• The Korean Journal of Physiology and Pharmacology
• /
• v.4 no.1
• /
• pp.73-79
• /
• 2000

This study investigated whether propofol, an intravenous, non-barbiturate anesthetic, could reduce brain damage following global forebrain ischemia. Transient global ischemia was induced in gerbils by occlusion of bilateral carotid arteries for 3 min. Propofol (50 mg/kg) was administered intraperitoneally 30 min before, immediately after, and at 1 h, 2 h, 6 h after occlusion. Thereafter, propofol was administered twice daily for three days. Treated animals were processed in parallel with ischemic animals receiving 10% intralipid as a vehicle or with sham-operated controls. In histologic findings, counts of viable neurons were made in the pyramidal cell layer of the hippocampal CA1 area 4 days after ischemia. The number of viable neurons in the pyramidal cell layer of CA1 area was similar in animals treated with a vehicle or a subanesthetic dose of propofol. In terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling (TUNEL) assay, semiquantitative analysis of dark-brown neuronal cells was made in the hippocampal CA1 area. There was no significant difference in the degree of TUNEL staining in the hippocampal CA1 area between vehicle-treated and propofol-treated animals. These results show that subanesthetic dose of propofol does not reduce delayed neuronal cell death following transient global ischemia in Mongolian gerbils.

• The Korean Journal of Physiology and Pharmacology
• /
• v.8 no.1
• /
• pp.1-5
• /
• 2004

Transient forebrain ischemia results in the delayed neuronal death in the CA1 area of the hippo-campus. The present study was performed to determine effects of aminoguanidine, a selective iNOS inhibitor, on the generation of peroxynitrite and delayed neuronal death occurring in the hippocampus following transient forebrain ischemia. Transient forebrain ischemia was produced in the conscious rats by four-vessel occlusion for 10 min. Treatment with aminoguanidine (100 mg/kg or 200 mg/kg, i.p.) or saline (0.4 ml/100 g, i.p.) was started 30 min following ischemia-reperfusion and the animals were then injected twice daily until 12 h before sacrifice. Immunohistochemical method was used to detect 3-nitrotyrosine, a marker of peroxynitrite production. Posttreatment of aminoguanidine (200 mg/kg) significantly attenuated the neuronal death in the hippocampal CA1 area 3 days, but not 7 days, after ischemia-reperfusion. 3-Nitrotyrosine immunoreactivity was enhanced in the hippocampal CA1 area 3 days after reperfusion, which was prevented by the treatment of aminoguanidine (100 mg/kg and 200 mg/kg). Our findings showed that (1) the generation of peroxynitrite in the hippocampal CA1 area 3 days after ischemia-reperfusion was dependent on the iNOS activity; (2) the postischemic delayed neuronal death was attenuated in the early phase through the prevention of peroxynitrite generation by an iNOS inhibitor.

• Fibers and Polymers
• /
• v.6 no.2
• /
• pp.131-138
• /
• 2005

A theoretical model is proposed in order to investigate rheological behavior of bubble suspension with large deformation. Theoretical constitutive equations for dilute bubble suspensions are derived by applying a deformation theory of ellipsoidal droplet [1] to a phenomenological suspension theory [2]. The rate of deformation tensor within the bubble and the time evolution of interface tensor are predicted by applying the proposed constitutive equations, which have two free fitting parameters. The transient and steady rheological properties of dilute bubble suspensions are studied for several capillary numbers (Ca) under simple shear flow and uniaxial elongational flow fields. The retraction force of the bubble caused by the interfacial tension increases as bubbles undergo deformation. The transient and steady relative viscosity decreases as Ca increases. The normal stress difference (NSD) under the simple shear has the largest value when Ca is around 1 and the ratio Of the first NSD to the second NSD has the value of 3/4 for large Ca but 2 for small Ca. In the uniaxial elongational flow, the elongational viscosity is three times as large as the shear viscosity like the Newtonian fluid.

• Journal of Ginseng Research
• /
• v.39 no.4
• /
• pp.398-405
• /
• 2015

Background: Ginseng has been used as a tonic for invigoration of the human body. In a previous report, we identified a novel candidate responsible for the tonic role of ginseng, designated gintonin. Gintonin induces $[Ca^{2+}]_i$ transient in animal cells via lysophosphatidic acid receptor activation. Gintonin-mediated $[Ca^{2+}]_i$ transient is linked to anti-Alzheimer's activity in transgenic Alzheimer's disease animal model. The previous method for gintonin preparation included multiple steps. The aim of this study is to develop a simple method of gintonin fraction with a high yield. Methods: We developed a brief method to obtain gintonin using ethanol and water. We extracted ginseng with fermentation ethanol and fractionated the extract with water to obtain water-soluble and water-insoluble fractions. The water-insoluble precipitate, rather than the water-soluble supernatant, induced a large $[Ca^{2+}]_i$ transient in primary astrocytes. We designated this fraction as gintonin-enriched fraction (GEF). Results: The yield of GEF was approximately 6-fold higher than that obtained in the previous gintonin preparation method. The apparent molecular weight of GEF, determined using sodium dodecyl sulfate-polyacrylamide gel electrophoresis, was equivalent to that obtained in the previous gintonin preparation method. GEF induced $[Ca^{2+}]_i$ transient in cortical astrocytes. The effective dose (ED50) was $0.3{\pm}0.09{\mu}g/mL$. GEF used the same signal transduction pathway as gintonin during $[Ca^{2+}]_i$ transient induction in mouse cortical astrocytes. Conclusion: Because GEF can be prepared through water precipitation of ginseng ethanol extract and is easily reproducible with high yield, it could be commercially utilized for the development of gintoninderived functional health food and natural medicine.

• The Korean Journal of Physiology and Pharmacology
• /
• v.10 no.4
• /
• pp.167-172
• /
• 2006

In the present study, we developed a simple method to predict the neuronal cell death in the mouse hippocampus and striatum following transient global forebrain ischemia by evaluating both cerebral blood flow and the plasticity of the posterior communicating artery (PcomA). Male C57BL/6 mice were anesthetized with halothane and subjected to bilateral occlusion of the common carotid artery (BCCAO) for 30 min. The regional cerebral blood flow (rCBF) was measured by laser Doppler flowmetry. The plasticity of PcomA was visualized by intravascular perfusion of India ink solution. When animals had the residual cortical microperfusion less than 15% as well as the smaller PcomA whose diameter was less than one third compared with that of basilar artery, neuronal damage in the hippocampal subfields including CA1, CA2, and CA4, and in the striatum was consistently observed. Especially, when mice met these two criteria, marked neuronal damage was observed in CA2 subfield of the hippocampus. In contrast, after transient BCCAO, neuronal damage was consistently produced in the striatum, dependent more on the degree of rCBF reduction than on the plasticity of PcomA. The present study provided simple and highly reproducible criteria to induce the neuronal cell death in the vulnerable mice brain areas including the hippocampus and striatum after transient global forebrain ischemia.

• The Korean Journal of Physiology and Pharmacology
• /
• v.3 no.6
• /
• pp.623-630
• /
• 1999

Decreased cardiac contractility occurs in endotoxicosis, but little is known about the ionic mechanism responsible for myocardial dysfunction. In this study, we examined the changes in $Ca{2+}$ and $K^+$ currents in cardiac myocytes from endotoxin-treated rat. Ventricular myocytes were isolated from normal and endotoxemic rats (ex vivo), that were treated for 10 hours with Salmonella enteritidis lipopolysaccharides (LPS; 1.5 mg/kg) intravenously. Normal cardiac myocytes were also incubated for 6 hours with 200 ng/ml LPS (in vitro). L-type $Ca{2+}$ current $(I_{Ca,L})$ and transient outward $K^+$ current $(I_{to})$ were measured using whole cell patch clamp techniques. Peak $I_{Ca,L}$ was reduced in endotoxemic myocytes (ex vivo; 6.00.4 pA/pF, P＜0.01) compared to normal myocytes (control; 10.90.6 pA/pF). Exposure to endotoxin in vitro also attenuated $I_{Ca,L}$ (8.40.4 pA/pF, P＜0.01). The amplitude of $(I_{to})$ on depolarization to 60 mV was reduced in endotoxin treated myocytes (16.51.5 pA/pF, P＜0.01, ex vivo; 20.00.9 pA/pF, P＜0.01 , in vitro) compared to normal myocytes (control; 24.71.0 pA/pF). There was no voltage shift in steady-state inactivation of $I_{Ca,L}$ and $(I_{to})$ between groups. These results suggest that endotoxin reduces $Ca{2+}$ and $K^+$ currents of rat cardiac myocytes, which may lead to cardiac dysfunction.

• Journal of the Korean Ceramic Society
• /
• v.49 no.2
• /
• pp.197-203
• /
• 2012

In this study, in order to improve densification of $La_{0.8}Ca_{0.2}Cr_{0.9}Co_{0.1}O_{3-\delta}$ (LCCC), which is known for one of the most proper candidate interconnector materials in the solid oxide fuel cells, $CaCrO_4$ was prepared via solid oxide synthesis route and added to the LCCC with different amount and particle sizes. As the amount of the $CaCrO_4$ increased, porosity of the sintered samples increased, and the pore size was proportional to the particle size of the $CaCrO_4$. This supports the fact that the $CaCrO_4$ phase forms liquid during sintering and permeate into the matrix leaving behind large pores. Then the liquid reacts with the matrix through the solid solution. However, when the samples were sintered with a slow ramp up rates, the porosity decreased. This is thought to be caused by the progressive solid solution of $CaCrO_4$ before the temperature reach to the melting temperature and forms a fluent amount of liquids. The sintering behavior of the LCCC with the addition of $CaCrO_4$ was analyzed through the transient liquid phase sintering on the basis of the microstructure observation and phase identification by x-ray diffraction.

• The Korean Journal of Physiology and Pharmacology
• /
• v.23 no.5
• /
• pp.357-366
• /
• 2019

$G{\alpha}_q$-coupled receptor stimulation was implied in the activation process of transient receptor potential canonical (TRPC)1/4 and TRPC1/5 heterotetrameric channels. The inactivation occurs due to phosphatidylinositol 4,5-biphosphate ($PI(4,5)P_2$) depletion. When $PI(4,5)P_2$ depletion was induced by muscarinic stimulation or inositol polyphosphate 5-phosphatase (Inp54p), however, the inactivation by muscarinic stimulation was greater compared to that by Inp54p. The aim of this study was to investigate the complete inactivation mechanism of the heteromeric channels upon $G{\alpha}_q$-phospholipase $C{\beta}$ ($G{\alpha}_q-PLC{\beta}$) activation. We evaluated the activity of heteromeric channels with electrophysiological recording in HEK293 cells expressing TRPC channels. TRPC1/4 and TRPC1/5 heteromers undergo further inhibition in $PLC{\beta}$ activation and calcium/protein kinase C (PKC) signaling. Nevertheless, the key factors differ. For TRPC1/4, the inactivation process was facilitated by $Ca^{2+}$ release from the endoplasmic reticulum, and for TRPC1/5, activation of PKC was concerned mostly. We conclude that the subsequent increase in cytoplasmic $Ca^{2+}$ due to $Ca^{2+}$ release from the endoplasmic reticulum and activation of PKC resulted in a second phase of channel inhibition following $PI(4,5)P_2$ depletion.

• International Journal of Oral Biology
• /
• v.35 no.3
• /
• pp.129-135
• /
• 2010

Recent studies have implicated reactive oxygen species (ROS) as determinants of the pathological pain caused by the activation of peripheral neurons. It has not been elucidated, however, how ROS activate the primary sensory neurons in the pain pathway. In this study, calcium imaging was performed to investigate the effects of NaOCl, a ROS donor, on the intracellular calcium concentration ($[Ca^{2+}]i$) in acutely dissociated dorsal root ganglion (DRG) neurons. DRG was sequentially treated with 0.2 mg/ml of both protease and thermolysin, and single neurons were then obtained by mechanical dissociation. The administration of NaOCl then caused a reversible increase in the $[Ca^{2+}]i$, which was inhibited by pretreatment with phenyl-N-tertbuthylnitrone (PBN) and isoascorbate, both ROS scavengers. The NaOCl-induced $[Ca^{2+}]i$ increase was suppressed both in a calcium free solution and after depletion of the intracellular $Ca^{2+}$ pool by thapsigargin. Additionally, this increase was predominantly blocked by pretreatment with the transient receptor potential (TRP) antagonists, ruthenium red ($50\;{\mu}M$) and capsazepine ($10\;{\mu}M$). Collectively, these results suggest that an increase in the intracellular calcium concentration is produced from both extracellular fluid and the intracellular calcium store, and that TRP might be involved in the sensation of pain induced by ROS.

• The Korean Journal of Physiology
• /
• v.29 no.2
• /
• pp.233-241
• /
• 1995

The nonapeptide bradykinin has been shown to exhibit an array of biological activities including relaxation/contraction of various smooth muscles. In order to investigate the effects of bradykinin on the contractility and the electrical activity of antral circular muscle of guinea-pig stomach, the isometric contraction and membrane potential were recorded. Also, using standard patch clamp technique, the $Ca^{2+}-activated$ K currents were recorded to observe the change in cytosolic $Ca^{2+}$ concentration. $0.4 {\mu}M$ bradykinin induced a triphasic contractile response (transient contraction-transient relaxation-sustained contraction) and this response was unaffected by pretreatment with neural blockers (tetrodotoxin, atropine and guanethidine) or with apamin. Bradykinin induced hyperpolarization of resting membrane potential and enhanced the amplitude of slow waves and spike potentials. The enhancement of spike potentials was blocked by neural blockers. Both the bradykinin-induced contractions and changes in membrane potential were reversed by the selective $B_2$-receptor antagonist $(N{\alpha}-adamantaneacetyl-_{D}-Arg-[Hyp, Thy,_{D}-Phe]-bradykinin)$. In whole-cell patch clamp experiment, we held the membrane potential at -20 mV and spontaneous and transient changes of Ca-activated K currents were recorded. Bradykinin induced a large transient outward current, consistent with a calcium-releasing action of bradykinin front the intracellular calcium pool, because such change was blocked by pretreatment with caffeine. Bradykinin-induced contraction was also blocked by pretreatment with caffeine. From these results, it is suggested that bradykinin induces a calciumrelease and contraction through the $B_{2}$ receptor of guinea-pig gastric smooth muscle. Enhancement of slow wave activity is an indirect action of bradykinin through enteric nerve cells embedded in muscle strip.