• Journal of Life Science
• /
• v.10 no.6
• /
• pp.584-590
• /
• 2000

Natural products are one of the useful source of cardiovascular drugs, in particular, when they have antioxidant activity. Gagaminine, an alkaloid isolated from the roots of Cynanchum wilfordi Hemsley, has been reported to potently inhibit the aldehyde oxidase activity ({TEX}$IC_{50}${/TEX}=0.8$\mu$M) and reduce lipid peroxidation. However, the effect of gagaminine on vascular smooth muscle has not yet been investigated. In the present study, we examined whether gagaminine relaxes vascular smooth muscle by isometric tension study. In order to observe its relaxation effect on the arteries, conductivel vessel (rat thoracic aorta) and resistance vessel (pig coronary artery) were purposely used. Results indicated that gagaminine relaxed in a concentration-dependent manner $\alpha$-adrenoceptor agonist, phenylephrine (PE)-induced contraction of rat aorta. Pretreatment with gagaminine inhibited PE-induced contraction, noncompetitively. {TEX}$Ca^{2+}${/TEX}-induced contraction was significantly diminished by gagaminine. In pig coronary artery, gagaminine relaxed thromboxane receptor (U 46619)-mediated contraction in dose-dependent manner. Pretreatment with gagaminine also reduced the maximum contraction induced by KCl. These observations strongly suggest that agagminnine relaxes vascular smooth muscle, irrespective of both resistance and conductive artery. We demonstrate that gagaminine, a potent natural antioxidant, has a significant vasodilatory effect and its action mechanism van be ascribed at least in part to {TEX}$Ca^{2+}${/TEX} antagonistic action as evidenced by inhibition {TEX}$Ca^{2+}${/TEX}-induced contraction (rat aorta) and KCl-induced contraction (porcine artery). Furthermore, neither $\alpha$ -adrenoceptor nor thromboxane receptor seems responsible for the relaxation of gagaminine.

• Clinical and Experimental Pediatrics
• /
• v.57 no.10
• /
• pp.461-463
• /
• 2014

Decreased exercise capacity after Fontan surgery is relatively common and the failure of the Fontan state gradually increases with age. However, there is no further treatment for patients with Fontan circulation. Pulmonary vasodilation therapy is an effective method to solve this problem because pulmonary vascular resistance is a major factor of the Fontan problem. Inhaled iloprost is a chemically stable prostacyclin analogue and a potent pulmonary vasodilator. We experienced two cases of Fontan patients treated with inhaled iloprost for 12 weeks. The first patient was an 18-year-old female with pulmonary atresia with an intact ventricular septum, and the second patient was a 22-year-old male with a double outlet right ventricle. Fifteen years have passed since both patients received Fontan surgery. While the pulmonary pressure was not decreased significantly, improved exercise capacity and cardiac output were observed without any major side effects in both patients. The iloprost inhalation therapy was well tolerated and effective for the symptomatic treatment of Fontan patients.

• Journal of Chest Surgery
• /
• v.13 no.3
• /
• pp.237-242
• /
• 1980

This is a case report of spontaneous regression of elevated pulmonary vascular resistance after the age of 6 years in a patient with partial endocardial cushion defect. The patient was first evaluated and considered to be highly risky for surgical correction because of obstructive type of pulmonary hypertension and presisting congestive heart failure at the age of 6 years, during which time medical treatment for congestive heart failure and sufferring from respiratory infection were only provided. Finally the patient was reevaluated at the age of 16 years, in January of 1980 when cardiac catheterization was revealed markedly reduced pulmonary vascular resistance and pulmonary hypertension as well. The patient was operated upon with uneventful postoperative recovery. So we report this case with review of the literatures regarding natural history regarding natural history of partial endocardial cushion defect.

• Journal of Chest Surgery
• /
• v.23 no.4
• /
• pp.659-666
• /
• 1990

We evaluated 68 patients with mitral valve disease who underwent mitral valve replacement from April, 1986, to December, 1988. Among them 20 patients showed increased systolic pulmonary arterial pressure greater than 60 mmHg and postoperative hemodynamic data were obtained in 19 patients average 13 months after mitral valve replacement. The results were as followings. 1. Average pulmonary systolic pressure decreased from 84.8$\pm$4.5 preoperatively to 33. 0$\pm$1.9mmHg postoperatively[P<0.001]. 2. Average pulmonary vascular resistance index decreased from 1425$\pm$148 preoperatively to 287+35.8 dyne * sec * cm2 * m postoperatively[P<0.001]. 3. Average cardiac index rose from 1.927$\pm$0.169 preoperatively to 2.625$\pm$0.159 L/min/m2 postoperatively [P <0.005]. This study shows that pulmonary hypertension and the increased pulmonary vascular resistance index due to mitral valve disease can regress significantly after mitral valve replacement.

• Journal of the Korean Society of Physical Medicine
• /
• v.5 no.4
• /
• pp.633-644
• /
• 2010

Purpose : This study was to investigate vascular dementia elders's activities of daily living, quality of life index and to determine how much vascular dementia elders is influenced by the 12 weeks combined exercise program with aerobic training and resistance exercise. Methods : Thirty patients with vascular dementia over 65 in B geriatrics hospital were recruited this study. Activities of daily living were measured by I-ADL(instrumental-activities of daily living) and B-ADL(basic-Activities of daily living) and quality of life index was measured by GQOL-D(geriatric quality of life scaledementia). Statistical analysis was used repeated one-way ANOVA to test mean difference by using SPSS 12.0 for windows. Results : After comparing the activities of daily living of experimental group that of control group according to the period of exercise, there were statistically significant differences in I-ADL, B-ADL score test and GQOL-D index test of both experimental and control groups. There was also a significant difference in comparing the results of 12 weeks exercise of the groups. Conclusion : 12 weeks combined exercise program had a good influence on vascular dementia elders's activities of daily living and quality of life index.

• International Journal of Vascular Biomedical Engineering
• /
• v.1 no.2
• /
• pp.20-29
• /
• 2003

A new treatment for coronary artery occlusive disease is being developed in which a shunt or conduit is placed directly connecting the left ventricle with the diseased artery at a point distal to the obstruction. To aid in assessing and optimizing its benefit, a computational model of the cardiovascular system was developed and used to explore various design conditions. Simulation results indicate that in complete LAD occlusion, flow can be returned to approximately 65% of normal if the conduit resistance is equal for forward and reverse flow, increasing to 80% in the limit in which backflow resistance is infinite. Increases in flow rate produced by asymmetric flow resistance are considerably enhanced in the case of a partial LAD obstruction since the primary effect of resistance asymmetry is to prevent leakage back into the ventricle("steal") during diastole. Increased arterial compliance has little effect on net flow with a symmetric shunt, but leads to considerable augmentation when the resistance is asymmetric. These results suggest that an LV-LAD conduit will be beneficial when stenosis resistance(Rst) > 27 PRU if resistance is symmetric.

• The Korean Journal of Physiology and Pharmacology
• /
• v.20 no.6
• /
• pp.641-647
• /
• 2016

Pulmonary arterial hypertension (PAH) is a progressive disease characterized by vascular remodeling of pulmonary arteries (PAs) and increased vascular resistance in the lung. Monocrotaline (MCT), a toxic alkaloid, is widely used for developing rat models of PAH caused by injury to pulmonary endothelial cells; however, characteristics of vascular functions in MCT-induced PAH vary and are not fully understood. Here, we investigated hypoxic pulmonary vasoconstriction (HPV) responses and effects of various vasoconstrictors with isolated/perfused lungs of MCT-induced PAH (PAH-MCT) rats. Using hematoxylin and eosin staining, we confirmed vascular remodeling (i.e., medial thickening of PA) and right ventricle hypertrophy in PAH-MCT rats. The basal pulmonary arterial pressure (PAP) and PAP increase by a raised flow rate (40 mL/min) were higher in the PAH-MCT than in the control rats. In addition, both high $K^+$ (40 mM KCl)- and angiotensin II-induced PAP increases were higher in the PAH-MCT than in the control rats. Surprisingly, application of a nitric oxide synthase inhibitor, L-$N^G$-Nitroarginine methyl ester (L-NAME), induced a marked PAP increase in the PAH-MCT rats, suggesting that endothelial functions were recovered in the three-week PAH-MCT rats. In addition, the medial thickening of the PA was similar to that in chronic hypoxia-induced PAH (PAH-CH) rats. However, the HPV response (i.e., PAP increased by acute hypoxia) was not affected in the MCT rats, whereas HPV disappeared in the PAH-CH rats. These results showed that vascular contractility and HPV remain robust in the MCT-induced PAH rat model with vascular remodeling.

• The Korean Journal of Physiology and Pharmacology
• /
• v.24 no.4
• /
• pp.287-298
• /
• 2020

Ca²⁺ signaling of endothelial cells plays a critical role in controlling blood flow and pressure in small arteries and arterioles. As the impairment of endothelial function is closely associated with cardiovascular diseases (e.g., atherosclerosis, stroke, and hypertension), endothelial Ca²⁺ signaling mechanisms have received substantial attention. Increases in endothelial intracellular Ca²⁺ concentrations promote the synthesis and release of endothelial-derived hyperpolarizing factors (EDHFs, e.g., nitric oxide, prostacyclin, or K⁺ efflux) or directly result in endothelial-dependent hyperpolarization (EDH). These physiological alterations modulate vascular contractility and cause marked vasodilation in resistance arteries. Transient receptor potential (TRP) channels are nonselective cation channels that are present in the endothelium, vascular smooth muscle cells, or perivascular/sensory nerves. TRP channels are activated by diverse stimuli and are considered key biological apparatuses for the Ca²⁺ influx-dependent regulation of vasomotor reactivity in resistance arteries. Ca²⁺-permeable TRP channels, which are primarily found at spatially restricted microdomains in endothelial cells (e.g., myoendothelial projections), have a large unitary or binary conductance and contribute to EDHFs or EDH-induced vasodilation in concert with the activation of intermediate/small conductance Ca²⁺-sensitive K⁺ channels. It is likely that endothelial TRP channel dysfunction is related to the dysregulation of endothelial Ca²⁺ signaling and in turn gives rise to vascular-related diseases such as hypertension. Thus, investigations on the role of Ca²⁺ dynamics via TRP channels in endothelial cells are required to further comprehend how vascular tone or perfusion pressure are regulated in normal and pathophysiological conditions.

• Toxicological Research
• /
• v.30 no.3
• /
• pp.141-148
• /
• 2014

Endothelium-derived relaxing factors (EDRFs), including nitric oxide (NO), prostacyclin ($PGI_2$), and endothelium-derived hyperpolarizing factor (EDHF), play pivotal roles in regulating vascular tone. Reduced EDRFs cause impaired endothelium-dependent vasorelaxation, or endothelial dysfunction. Impaired endothelium-dependent vasorelaxation in response to acetylcholine (ACh) is consistently observed in conduit vessels in human patients and experimental animal models of hypertension. Because small resistance arteries are known to produce more than one type of EDRF, the mechanism(s) mediating endothelium-dependent vasorelaxation in small resistance arteries may be different from that observed in conduit vessels under hypertensive conditions, where vasorelaxation is mainly dependent on NO. EDHF has been described as one of the principal mediators of endothelium-dependent vasorelaxation in small resistance arteries in normotensive animals. Furthermore, EDHF appears to become the predominant endothelium-dependent vasorelaxation pathway when the endothelial NO synthase (NOS3)/NO pathway is absent, as in NOS3-knockout mice, whereas some studies have shown that the EDHF pathway is dysfunctional in experimental models of hypertension. This article reviews our current knowledge regarding EDRFs in small arteries under normotensive and hypertensive conditions.

• Journal of Chest Surgery
• /
• v.33 no.1
• /
• pp.1-6
• /
• 2000

Background: TNF-$\alpha$ plays a major role in producing left ventricular dysfunction cardio-myopathy pulmonary edema and inhibits the compensatory mechanism of congestive heart failure. IL-6 is an acute reactant of immune reaction and also known to control immune reaction but its function in the myocyte was not clearly investigated. Author's performed this experiment to investigate the contents of TNF-$\alpha$ and IL-6 on the assumption that TNF-$\alpha$ and IL-6 may reside in nonfailing heart that has gone cardiac surgery and play some role in cardiac function. Material and Method : Right auricular tissues were sampled from 12 patients who had undergone total corrective surgery for both congenital and acquired heart diseases from January 1998 to June 1998 in Kosin Universcfy Gospel hospital. The quantitive analysis of TNF-$\alpha$ and IL-6 were assessed by ELISA method in right auricular tissue. Hemodynamic values about the pressure of ventricle atrium aorta pulmonary artery and cardiac index pulmonary and systemic vascular resistance and cardiac output were measured by echocardiography and cardiac catheterization and biochemical analyses of LDH & AST were done before operation. statistical analysis was by Paired Student t-test. Patients were divided into children(under 15 years olds) and adults groups and the data was compared beween two groups. Conclusion: Mild pulmonary hypertension and increased pulmonary vascular resistance were existed in both group. The contents of tissue TNF-$\alpha$ IL-6 in each group were independent of each data.