• Journal of Chest Surgery
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• v.41 no.2
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• pp.170-176
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• 2008

Background: Bioprosthetic devices for treating cardiovascular diseases and defects may provide alternatives to autologous and homograft tissue. We evaluated the mechanical and physical conditions of a porcine pericardial bioprosthesis treated with Glutaraldehyde (GA), Ethanol, or Sodium dodecylsulfate (SDS) before implantation. Material and Method: 1) Thirty square-shaped pieces of porcine pericardium were fixed in 0.625%, 1.5% or 3% GA solution. 2) The tensile strength and thickness of these and other bioprosthesis, including fresh porcine pericardium, fresh human pericardium, and commercially produced heterografts, were measured. 3) The tensile strength and thickness of the six treated groups (GA-Ethanol, Ethanol-GA, SDS only, SDS-GA, Ethanol-SDS-GA and SDS-Ethanol-GA) were measured. Result: 1) Porcine pericardium fixed in 0.625% GA the thinnest and had the lowest tensile strength, with thickness and tensile strength increasing with the concentration of GA solution. The relationship between tensile strength and thickness of porcine pericardium increased at thicknesses greater than 0.1mm (correlation-coefficient 0.514, 0<0.001). 2) There were no differences in tensile strength or thickness between commercially-produced heterografts. 3) Treatment of GA, ethanol, or SDS minimally influenced thickness and tensile strength of porcine pericardium, except for SDS alone. Conclusion: Porcine pericardial bioprosthesis greater than 0.1 mm thick provide better handling and advantageous tensile strength. GA fixation did not cause physical or mechanical damage during anticalcification or decellularization treatment, but combining SDS-ethanol pre-treatment and GA fixation provided the best tensile strength and thickness.

• Journal of Chest Surgery
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• v.41 no.5
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• pp.541-549
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• 2008

Background: Vasoconstrictor-induced reduction in arterial graft diameter can cause significant flow deprivation. The aim of this study was to evaluate the effect of vasodilator pretreatment on vasoconstrictor-induced blood vessel spasm in vitro. Material and Method: Rabbit brachial arteries (BA) and celiac arteries (CA) were cut into rings $(3{\sim}4mm)$ and suspended with a force displacement transducer (TSD $125C^{(R)}$, Biopac Inc. USA) in a tissue bath filled with 5 mL modified Krebs solution bubbled with 5% $CO_2$ and 95% $O_2\;at\;38^{\circ}C$. The rings were contracted with vasoconstrictors, and the developed tension changes were considered control values. The rings were then pre- treated with $30{\mu}M$ nitroglycerin, nicardipine, verapamil, and papaverine, respectively, for 40 minutes and rinsed with the physiologic buffered salt solution three times every 15 min. The vasoconstrictor-induced tension changes after the previous procedure were considered experimental values. Data are expressed as the percentage tension induced by vasoconstrictors before and after pretreatment with vasodilators. Result: Nicardipine depressed vasoconstriction induced by norepinephrine, angiotensin II (All), and U46619 in both the BA and the CA more significantly than did nitroglycerin (p<0.01) and verapamil (p<0.05). Verapamil depressed vasoconstriction induced by 5-hydroxytryptamine (5HT), All, and U46619 in the BA and by 5HT in the CA more significantly than did nitroglycerin (p<0.01). Conclusion: These findings suggest that both nicardipine and verapamil effectively depressed vasoconstrictor action. Nicardipine is thought to be more effective than verapamil for the prevention of vasoconstrictor action.

• Journal of Chest Surgery
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• v.43 no.1
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• pp.1-10
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• 2010

Background: Bioprosthetic materials have been made using glutaraldehyde fixation of porcine or bovine pericardium during cardiovascular surgery. But these bioprostheses have the problems of calcification and mechanical failure. We determined changes in tensile strength and elasticity of pericardium after glutaraldehyde, solvent, decellularization and detoxification. Material and Method: Tissues were allocated to four groups: glutaraldehyde with and without solvent, decellularization, and detoxification. We studied tensile strength and strain on tissues. We measured the tensile strength of fresh pericardium stretched in six directions (with 5 mm width), and % strain, which we calculated from the breaking point when we pulled the pericardium in two directions. Result: Tensile strength was reduced when we used the usual concentrated glutaraldehyde fixation (n=83, $MPa=11.47{\pm}5.40$, p=0.006), but there was no change when we used solvent. Elasticity was increased after glutaraldehyde fixation (n=83, strain $(%)=24.55{\pm}9.81$, p=0.00), but there was no change after solvent. After decellularization of pericardium, the tensile strength was generally reduced. The decrease in tensile strength after concentrated glutaraldehyde fixation for a long time was significantly greater less than after concentrated solvent (p=0.01, p=0.00). After detoxification, the differences in strength and strain were not significant. Conclusion: After glutaraldehyde treatment of pericardium there is no loss in tensile strength (even though we did the glutaraldehyde, solvent and detoxification treatments LOGIC IS UNCLEAR). Also, these treatments had a tendency to increase elasticity. Although post-treatment decellularization led to a significant loss in strength, this effect could be attenuated using a low concentration of solvent or hypertonic solution.

• The Korean Journal of Pharmacology
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• v.24 no.2
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• pp.197-201
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• 1988

Effects of high concentration of KC1 and caffeine on cytosolic $Ca^{2+}$ level $([Ca^{2+}]_{cyt})$, measured simultaneously with muscle tension using a fluorescent intracellular $Ca^{2+}$ indicator fura 2, were examined in isolated smooth muscle of rat aorta. High $K^+$ (72.7 mM) solution induced sustained increase in both $([Ca^{2+}]_{cyt})$ and tension. In contrast to this, caffeine (20 mM) induced a rapid increase in $([Ca^{2+}]_{cyt})$ followed by a decrease to a level which was higher than the resting level. However, muscle tension showed only a transient increase followed by a decrease below the resting level. In a $Ca^{2+}-free$ solution, high $K^+-induced$ neither $([Ca^{2+}]_{cyt})$ nor tension, whereas caffeine induced a transient increase in both $([Ca^{2+}]_{cyt})$ and muscle tension. These results suggest that high $K^+-induced$ contraction in vascular smooth muscle of rat aorta is due to $Ca^{2+}$ influx whereas caffeine-induced contraction is due to $Ca^{2+}$ release from cellular store. Further, caffeine seems to have an additional effect to decrease the sensitivity of the contractile elements to $Ca^{2+}$.

• Journal of Chest Surgery
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• v.29 no.5
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• pp.487-494
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• 1996

The neurogenic responses of tracheal smooth muscles to electrical field stimulation (EFS) is biphasic, consisting firstly of cholinergic contraction followed by a slow and sustained relaxation. It is well known that a sustained relaxation involves the inhibitory non-adrenergic non-cholinergic systems. This study was done to Investigate the relaxing agents and their action mechanisms by use of an organ bath with plati- ilum . The tracheal smooth muscle relaxation due to EFS was suppressed by L-NAME, the WO (Nitric Oxide) synthase inhibitor, and these effects were reversed by L-arginine, the precursor of NO. Also, L-WAME (HG-nitro-L-arginine methyl ester) increased the basal tension. Nitroprusside, the NO-donor, suppressed the tracheal basal tension greatly. Methylene blue, the inhibitor of guanylate cyclase, decreased EFS-induced relaxations and increa ed basal tension. Forskolin and isoprenaline, which are activators of adenylate cyclase, suppressed tracheal basal tension in the same way as nitroprusside. TEA (tetraethylammonium), the non-specific K'channel blocker, and apamin, the Ca"-activated K'channel blocker, increased tracheal basal tension and EFS-induced relaxations. Our results indicate that Pr3 Is released upon stimulation of the NANC (Won Adrenergic Won Cholinergic) nerves in guinea-pig tracheal smooth muscle and that the release of NO related with the K+ channel, as well as the release of other inhibitory agents< e. g.)VIP (Vasoactive Intestinal Polypeptide), PHI (Peptide Histidine Isoleusine) > mediated via CAMP (cyclic Adenosine Monophosphate) may be Involved In sustained relaxation.

• Journal of Ginseng Research
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• v.26 no.1
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• pp.1-5
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• 2002

It has been well known that Korea red ginseng has an antihypertensive effect. The antihypertensive effect may be due to its ability to change the peripheral resistance. Change of vascular tone in the resistance-sized artery contribute to the peripheral resistance, thereby regulate the blood pressure. Therefore, we investigated to clarify the vasorelaxing mechanism induced by crude saponin of Korea red ginseng in the resistance-sized mesenteric artery of rats. The resistance-sized mesenteric artery was isolated and cut into a ring. The ring segment was immersed in HEPES-buffered solution and its isometric tension was measured using myograph force-displacement transducer. Crude saponin of ginseng relaxed the mesenmetric arterial rings precontracted with norepinephrine (3$\mu$M) in dose-dependent manner (0.01 mg/㎖ -1 mg/㎖. The relaxation by crude saponin was smaller in endothelium-intact preparation than that in endothelium-denuded preparation. The contraction induced by A23187 or phorbol 12,13-dibutyrate was not affected by crude saponin of ginseng. The vasorelaxing effect of crude saponin of ginseng was significantly attenuated by the increase of the extracellular K$\^$+/ concentration. Crude saponin-induced vasorelaxation was not affected by tetraethylammonium (1 mM), glybenclamide (10$\mu$M), and 4-aminopyridine (0.1 mM) in these preparations. Ba$\^$2+/(10$\mu$M ∼100$\mu$M) markedly reduced the crude saponin-induced vasorelakation dose-dependently. From the above results, we suggest that crude saponin of ginseng may stimulate K$\^$+/ efflux and hyperpolarize the membrane, thereby cause the vasorelaxation in the resistance-sized mesenteric artery of rats.

• The Korean Journal of Pharmacology
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• v.31 no.3
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• pp.285-290
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• 1995

This study was undertaken to define the varying responses of vascular smooth muscle to different wavelengths of ultraviolet radiation and to relate them to the changes in cyclic GMP contents. The ring preparations of rat thoracic aorta with intact or removed endothelium were irradiated with the ultraviolet or visible light (UVR) of wavelengths in step of 10 nm between 250 and 500 nm from xenon lamp of a spectrofluorometer, and the changes in vascular tension were recorded. For cyclic GMP assay, the preparations, pretreated with phenylephrine as in the tension experinents, were frozen after irradiation and homogenated in trichloroacetic acid. The supernatant was extracted with ether and the cyclic GMP contents were measured with radioimmunoassay. In the endothelium-intact preparations, biphasic responses, vasoconstriction (UVR-contraction) followed by vasodilatation (UVR-dilatation), were observed. The maximal UVR-contraction was observed at 320 nm, while the maximal vasodilatation was elicited at 420 nm. In the endothelium-removed rings, however, only vasodilatation was observed, with the maximal vasodilatation taking place at 370 nm. The cyclic GMP contents were not affected by the Irradiation with 320 nm for 30 sec or 1 min in the endothelium-intact preparations, while it was significantly increased by 380 and 420 nm. In the endothelium-removed preparations, UVR of 370 nm markedly increased the cyclic GMP contents. The present study indicates that the increase in cyclic GMP is closely related to vasodilatation induced by UVR of 420 nm in the endothelium-intact or 370 nm in the denuded preparations, whereas it is not involved in the vasoconstriction induced by UVR of 320 nm in the intact rings, and the mechanism leading to UVR-contraction remains to be clarified. These observations suggest that nitric oxide-cyclic GMP system is closely related to the UVR-dilatation in rat aortic preparation, while it is not involved in the UVR contraction.

• Journal of Food Hygiene and Safety
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• v.11 no.2
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• pp.83-87
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• 1996

The objective of this study is to investigate the direct effects of green tea catechins(GTC) on vascular smooth muscle tension and 45Ca2+ Uptake in rat aorta. The methods used in this study are isometric tension measurements using physiograph, Lanthanum method for 45Ca2+(2 uCi/ml) uptake measurement in rat aorta. GTC modified tension induced by 40 mM KCl or 1 uM norepinephrine in rat aorta. Low concentrations of GTC(<0.5mg/ml) increased tension by 40 mM KCl or 1 uM norepinephrine, individually. However, high conecentration of GTC(>0.5 mg/ml) inhibiited tension by 40 mM KCl or 1 uM norepinephrine, individually. GTC increased 45Ca uptake induced by 40 mM KCl in a dose-dependent manner. From these results, GTC has the dual actions in vascular smooth muscle in vitro. Low concentrations of GTC augments tension by K or norepinephrine. However, high concentrations of GTC inhibits tension by K or norepinephrine GTC may have Ca2+ channel activation, action, which may result in unphysiological vasodilation by Ca2+ overload in vascular smooth muscle.

• Journal of Chest Surgery
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• v.31 no.2
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• pp.102-107
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• 1998

It has not been clear whether L-arginine plays solely a role contributing to vascular nitric oxide (NO) synthesis. To investigate the mechanisms by which L-arginine induces vasorelaxation, effects of L-arginine on the isometric tension, and tissue NOx and cyclic guanosine monophosphate(cGMP) contents were examined in the isolated rat thoracic aorta. L-Arginine induced a dose-dependent relaxation of aortic rings only with intact endothelium only. The vasorelaxation response to low concentrations of L-arginine was abolished by the pretreatment with NG-nitro-L-arginine methyl ester(L-NAME, 10-4 mol/L), whereas the relaxation caused by higher concentrations L-arginine(10-5-10-3 mol/L) was maintained and even more pronounced in the presence of L-NAME. L-Arginine did not affect the vascular tension precontracted with KCl. The vascular tissue contents of NOx/cGMP were not significantly affected by L-arginine, while they were decreased by L-NAME. L-Arginine could not completely recover the NOx/cGMP decreased by L-NAME. Methylene blue only partially antagonized the relaxation response to L-arginine. Indomethacin did not affect the L-arginine-induced vasorelaxation, whereas ouabain markedly attenuated the relaxation. It is suggested that L-arginine induces vasorelaxation not only through its contribution to NO synthesis, but also through enhancing another endothelium-dependent mechanism which is NO/cGMP-independent and cyclooxygenase- independent.

• Proceedings of the KOR-BRONCHOESO Conference
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• 1991.06a
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• pp.25-25
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• 1991

최근 교통사고의 증가, 심폐술의 보편화 및 보조호흡을 필요로 하는 환자의 증가에 따라 경구적 혹은 기관절개술을 통해 기관내 삽관을 장기간 유치하는 경우가 많아져서 이에 따른 합병증으로 기관협착증의 빈도가 높아지게 되었다. 기관내 삽관후 기관협착증을 초래하는데에는 관의 외경, 삽관시 외상, 삽관유치기간, 기계적 보조호흡시 관의 이동, cuff 의 압력 등의 요인이 작용한다. 이러한 요인에 의해 기관내 삽관을 장기간 유치시 기관점막에 대한 지속적인 압박으로 점막하부의 압박괴사 및 혈관의 폐쇄로 인해 기관연골의 무혈성 괴사를 초래하여 환상의 기관협착이 병발하게 된다. 기관협착증에 대한 치료방법으로서는 여러 가지가 있으나 환상의 기관협착증인 경우는 협착부위의 절제 및 단단문합술을 시행하고 절제부위가 광범위한 경우는 release technique 을 이용하여 문합부위의 장력을 줄여주는 것이 효과적인 치료방법으로 알려져 있다. 저자들은 최근 기관내 삽관후에 병발한 환상기관협착증 3례(다발성 골절 1례, 기관지 천식 1례, 약물중독 1례)에 대해 기관절제 및 단단문합술을 경험하였기에 보고하고자 한다.