• Journal of Chest Surgery
• /
• v.24 no.5
• /
• pp.445-450
• /
• 1991

Forty eight patients diagnosed as atrial septal defect, had been operated from April 1986 to December 1990 at the Department of Thoracic and Cardiovascular Surgery, Inha University Hospital, were analysed retrospectively. Of the 48 patients, 12 patients, were male and 36 patients were female, Their ranged from 8 months to 51 years old, and the mean was 18.0 years old. The proceeding two symptoms were exertional dyspnea and frequent upper respiratory infection. But 10 patients [20.8%] were asymptomatic. Electrocardiographic findings were regular sinus rhythm in 100.0%, RVH in 29.2%, incomplete RBBB in 27.1%, and first degree AV block in 2.1%. Hemodynamic studies were performed in 38 of 48 patients. Significant pulmonary hypertension[over 50mmHg in systolic pulmonary arterial pressure], which is the most serious risk factor, was developed in 4 patients[8.3%]. There was statistical significance between size of defect[cm2/BSA-M2] and systolic pulmonary arterial pressure[sPAP] retrospectively[p=0.036]. We could not find the correlationship between age and Qs % size. Anatomically, secundum type constituted 97.9%, in which 43 patients were PFO type[91.6%] and 3 patients were IVC type[6.3%]. 38 of 48 ASD patients were repaired with patch closure[72.9%] and remains were repaired with direct closure[27.1%]. The operative result was excellent except two cases of transient postoperative arrhythmia. There was no operative mortality.

• Journal of Chest Surgery
• /
• v.22 no.6
• /
• pp.944-950
• /
• 1989

Children with congenital cardiac defects associated with high pulmonary artery pressure may die despite accurate surgery. Postoperative mortality and morbidity have been attributed to acute rises in pulmonary artery pressure and resistance. Acute pulmonary hypertensive crisis is defined as a paroxysmal event in which pulmonary arterial systolic pressure rises to or above systemic levels followed by a rapid fall in systemic pressure and a minor pulmonary hypertensive event is defined as an acute rise in pulmonary arterial pressure to more than 80 % of systemic levels but without a fall in systemic pressure. From Oct. 1988 to Jul. 1989, we experienced 23 patients who showed many pulmonary hypertensive crises after operation in the Department of Thoracic and Cardiovascular Surgery, Seoul National University Children\ulcorner Hospital. Their preoperative PAP/SAPs were 53 to 123 %[mean 93.3%] and diagnoses were VSD[7], TAPVR[5], TGA[4], AVSD[3], MS[1], DORV[1], Truncus arteriosus[1], and AP window[l]. There were 9 deaths among 23 patients and they showed many pulmonary hypertensive crisis episodes during postoperative intensive care, which was managed by sedation, hyperventilation, oxygen, and acidosis correction and which decreased after using tolazoline. In view of our experience, we recommend that pulmonary artery pressure should be monitored in congenital heart defected patient with preoperative pulmonary hypertension to confirm and to manage the pulmonary hypertensive crisis accurately and using tolazoline is helpful in the treatment of pulmonary hypertensive crisis.

• The Korean Journal of Pharmacology
• /
• v.32 no.2
• /
• pp.211-219
• /
• 1996

The inhibitory effect of cyclosporin A (CsA) on nitric oxide production is not related to the immunosuppressive action of the drug, but to the renal toxicity and arterial hyper-tension. In this study the experimental interventions to reverse the inhibition of nitric oxide production by cyclosporin A in rat aortic smooth muscle cells were examined. CsA inhibited the accumulation of nitrite, the stable end product of nitric oxide, in culture media in a concentration $(0.1{\sim}100{\mu}g/ml)-dependent$ manner. The inhibitory effect of CsA on nitrite accumulation were not antagonized by arginine (10 mM), a substrate of nitric oxide synthase, nor by calcium ionophore A23187 $(7{\mu}M)$. Forskolin, an activator of adenylate cyclase, which enhanced iNOS induction at transcriptional level, completely reversed the inhibitory action of CsA on nitrite accumulation. However, PMA (2 nM) and PDB (50 nM), PKC activators, increased the inhibitory action of CsA on nitrite accumulalion. From these results, it is suggested that cyclic AMP-elevating agents may be candidates of therapeutic agents in prevention and treatment of renal toxicity and arterial hypertension induced by CsA. Among conventional antihypertensive drugs, calcium channel blockers and ${\alpha}-blockers$ are preferred to ${\beta}-blockers$.

• Journal of Chest Surgery
• /
• v.9 no.1
• /
• pp.10-19
• /
• 1976

One hundred and seventy-four patients were treated in this Department since 1956. One hundred and fifteen patients of them were surgically treated. They were classified on the basis of the disease entity as follows; 48 case of thrombo-angiitis obliterance, 8 cases of Leriche syndrome, 12 cases of arterial embolism, 36 arterial aneurysm, 5 arterio-venous fistula, 15 arterial and venous injuries, 8 pulseless diseases, 2 coarctation of aortas, 15 varicose veins, 12 thrombophlebitis, 9 superior venacaval syndromes, 2 inferior vena caval obstructions and Raynaud's diseases. All the cases of the Burger's diseases were males, and half of them were in the fourth decades, 39 cases underwent undergone unilateral or bilateral sympathectomies. All the Leriche syndromes were males aged over fifty. Three cases out of six were suffering from diabetes mellitus. 2 cases underwent aorto-femoral bypass graft with Y-shaped dacrons. And two embolectomies were performed in 2 cases. Eight cases of arterial embolisms among 12 had mitral valvular diseases with auricular fibrillation The most common site of lodgement of emboli was femoral artery. Nine out of 14 underwent embolectomies with Fogarty catheters. There were 14 peripheral arterial aneurysms, 16 thoracic and/or abdominal aortic aneurysms, and 4 dissecting aneurysms. Most frequent cause of peripheral arterial aneurysms were external trauma. Thoracic and abdominal aortic aneurysms were non-traumatic. And four cases of the dissecting aneurysms had significant hypertension and aged over fifty. Among 5 cases of arteriovenous fistulas, 2 cases hand typical Branham's sign, and they were normalized after operation. Eight cases of pulseless disease were females and aged from three to twenty-five. Three out of them were treated surgically using dacron prosthetic grafts, but the results of the surgery were variable and not satisfactory. A case of coarctation of aorta was treated surgically with an excellent result. Fourteen out of 15 varicose veins underwent ligation of the saphenous vein system, exstirpation of the varicose veins, stripping or some combination of these methods. Two cases of superior vena caval syndromes were operated by bypass graft between the left innominate vein and the right auricle. Two cases of inferior vena caval obstructions were operated upon through right atrial route using extracorporial circulation. All the four cases of vena caval obstructions showed excellent results postoperatively. Two cases out of 12 thrombophlebitis underwent thrombectomies. One of two Raynaud's diseases was surgically treated with an excellent result.

• The Korean Journal of Physiology and Pharmacology
• /
• v.20 no.6
• /
• pp.605-611
• /
• 2016

Ketamine is an anesthetic with hypertensive effects, which make it useful for patients at risk of shock. However, previous ex vivo studies reported vasodilatory actions of ketamine in isolated arteries. In this study, we reexamined the effects of ketamine on arterial tones in the presence and absence of physiological concentrations of 5-hydroxytryptamine (5-HT) and norepinephrine (NE) by measuring the isometric tension of endothelium-denuded rat mesenteric arterial rings. Ketamine little affected the resting tone of control mesenteric arterial rings, but, in the presence of 5-HT (100~200 nM), ketamine ($10{\sim}100{\mu}M$) markedly contracted the arterial rings. Ketamine did not contract arterial rings in the presence of NE (10 nM), indicating that the vasoconstrictive action of ketamine is 5-HT-dependent. The concentration-response curves (CRCs) of 5-HT were clearly shifted to the left in the presence of ketamine ($30{\mu}M$), whereas the CRCs of NE were little affected by ketamine. The left shift of the 5-HT CRCs caused by ketamine was reversed with ketanserin, a competitive 5-$HT_{2A}$ receptor inhibitor, indicating that ketamine facilitated the activation of 5-$HT_{2A}$ receptors. Anpirtoline and BW723C86, selective agonists of 5-$HT_{1B}$ and 5-$HT_{2B}$ receptors, respectively, did not contract arterial rings in the absence or presence of ketamine. These results indicate that ketamine specifically enhances 5-$HT_{2A}$ receptor-mediated vasoconstriction and that it is vasoconstrictive in a clinical setting. The facilitative action of ketamine on 5-$HT_{2A}$ receptors should be considered in ketamine-induced hypertension as well as in the pathogenesis of diseases such as schizophrenia, wherein experimental animal models are frequently generated using ketamine.

• KIPS Transactions on Computer and Communication Systems
• /
• v.5 no.6
• /
• pp.135-142
• /
• 2016

We proposed the new method to estimate the blood pressure with the differential value of the digital arterial pulse waveform and BP relation equation. To get the digital arterial pulse waveform, we use the arterial pulse waveform measurement system that has digital air-pressure sensor device and smart phone. The acquired digital arterial pulse waveforms are classified as hypertension group, normal group, and hypotension group, and we can derive the average differential value between the highest point and lowest point of a single waveform of individuals along with the group. In this study, we found the functional correlation between the blood pressure and differential value as a form of BP relation equation through the regression process on the average of differential value and blood pressure value from a tonometer. The Experimental results show the BP relation equation can give easy blood pressure estimation method with a high accuracy. Although this estimation method has over 66 % error rate and does not give the high level of the accuracy for the diastolic compares to the commercial tonometer, the estimation results for the systolic show the high accuracy that has less than 10 % error rate.

• The Korean Journal of Physiology and Pharmacology
• /
• v.24 no.1
• /
• pp.111-119
• /
• 2020

In vascular smooth muscle, K⁺ channels, such as voltage-gated K⁺ channels (Kv), inward-rectifier K⁺ channels (Kir), and big-conductance Ca²⁺-activated K⁺ channels (BK_Ca), establish a hyperpolarized membrane potential and counterbalance the depolarizing vasoactive stimuli. Additionally, Kir mediates endothelium-dependent hyperpolarization and the active hyperemia response in various vessels, including the coronary artery. Pulmonary arterial hypertension (PAH) induces right ventricular hypertrophy (RVH), thereby elevating the risk of ischemia and right heart failure. Here, using the whole-cell patch-clamp technique, we compared Kv and Kir current densities (I_Kv and I_Kir) in the left (LCSMCs), right (RCSMCs), and septal branches of coronary smooth muscle cells (SCSMCs) from control and monocrotaline (MCT)-induced PAH rats exhibiting RVH. In control rats, (1) I_Kv was larger in RCSMCs than that in SCSMCs and LCSMCs, (2) I_Kv inactivation occurred at more negative voltages in SCSMCs than those in RCSMCs and LCSMCs, (3) I_Kir was smaller in SCSMCs than that in RCSMCs and LCSMCs, and (4) I_BKCa did not differ between branches. Moreover, in PAH rats, I_Kir and I_Kv decreased in SCSMCs, but not in RCSMCs or LCSMCs, and I_BKCa did not change in any of the branches. These results demonstrated that SCSMC-specific decreases in I_Kv and I_Kir occur in an MCT-induced PAH model, thereby offering insights into the potential pathophysiological implications of coronary blood flow regulation in right heart disease. Furthermore, the relatively smaller I_Kir in SCSMCs suggested a less effective vasodilatory response in the septal region to the moderate increase in extracellular K⁺ concentration under increased activity of the myocardium.

• BMB Reports
• /
• v.55 no.11
• /
• pp.565-570
• /
• 2022

Pulmonary arterial hypertension (PAH) is a progressive and devastating disease whose pathogenesis is associated with a phenotypic switch of pulmonary arterial vascular smooth muscle cells (PASMCs). Bone morphogenetic protein (BMP) signaling and potassium two pore domain channel subfamily K member 3 (KCNK3) play crucial roles in PAH pathogenesis. However, the relationship between BMP signaling and KCNK3 expression in the PASMC phenotypic switching process has not been studied. In this study, we explored the effect of BMPs on KCNK3 expression and the role of KCNK3 in the BMP-mediated PASMC phenotypic switch. Expression levels of BMP receptor 2 (BMPR2) and KCNK3 were downregulated in PASMCs of rats with PAH compared to those in normal controls, implying a possible association between BMP/BMPR2 signaling and KCNK3 expression in the pulmonary vasculature. Treatment with BMP2, BMP4, and BMP7 significantly increased KCNK3 expression in primary human PASMCs (HPASMCs). BMPR2 knockdown and treatment with Smad1/5 signaling inhibitor substantially abrogated the BMP-induced increase in KCNK3 expression, suggesting that KCNK3 expression in HPASMCs is regulated by the canonical BMP-BMPR2-Smad1/5 signaling pathway. Furthermore, KCNK3 knockdown and treatment with a KCNK3 channel blocker completely blocked BMP-mediated anti-proliferation and expression of contractile marker genes in HPAMSCs, suggesting that the expression and functional activity of KCNK3 are required for BMP-mediated acquisition of the quiescent PASMC phenotype. Overall, our findings show a crosstalk between BMP signaling and KCNK3 in regulating the PASMC phenotype, wherein BMPs upregulate KCNK3 expression and KCNK3 then mediates BMP-induced phenotypic switching of PASMCs. Our results indicate that the dysfunction and/or downregulation of BMPR2 and KCNK3 observed in PAH work together to induce aberrant changes in the PASMC phenotype, providing insights into the complex molecular pathogenesis of PAH.

• Korean Journal of Radiology
• /
• v.20 no.4
• /
• pp.631-640
• /
• 2019

Objective: To evaluate the value of airway computed tomography (CT) in patients with obstructive sleep apnea (OSA) as a predictor of cerebrocardiovascular disease (CCVD) clinically, by quantitatively analyzing carotid arterial calcification (CarAC). Materials and Methods: This study included 287 patients aged 40-80 years, who had undergone both polysomnography (PSG) and airway CT between March 2011 and October 2015. The carotid arterial calcium score (CarACS) was quantified using the modified Agatston method on each upper airway CT. The OSA severity was categorized as normal, mild, moderate, and severe using the PSG results. Clinical characteristics, comorbid diseases, and lipid profiles of all patients were analyzed, and the prevalence of CCVDs was investigated during the follow up period (52.2 ± 16.0 months). Results: CCVD occurred in 27 patients (9.3%) at the end of follow-up, and the CCVD-present groups showed a significantly older mean age (57.5 years vs. 54.2 years), higher prevalence of hypertension (59% vs. 34%) and CarAC (51.9% vs. 20.8%), whereas sex, other comorbid diseases, and severity of OSA were not significantly different from the CCVD-absent group. A univariate analysis showed that age, hypertension, incidence of CarAC, and CarACS were risk factors for the occurrence of CCVD events. In a multivariate analysis, the incidence of CarAC was the only independent risk factor for CCVD. Conclusion: CarAC is an independent risk factor for CCVD, whereas the severity of OSA is not a contributory risk factor in patients with OSA. Therefore, additional analysis of CarACS based on airway CT scans may be useful for predicting CCVD.

• Biomolecules & Therapeutics
• /
• v.25 no.5
• /
• pp.471-481
• /
• 2017

The canonical transient receptor potential channels (TRPCs) constitute a series of nonselective cation channels with variable degrees of $Ca^{2+}$ selectivity. TRPCs consist of seven mammalian members, TRPC1, TRPC2, TRPC3, TRPC4, TRPC5, TRPC6, and TRPC7, which are further divided into four subtypes, TRPC1, TRPC2, TRPC4/5, and TRPC3/6/7. These channels take charge of various essential cell functions such as contraction, relaxation, proliferation, and dysfunction. This review, organized into seven main sections, will provide an overview of current knowledge about the underlying pathogenesis of TRPCs in cardio/cerebro-vascular diseases, including hypertension, pulmonary arterial hypertension, cardiac hypertrophy, atherosclerosis, arrhythmia, and cerebrovascular ischemia reperfusion injury. Collectively, TRPCs could become a group of drug targets with important physiological functions for the therapy of human cardio/cerebro-vascular diseases.