• The Korean Journal of Physiology
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• v.24 no.1
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• pp.91-102
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• 1990

The effects of extracellular $Ca^{2+}$ and various $Ca^{2+}$ antagonists on endothelium-dependent relaxation to acetylcholine were studied in the isolated rabbit thoracic aorta in order to elucidate the control mechanism of endothelium derived relaxing factor (EDRF) release. Endothelium was removed from aortic strips by gentle rubbing with cotton ball. The effect of hemoglobin on basal tension was also observed with hemolysate. The results obtained were as follows: 1) Endothelium-dependent relaxation (EDR) to acetylcholine (ACh) showed biphasic pattern; the initial rapid relaxation phase and the late slow relaxation phase. 2) With the depletion of the extracellular $Ca^{2+}$, EDR was gradually suppressed, especially the late slow relaxation. 3) Verapamil, nifedipine, $Mn^{2+}$ and $Cd^{2+}$ had not any effect on EDR, while $La^{3+}$ and $Co^{2+}$ suppressed EDR completely. 4) The resting tension of the strips with rubbed endothelium was not altered by the addition of hemoglobin. That of the strips with intact endothelium, however, was enhanced and EDR to ACh was completely blocked From these results, we suggest that extracellular $Ca^{2+}$ is necessary for ACh-induced slow relaxation while $Ca^{2+}$ antagonists have not any effect on EDR.

• Journal of Chest Surgery
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• v.42 no.3
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• pp.396-400
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• 2009

Operations using the da Vinci robot have performed in for many surgeries, but the adoption of robotics to general thoracic surgery has been slow. The patient (age 74, male) visited our hospital complaining of hiccups and dysphagia. The CT scan and endoscopic biopsy revealed esophageal cancer (squamous cell carcinoma). We performed transthoracic esophagectomy using a da Vinci robot and this was followed by gastric tube mobilization via laparoscopy. Cervical esophago-gastric anastomosis was done using the hand-sewn method. The gastric tube was brought into the neck through the retrosternal route. The patient was discharged without any complications. We report here on a case of successful da Vinci robotic esophgagectomy.

• Journal of Chest Surgery
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• v.43 no.2
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• pp.161-163
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• 2010

A 12-day-old female baby underwent a Norwood procedure for hypoplastic left heart syndrome. The left superior vena cava (LSVC), which was found incidentally during the operation, was divided to facilitate surgical exposure. After the operation, she developed signs of low cardiac output and died 7 hours afterward. Autopsy findings showed that the coronary sinus was atretic at the orifice without unroofing into both atria, rendering the LSVC the sole route of coronary sinus drainage. In patients with incidentally-found LSVC during surgery, special care should be taken to leave the LSVC intact because the LSVC may be the exclusive drainage vein of the coronary venous system.

• The Korean Journal of Pharmacology
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• v.28 no.2
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• pp.147-162
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• 1992

The objectives of the present experiments were to characterize the effects of the peptides belonging to the pancreatic polypeptide family on the contractility of cerebral arteries and to observe the interactions of these peptides with the cyclic nucleotide activators and the potassium channel openers. Dogs of either sex, $20{\sim}30\;Kg$ in weight, were sacrificed. Basilar and middle cerebral arteries from brain were isolated and prepared for myography in the PSS equilibrated with 95% $O_2$ and 5% $CO_2$ at $37^{\circ}C$. The endothelial cells of the spiral strips were removed by CHAPS solution (0.3% w/v, 15 seconds). 1. PP, PYY and NPY contracted the arterial strips concentration-dependently with a rank order of potency of PYY>NPY>PP. These peptides were 20 to 200 times more potent than norepinephrine, and only PYY showed a greater potency than 5-HT. 2. Cyclic nucleotide activators, forskolin (for cAMP) and sodium nitroprusside (for cGMP) reduced the basal tone and inhibited the PP-, PYY- and NPY- induced contractions by concentration-dependent manners. Forskolin was more potent in reducing basal tone than sodium nitroprusside. 3. Potassium channel openers, RP 49356, P 1060 and BRL 38227 reduced the basal tone concentration-dependently and tended to inhibit the PP-, PYY- and NPY- induced contractions. Notably, BRL 38227 with low concentration $(0.1\;{\mu}M)$ enhanced the contractions induced by those peptides while P 1060 inhibited the contractions concentration-dependently. 4. The combinations of the cyclic nucleotide activators and the potassium channel openers were slightly additive in reducing the basal tone. P 1060 and BRL 38227 enhanced the relaxant effect of sodium nitroprusside significantly. On the PYY-induced contration $(0.1\;{\mu}M)$, $K^+$ channel openers tended to inhibit the inhibitory actions of forskolin and sodium nitroprusside. P 1060 and BRL 38227 antagonized the inhibitory action of sodium nitroprusside significantly. The results of the present study may be summarized that in canine cerebral arteries, not only NPY but also PYY may play a role in a cerebrovascular spasm, and intracellular concentration of either cAMP or cGMP may be involved in the mechanism of vasoconstrictive actions of these peptides, which may be affected either positively or negatively by a $K^+$ channel opener.

• The Korean Journal of Pharmacology
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• v.31 no.1 s.57
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• pp.27-37
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• 1995

In anesthetized rats, we examined the possibility that endothelium-derived relaxing factor (EDRF) or nitric oxide (NO) released in response to cholinergic mechanism may contribute to the reflex autoregulation of cerebral blood flow. Suffusion with mock cerebrospinal fluid (CSF), containing acetylcholine (ACh, $10^{-9}{\sim}10^{-6}M$) evoked concentration-dependent vasodilatation of the resting pial artery (mean, $19.3{\pm}1.7{\mu}m$, n=36), which was significantly inhibited not only by $N{\omega}$-nitro-L-arginine (L-NNA, $10^{-5}M$) but also by methylene blue ($10^{-6}M$) and oxyhemoglobin ($10^{-6}M$). The muscarinic receptors in the endothelium of pial artery implicated in the release of EDRF were considered to be $M_1\;and\;M_3$ subtypes. When suffused with mock CSF containing L-arginine it caused a transient vasodilatation, which was strongly inhibited by LY 83583 ($10^{-5}M$), but not by L-NNA ($10^{-5}M$). Additionally, both ACh- and L-arginine-induced vasodilation were significantly inhibited by glibenclamide, a specific ATP-sensitive $K^+$ channel blocker. On the other hand, changes in pial arterial diameter were plotted as a function of changes in systemic arterial blood pressure. The slopes of regression lines for vasodilation and vasoconstriction were not affected by pretreatment with $10^{-5}M$ L-NNA, but significantly reduced by $3{\times}10^{-6}M$ glibenclamide. Thus it is suggested that the reflex vasodilation of rat pial arteries in response to a transient hypotension is not mediated by EDRF (NO).

• Journal of Chest Surgery
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• v.42 no.5
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• pp.588-596
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• 2009

Background: To clarify the effect of hypoxia on vascular contractility, we tried to show whether hypoxia induced the release of endothelium-derived relaxing factor (EDRF) and the nature of the underlying mechanism for this release. Material and Method: Isometric contractions were observed in rabbit aorta, and the released EDRF from the rabbit aorta was bioassayed by using rabbit denuded carotid artery. The intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) in the cultured rabbit aortic endothelial cells was recorded by a microfluorimeter with using Fura-2/AM. Hypoxia was evoked to the blood vessels or endothelial cells by eliminating the $O_2$ in the aerating gases in the external solution. Chemical hypoxia was evoked by applying deoxyglucose or $CN^-$. Result: Hypoxia relaxed the precontracted rabbit thoracic aorta that had its endothelium, and the magnitude of the relaxation was gradually increased by repetitive bouts of hypoxia. In contrast, hypoxia-induced relaxation was not evoked in the aorta that was denuded of endothelium. In a bioassay experiment, hypoxia released endothelium-derived relaxing factor (EDRF) and the release was inhibited by L-NAME or the $K^+$ channel blocker tetraethylammonium (TEA). In the cultured endothelial cells, hypoxia augmented the ATP-induced increase of the intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) and this increase was inhibited by TEA. Furthermore, chemical hypoxia also increased the $Ca^{2+}$ influx. Conclusion: From these results, it can be concluded that hypoxia might induce the release of NO from rabbit aortic endothelial cells by increasing $[[Ca^{2+}]_i$.

• The Korean Journal of Pharmacology
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• v.27 no.1
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• pp.45-52
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• 1991

The inhibitory effects of GS354 and GS389 on cytosolic $Ca^{2+}$ level ($[Ca^{2+}]_{1}$; measured with fura-2 fluorescence) and muscle tension in vascular smooth muscle of rat thoracic aorta were investigated. Both GS354 and GS389 inhibited the contractions induced by high $K^+$ or by norepinephrine. The vasodilator effect of GS354 was accompanied by a decrease in $[Ca^{2+}]_{1}$. The inhibitory effect on high $K^+-stimulated$ $[Ca^{2+}]_{1}$ was antagonized by a $Ca^{2+}$ channel activator, Bay K8644. However, the inhibitory effect on muscle tension was not antagonized by Bay K8644. These results suggest that GS354 inhibits $Ca^{2+}$ channels to decrease $[Ca^{2+}]_{1}$ and also decreases $Ca^{2+}$ sensitivity of contractile elements. The inhibitory effects of GS389 was accompanied by the increase in tissue fluorescence. This increment was not due to fura-2 fluorescence but to endogeneous pyridine nucleotides, suggesting that GS389 has an effect to inhibit mitochondrial function. Because of this interference, effects of GS389 on $[Ca^{2+}]_{1}$ was obscured. However, since sequential addition of Bay K8644 in the presence of GS389 further increased the fluorescence but not muscle tension, this compound seems to have the effects to inhibit $Ca^{2+}$ channels and to decrease $Ca^{2+}$ sensitivity of contractile elements.

• KSBB Journal
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• v.21 no.5
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• pp.376-383
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• 2006

Pine needle(Pinus densiflora sieb, et zucc) extract has been used to improve cardiovascular disorders, detoxification of nicotine, the infirmities of age and curing diseases of unidentified symptoms. It has various useful components including amino acids, vitamin C, terpenoids and chlorophyll. In this study we have identified 8 different yeast strains that are developed spontaneously causing self fermentation in the extract. The self-fermented pine extract(SFPE) inhibited the growth of some bacterial strains like E. coli, Bacillus subtilis and Staphylococcus aureus. The SFPE($0.2{\mu}{\ell}/ml{\sim}0.3{\mu}{\ell}/ml$) showed 90% NBT superoxide scavenging activities which is similar for all tested samples of different ages. The 7 years old SFPE(0.15 mg/ml and 0.3 mg/ml) caused relaxation of spontaneous contraction and relaxation rhythm of thoracic arterial tissues from rat. Therefore, SFPE has useful effects such as antibacterial, antioxidant and improved blood circulation and could be a good source of functional food development.

• The Korean Journal of Pharmacology
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• v.32 no.1
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• pp.39-49
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• 1996

In the present study, we observed change in intracellular $Ca^{2+}$$([Ca^{2+}]_i)$ as measured with the fluorescent $Ca^{2+}-indicator$ fura-2 in association with force development of the rat basilar arteries during activation by$K^+$ depolarizing solution and U46619, a thromboxane analogue, in the absence and the presence of calcitonin-gent related peptide (CGRP). CGRP (30 and 100 nM) caused a concentration-dependent inhibition of U46619-induced contraction with decrease in $[Ca^{2+}]_i$, whereas it did not exert any effect on the $K^+$ (90 mM)-induced contraction and increase in $[Ca^{2+}]_i$, Further, $[Ca^{2+}]_i-force$ relationships were determined by plotting the ratio of $F_{340}/F_{380}$ $([Ca^{2+}]_i)$ as a function of the force induced by U46619, and the results were compared with those obtained in the presence of CGRP. The curves obtained in the presence of CGRP (30 and 100 nM) were significantly moved to downward without right shift of the curves suggesting that CGRP inhibited the U46619-induced contraction only by mediation of reduction in $[Ca^{2+}]_i$ with out any change in the sensitivity of contractile apparatus to $Ca^{2+}$. The CGRP-induced attenuation of $[Ca^{2+}]_i$ and force development was significantly inhibited under pretreatment with CGRP $(8{\sim}37)$ fragment (100 nM), a CGRP1 receptor antagonist. Both the reduced contraction and reduction in $[Ca^{2+}]_i$ caused by CGRP were fully reversed by pretreatment with charybdotoxin (100 nM) and iberiotoxin (100 nM), large conductance $Ca^{2+}-activated$ $K^+$ channel blockers, but not by apamin (300 nM), a small conductance $Ca^{2+}-activated$ $K^+$ channel blocker, and glibenclamide ( 1 ${\mu}M$), an ATP-sensitive $K^+$ channel blocker. In conclusion, it is suggested that the CGRP1 receptor, upon activation by CGRP, are coupled to opening of $Ca^{2+}-activated$ $K^+$ channel and cause to decrease in $[Ca^{2+}]_i$, thereby leading to vasodilation of the rat basilar artery. However, it is not defined that the mechanism underlying vasodilation whether the $K^+$ channel blockers, charybdotoxin and iberiotoxin directly block the CGRP receptors and that CGRP-evoked relaxation is dependent on the cyclic AMP or $K^+$ channel opening or both actions.

• Journal of Chest Surgery
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• v.31 no.5
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• pp.472-480
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• 1998

We reviewed the surgical results of intracardiac lateral tunnel Fontan procedure for the repair of functional single ventricles. Between 1990 and 1996, 104 patients underwent total cavopulmonary anastomosis. Patients' age and body weight averaged 35.9(range 10 to 173) months and 12.8(range 6.5 to 37.8) kg. Preoperative diagnoses included 18 tricuspid atresias and 53 double inlet ventricles with univentricular atrioventricular connection and 33 other complex lesions. Previous palliative operations were performed in 50 of these patients, including 37 systemic to pulmonary artery shunts, 13 pulmonary artery bandings, 15 surgical atrial septectomies, 2 arterial switch procedures, 2 resections of subaortic conus, 2 repairs of total anomalous pulmonary venous connection and 1 Damus-Stansel-Kaye procedure. In 19 patients bidirectional cavopulmonary shunt operation was performed before the Fontan procedure and in 1 patient a Kawashima procedure was required. Preoperative hemodynamics revealed a mean pulmonary artery pressure of 14.6(range 5 to 28) mmHg, a mean pulmonary vascular resistance of 2.2(range 0.4 to 6.9) wood-unit, a mean pulmonary to systemic flow ratio of 0.9(range 0.3 to 3.0), a mean ventricular end-diastolic pressure of 9.0 (range 3.0 to 21.0) mmHg, and a mean arterial oxygen saturation of 76.0(range 45.6 to 88.0)%. The operative procedure consisted of a longitudinal right atriotomy 2cm lateral to the terminal crest up to the right atrial auricle, followed by the creation of a lateral tunnel connecting the orifices of either the superior caval vein or the right atrial auricle to the inferior caval vein, using a Gore-Tex vascular graft with or without a fenestration. Concomitant procedures at the time of Fontan procedure included 22 pulmonary artery angioplasties, 21 atrial septectomies, 4 atrioventricular valve replacements or repairs, 4 corrections of anomalous pulmonary venous connection, and 3 permanent pacemaker implantations. In 31, a fenestration was created, and in 1 an adjustable communication was made in the lateral tunnel pathway. One lateral tunnel conversion was performed in a patient with recurrent intractable tachyarrhythmia 4 years after the initial atriopulmonary connection. Post-extubation hemodynamic data revealed a mean pulmonary artery pressure of 12.7(range 8 to 21) mmHg, a mean ventricular end-diastolic pressure of 7.6(range 4 to 12) mmHg, and a mean room-air arterial oxygen saturation of 89.9(range 68 to 100) %. The follow-up duration was, on average, 27(range 1 to 85) months. Post-Fontan complications included 11 prolonged pleural effusions, 8 arrhythmias, 9 chylothoraces, 5 of damage to the central nervous system, 5 infectious complications, and 4 of acute renal failure. Seven early(6.7%) and 5 late(4.8%) deaths occured. These results proved that the lateral tunnel Fontan procedure provided excellent hemodynamic improvements with acceptable mortality and morbidity for hearts with various types of functional single ventricle.