• Journal of Industrial Convergence
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• v.21 no.10
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• pp.57-63
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• 2023

This study aims to elucidate the effect of glycyrrhizic acid on smooth muscle contraction and to determine the detailed mechanism incorporated. We hypothesized that glycyrrhizic acid played a role in the agonist-sensitive management of smooth muscle contraction. Stripped smooth muscles of Sprague-Dawley rats were prepared in organ baths and isometric tensions were converted, stored and analyzed by using isometric transducers, a physiograph and one way ANOVA. Interestingly, glycyrrhizic acid attenuated the thick filament regulating agonist (fluoride or thromboxane mimetic)-sensitive contraction (p=0.113, 0.008, 0.004 (Student's t-test), p=0.113, 0.008, 0.004 (One way ANOVA) at 0.01, 0.03, 0.1 mM fluoride, and p=0.156, 0.004, 0.003 (Student's t-test), p=0.156, 0.004, 0.003 (One way ANOVA) at 0.01, 0.03, 0.1 mM thromboxane mimetic) and did not attenuate the thin filament regulating agonist (phorbol ester)-induced contraction (p=0.392, 0.086, 0.065 (Student's t-test), p=0.392, 0.086, 0.065 (One way ANOVA) at 0.01, 0.03, 0.1 mM phorbol ester). It is suggesting that endothelial EDRF (NO) synthesis and accessory pathways besides endothelial EDRF (NO) synthesis such as ROCK restriction might be incorporated in the glycyrrhizic acid-induced modulation of smooth muscle contraction inhibiting acto-myosin interaction.

• Tuberculosis and Respiratory Diseases
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• v.57 no.1
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• pp.37-46
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• 2004

Background : Lung pericytes are important constituent cells of blood-air barrier in pulmonary microvasculature. These cells take part in the control of vascular contractility and permeability. In this study, it was hypothesized that change of lung pericytes might be attributable to pathologic change in microvasculature in acute lung injury. The purpose of this study was how hypoxia change proliferation and genetic expression in lung pericytes. Methods : From the lungs of several Sprague-Dawley rats, performed the primary culture of lung pericytes and subculture. Characteristics of lung pericytes were confirmed with stellate shape in light microscopy and immunocytochemistry. 2% concentration of oxygen and $200{\mu}M$ $CoCl_2$ were treated to cells. Tryphan blue method and reverse transcription-polymerase chain reaction were done. Results : 1. We established methodology for primary culture of lung pericytes. 2. Hypoxia inhibited cellular proliferation in pericytes. 3. Hypoxia could markedly induce vascular endothelial growth factor(VEGF) and smad-2. 4. Hypoxia-inducible factor-$1{\alpha}$(HIF-$1{\alpha}$) was also induced by 2% oxygen. Conclusion : Viability of lung pericytes are inhibited by hypoxia. Hypoxia can stimulate expression of hypoxia-responsive genes. Pericytic change may be contributed to dysfunction of alveolar-capillary barrier in various pulmonary disorders.

• Journal of Chest Surgery
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• v.32 no.3
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• pp.224-236
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• 1999

Background: To evaluate the short-term effect of dynamic cardiomyoplasty on circulatory function and detect the related factors that can affect it, experimental cardiomyoplasties were performed under the state of normal cardiac function and heart failure. Material and Method: A total of 10 mongrel dogs weighing 20 to 30kg were divided arbitrarily into two groups. Five dogs of group A underwent cardiomyoplasty with latissimus dorsi(LD) muscle mobilization followed by a 2-week vascular delay and 6-week muscle training. Then, hemodynamic studies were conducted. In group B, doxorubicin was given to 5 dogs in an IV dose of 1 mg/kg once a week for 8 weeks to induce chronic heart failure, and simultaneous muscle training was given for preconditioning during this period. Then, cardiomyoplasties were performed and hemodynamic studies were conducted immediately after these cardiomyoplasties in group B. Result: In group A, under the state of normal cardiac function, only mean right atrial pressure significantly increased with the pacer-on(p<0.05) and the left ventricular hemodynamic parameters did not change significantly. However, with pacer-on in group B, cardiac output(CO), rate of left ventricular pressure development(dp/dt), stroke volume(SV), and left ventricular stroke work(SW) increased by 16.7${\pm}$7.2%, 9.3${\pm}$3.2%, 16.8${\pm}$8.6%, and 23.1${\pm}$9.7%, respectively, whereas left ventricular end-diastole pressure(LVEDP) and mean pulmonary capillary wedge pressure(mPCWP) decreased by 32.1${\pm}$4.6% and 17.7${\pm}$9.1%, respectively(p<0.05). In group A, imipramine was infused at the rate of 7.5mg/kg/hour for 34${\pm}$2.6 minutes to induce acute heart failure, which resulted in the reduction of cardiac output by 17.5${\pm}$2.7%, systolic left ventricular pressure by 15.8${\pm}$2.5% and the elevation of left ventricular end-diastole pressure by 54.3${\pm}$15.2%(p<0.05). With pacer-on under this state of acute heart failu e, CO, dp/dt, SV, and SW increased by 4.5${\pm}$1.8% and 3.1${\pm}$1.1%, 5.7${\pm}$3.6%, and 6.9${\pm}$4.4%, respectively, whereas LVEDP decreased by 11.7${\pm}$4.7%(p<0.05). Comparing CO, dp/dt, SV, SW and LVEDP that changed significantly with pacer-on, both under the state of acute and chronic heart failure, augmentation widths of these left ventricular hemodynamic parameters were significantly larger under the state of chronic heart failure(group B) than acute heart failure(group A)(p<0.05). On gross inspection, variable degrees of adhesion and inflammation were present in all 5 dogs of group A, including 2 dogs that showed no muscle contraction. No adhesion and inflammation were, however, present in all 5 dogs of group B, which showed vivid muscle contractions. Considering these differences in gross findings along with the following premise that the acute heart failure state was not statistically different from the chronic one in terms of left ventricular parameters(p>0.05), the larger augmentation effect seen in group B is presumed to be mainly attributed to the viability and contractility of the LD muscle. Conclusion: These results indicate that the positive circulatory augmentation effect of cardiomyoplasty is apparent only under the state of heart failure and the preservation of muscle contractility is important to maximize this effect.

• 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 $[[Ca^{2+}]_i$.