channel phosphorylation and direct GTP-binding protein mediated effect might be responsible for the the activation of Ca(2+)-activated K+ channel by ISO in rabbit coronary smooth muscle cells. And this K+ channel activation also contributes to the ISO-induced vasorelaxation.

Animals↗
PubMed1995

Effects of mastoparan on a vascular contractility in rabbit aorta.

Mastoparan is an amphiphilic tetradecapeptide derived from wasp venom which activates G-proteins. Several secondary effects have been attributed to this peptide, including activation of phospholipase and phosphatidylinositol kinase. The aim of the present study was to investigate the effects of mastoparan on vascular contractility. Rabbit aortic rings were cut and mounted on a force transducer to record isometric tension on a polygraph. The effects of mastoparan were then investigated on the contractile responses in the isolated rabbit aorta with or without endothelium. The results were summarized as follows; 1. Mastoparan caused biphasic response, a transient relaxation followed by a further contraction, in norepinephrine (NE)-precontracted ring with endothelium. These effects were not observed in the aorta in the absence of endothelium. 2. Mastoparan-induced transient relaxation was significantly inhibited by treatment with a N-omega-nitro-L-arginine or methylene blue. 3. When an inhibitor of phospholipase C, neomycin was added to the precontracted aortic ring with NE, the transient relaxation induced by mastoparan was inhibited, but sustained contraction was not inhibited. 4. When an inhibitor of phospholipase A2, quinacrine and inhibitor of the cyclooxygenase pathway, indomethacin, were added to a precontracted ring with NE, the transient relaxation induced by mastoparan was not inhibited, but sustained contraction was inhibited. 5. Mastoparan induced a contraction of the aorta either with or without endothelium. Indomethacin and nifedipine inhibited mastoparan-induced contraction. From the above results, we concluded that mastoparan acts on the endothelium and modifies the release of endothelium-derived relaxing factors such as nitric oxide and also endothelium-derived contracting factors such as metabolites of arachidonic acid.

Animals↗
PubMed1994

Fatty acids directly increase the activity of Ca(2+)-activated K+ channels in rabbit coronary smooth muscle cells.

The large conductance Ca2+ activated K+ channel (BK channel) has been considered to play an important role in the excitability and contractility of vascular smooth muscle cells. Activation of the BK channel causes the hyperpolarization and relaxation of vascular smooth muscle cells. It has been reported that fatty acids can affect the BK channel activity and its concentration is increased significantly during myocardial ischemia. These reports suggest that fatty acids may contribute to the ischemic coronary vasodilation by increasing the BK channel activity. However, the underlying mechanism of fatty acid-induced activation of the BK channel is still uncertain. In the present study, we measured the effect of fatty acids on the BK channel activity in rabbit coronary smooth muscle cells by using patch clamp method and also examined its underlying mechanism. Arachidonic acid (AA) dissolved in DMSO activated the BK channel in a dose-dependent manner (from 0.5 to 10 microM), and DMSO (0.1%) alone had no effect on the activity of the BK channel. Arachidonic acid activated BK channels in both cell-attached and inside-out patches, but the onset and recovery of this effect were slower in the cell-attached patch configuration. The BK channel activity was also increased by other fatty acids, including myristic acid, linoleic acid, palmitoleic acid and palmitic acid. Long chain fatty acids were more effective than short chain fatty acids (myristic acid), and there was no statistical difference between the effect of saturated (palmitic acid) and unsaturated fatty acids (palmitoleic acid) on the BK channel activity. The concentration of Ca2+ and Mg2+ in the bathing solution had no appreciable effects on the AA-induced increase of BK channel activity. From the above results, it may be concluded that fatty acids directly increase the BK channel activity and may contribute to the ischemic coronary vasodilatation in rabbit coronary smooth muscle cells.

Animals↗
PubMed1994

Effect of hypothermic cardioplegia on cardiac protection--I. Effect of hypothermic cardioplegia on the cytosolic Ca2+ concentration in rat ventricular myocytes.

Cytosolic Ca2+ concentration of rat ventricular cells was measured under varying experimental conditions by using a fluorescent Ca2+ indicator, Fura-2. Resting [Ca2+]i of rat myocyte was 150 +/- 30 nM (n = 39), and this value was compatible with others. The Perfusion of cardioplegic solution significantly increased [Ca2+]i, and this effect was further augmented by hypothermia (p < 0.05). Application of nifedipine (5 x 10(-7) M) to the perfusate or pretreatment of caffeine (10 mM) had no apparent effect on this cardioplegia-induced [Ca2+]i change. But Ni2+ (5 mM), an antagonist of Na+/Ca2+ exchange mechanism, prevented the [Ca2+]i change during cardioplegia (p < 0.05). Magnitude of cardioplegia-induced [Ca2+]i increase was also dependent on the Ca2+ concentration of cardioplegic solution. These results suggest that Na+/Ca2+ exchange may play an important role in cardioplegia-induced [Ca2+]i change. To rule out the possibility whether the protective effect of hypothermic cardioplegia is due to the preservation of high-energy phosphate store or decreasing the transmembrane ionic fluxes by phase transition, we exhausted a energy store of cardiac cell by application of 2,4 dinitrophenol to the bath and measured its effect on [Ca2+]i change during cardioplegia. Hypothermic cardioplegia delayed the onset of [Ca2+]i increase and decreased its amplitude compared to those of normothermic cardioplegia. From the above results, hypothermic cardioplegia may protect the cardiac cells from ischemic insult by preserving a high-energy phosphate store. Application of Ni2+ to the cardioplegic solution or reduction of external Ca2+ concentration also had some protective effect, since it prevented [Ca2+]i increase during cardioplegia.

Animals↗
PubMed1992

High-pass resolution perimetry in eyes with ocular hypertension and primary open-angle glaucoma.

We analyzed the results of high-pass resolution perimetry on normal eyes, eyes with ocular hypertension, and eyes with primary open-angle glaucoma. The subjects were matched for age and lens density. We controlled for refraction, visual acuity, pupil size, miotic medications, and learning effects. Under these conditions the glaucomatous eyes showed a significant reduction in overall resolution threshold compared to both normal (P less than or equal to .01) and hypertensive eyes (P less than .01). The hypertensive eyes were not significantly different from normal. Standard increment threshold fields and high-pass resolution visual fields had an agreement of abnormality of 67%. Resolution perimetry showed a 92% agreement with standard perimetry in the location of the defect, when the defect was apparent on both tests. These results indicated that resolution perimetry may be useful for diagnosis and management of primary open-angle glaucoma.

Aged↗
PubMed1992

Effects of vanadate on vascular contractility and membrane potential in the rabbit aorta.

Isolated rabbit aortic ring with intact endothelial cell preparations precontracted with NE (10(-7) M) were relaxed by vanadate in a dose dependent manner (from 0.2 to 2 mM). Application of vanadate and ACh during the tonic phase of high K+(100 mM)-induced contraction showed a slight relaxation in contrast to that in NE-induced contraction, but sodium nitroprusside (10 microM) more effectively relaxed the aortic ring preparations in high K+ contraction than that of vanadate. Vanadate-induced relaxation in NE-contracted aortic rings was reversed by application of BaCl2 (50 microM) or glibenclamide (10 microM). Furthermore, Vanadate hyperpolarized membrane potential of smooth muscle cells in endothelium-intact aortic strips and this effect was abolished by application of glibenclamide. The above results suggest that vanadate release EDHF (Endothelium-Derived Hyperpolarizing Factor), in addition to EDRF (Endothelium-Derived Relaxing Factor) from endothelial cell. This EDHF hyperpolarize the smooth muscle cell membrane potential via opening of the ATP-sensitive K+ channel and close a voltage dependent Ca++ channel. So it is suggested that the vanadate-induced relaxation of rabbit thoracic aortic rings may be due to the combined effects of EDRF and EDHF.

Animals↗
PubMed1992

Effects of Na+, K(+)-pump inhibitors on acetylcholine-induced relaxation in the rabbit aorta.

The purpose of this study was to investigate the effects of inhibitors of the Na+, K(+)-pump and membrane depolarizing agents on endothelium-dependent acetylcholine-induced relaxation in the rabbit thoracic aorta. Aortic rings were prepared from the rabbit descending thoracic aorta and the contractility of the ring was measured in various conditions such as application of ouabain, exposure to K(+)-free Krebs-Henseleit solution and high K+. Ouabain or exposure to K(+)-free Krebs-Henseleit solution inhibited acetylcholine or sodium nitroprusside-induced relaxation. KCl also inhibited the acetylcholine or sodium nitroprusside-induced relaxation. These results suggest that the Na+, K(+)-pump may play a role in endothelium-dependent acetylcholine-induced relaxation.

Acetylcholine↗
PubMed1991

Esophagogastric neoplasms: palliation with a modified gianturco stent.

Self-expanding metallic stents of a modified Gianturco design were used for palliative treatment of malignant esophagogastric strictures. Over a 10-month period, 10 stents were placed in nine patients. All patients with severe dysphagia due to malignant strictures in whom all other treatment options had failed were candidates for these stents. Neither extensive length of esophageal involvement nor complete esophageal obstruction was a contraindication. All stents were placed with fluoroscopic guidance without any technical failures or procedural morbidity or mortality. Mild reflux occurred in three patients in whom the stent tubes straddled the distal esophageal sphincter. Five patients were still alive after 1-8 months. The remaining four patients died 6-28 weeks after stent placement; all stents were patent at the time of death. These stents are easy to insert, safe, and reasonably effective for short-term palliative treatment of esophagogastric neoplasms.

Adenocarcinoma↗
PubMed1989

Impaired interleukin-2 receptor expression on lymphocytes from patients with chronic active hepatitis type B.

To evaluate cell mediated immunopathogenic mechanisms in chronic hepatitis B virus (HBV) infection, we investigated the changes of T4/T8 ratios from the peripheral blood, the percentages of IL-2 receptor expression after stimulation of mitogens (Con A, PHA) and a specific antigen (Hepatitis type B surface antigen, HBs), and the proliferative response mediated by IL-2 receptors after rIL-2 stimulation on mixed mononuclear cell. These experiments were performed comparatively in 5 groups which consisted of serologically negative normal subjects, chronic HBV carriers, patients with chronic active hepatitis (CAH) type B, patients with acute hepatitis (AH) type B, and the antibody positive healthy subjects. There were significant decreases of T4/T8 ratios in chronic HBV carriers, in patients with CAH type B, and in patients with AH type B, compared with negative normal controls. There were no significant differences between patients with CAH type B and the HBs negative normal controls in the percentage of IL-2 receptor positive cells after in-vitro HBs-stimulation and the proliferative response assessed by the incorporation of 3H-thymidine, whereas in patients with AH type B there were significant increases in both. Thus, in addition to a relatively decreased T4/T8 ratio, the impairment of IL-2 receptor expression on the lymphocytes after HBs-stimulation caused a defective response of cellular proliferation, and this might be one of the leading immunopathogenic roles in chronic HBV infection.

Adult↗
PubMed1989

Percutaneous transcatheteral biliary biopsy (PTBB)--a report of two cases.

In two patients with obstructive jaundice, percutaneous transhepatic cholangiography (PTC) and percutaneous transhepatic biliary drainage (PTBD) were performed. During PTBD, the percutaneous transcatheteral biliary biopsy (PTBB) with the biopsy forceps of the gastrofiberscope was performed through the biliary stent catheter. Biopsy specimens were successfully obtained and histopathologic findings were satisfactory in both cases.

Aged↗