• 한국임상수의학회지
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• 제32권1호
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• pp.101-104
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• 2015

4년령의 수컷 골든 리트리버 견이 복부 팽만 및 호흡곤란을 주증상으로 내원하였으며, 신체 검사 결과 부정맥과 심잡음이 청진되었다. 흉복부 방사선 검사 결과 전반적인 심비대, 흉수 및 복수가 관찰되었다. 심초음파 검사에서 비정상적인 승모판 및 삼첨판의 움직임과 역류가 관찰되었으며, 좌심실의 편심성 비대와 좌심방 비대가 보였다. 컬러 도플러 영상에서 확장기에 승모판 입구로부터 좌심실로 유입되는 와류가 관찰되었으며, 수축기에는 좌심방 및 우심방으로의 와류가 보였다. 도플러 검사로 확장기 승모판 유입 속도가 매우 증가하였으며 pressure half time이 지연되었다는 것을 알 수 있었다. 심초음파 검사 결과에 기초하여 승모판 협착증과 병발된 승모판 이형성증과 삼첨판 이형성증을 진단하였다.

• Journal of Chest Surgery
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• 제28권2호
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• pp.136-142
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• 1995

A clinical study was performed on 69 cases of isolated PDA surgically treated at the Department of Thoracic and Cardiovascular surgery of Kyung-Hee University Hospital from Mar. 1986 to Feb. 1994. Retrospective clinical analysis of these patients were as follows: 1.23 males and 46 females ranged in age from 16 days to 49 years. [mean 8.69yrs.,sex ratio M:F=1:2 2. Chief complaints were frequent URI in 44%, dyspnea on exertion in 16%,palpitation in 8%, easy fatigability in 6%, and no subjective symptoms in 26%. 3. On auscultation, typical continuous machinery murmur heard in 84%, and systolic murmur in 16% on Lt 2nd or 3rd intercostal space. 4. Simple chest x- ray showed increased pulmonary vascularity in 67%, cardiomegaly in 61%,and within normal limit in 16%. 5. EKG findings were LVH in 42%, biventricular hypertrophy in 17%, RVH in 3%, and within normal limit in 38%. 6. Echocardiogram was performed from all patient, and direct visualization of ductus in 93% 7. Cardiac catheterization was performed in 39 patients. The mean value of the results were;Differance SaO2[MPA-RV =11.03$\pm$ 5.26%,Qp/Qs=2.44$\pm$1.35,systolic pulmonary arterial pressure=40.69 $\pm$ 17.69mmHg. 8. 66 patients were operated through the left posterolateral thoracoctomy ; closure of ductus by double ligation in 43 cases, triple ligation in 23 cases.3 patients were operated by simple closure under cardiopulmonary bypass. 9. There was no death associated with the operation. The operative complications were atelectasis in 8 cases, pneumonia in 4 cases recannalization in 2 cases, and hoarseness in one case. 10. Systemic diastolic pressure was increased 8.12$\pm$ 0.13mmHg, and pulse pressure was decreased about 9.52 $\pm$ 1.87mmHg.

• Asian-Australasian Journal of Animal Sciences
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• 제10권5호
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• pp.528-533
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• 1997

Twenty four female Sprague-Dawley rats weighing about 190 g were used to examine changes in muscle cAMP concentrations and steady-state levels of skeletal muscle ${\alpha}$-actin mRNA during chronic administration of cimaterol, a ${\beta}$-adrenergic agonist. Cimaterol was mixed in a powdered rat diet at 10 mg/kg diet. At 3 and 21 days after the start of treatment, skeletal muscle and heart samples were collected for the measurement of cAMP concentrations and skeletal muscle ${\alpha}$-actin mRNA levels. Cimaterol increased (p < 0.01) body weight gain gradually during the first seven days of the trial period, but not thereafter. Most skeletal muscle weights and the ratio of muscle weight to body weight were increased (p < 0.05) by cimaterol treatment both at 3 and 21 days. Heart weight was also increased (p < 0.05) by cimaterol treatment at 3 and 21 days, but the ratio of heart weight to body weight was increased (p < 0.05) only at 3 day. Cimaterol decreased (p < 0.05) cAMP concentration of gastrocnemius muscle at both 3 and 21 days after treatment. However, cimaterol tended (p = 0.07) to increase cAMP concentration at 3 days in the heart. Cimaterol tended (p = 0.08) to increase the steady-state level of ${\alpha}$-actin mRNA by 60% in gastrocnemius muscle at 3 days but had no effect at 21 days. The results indicate that the pattern of hypertrophic response to chronic dietary administration of cimaterol is different between cardiac and skeletal muscle. In skeletal muscles it appears that the hypertrophy induced by cimaterol is partly due to stimulated myofibrillar protein synthesis at a pre-translational level.

• 대한한의학방제학회지
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• 제28권3호
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• pp.271-280
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• 2020

Hypertension has been approved to cause disharmony between the heart and kidney such as cardiac hypertrophy and kidney dysfunction. In traditional oriental medicine Paeo-tang (PET) has been shown to have effects on blood circulation improvement. However, the beneficial effect of PET on hypertension remains unknown. In this study, we investigated that PET attenuates blood pressure and improves cardiovascular and renal function in NG-nitro-L-arginine methylester (L-NAME) rat model. Hypertensive rat models were induced by the administration of L-NAME (40 mg/kg/day) and then PET (50 or 100 mg/kg/day) or Olmetec was treated for 2 weeks. PET treatment significantly suppressed the systolic blood pressure and decreased intima-media thickness in the thoracic aorta. PET ameliorated endothelium-dependent and independent vascular relaxation in the L-NAME-induced vascular dysfunction. PET ameliorated the functional decline in the kidney such as albumin and blood urea nitrogen in plasma. These results demonstrated that PET possesses protective effects against L-NAME-induced hypertension.

• The Korean Journal of Physiology and Pharmacology
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• 제22권4호
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• pp.447-456
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• 2018

Angiotensin-(1-9) [Ang-(1-9)], generated from Ang I by Ang II converting enzyme 2, has been reported to have protective effects on cardiac and vascular remodeling. However, there is no report about the effect of Ang-(1-9) on pulmonary hypertension. The aim of the present study is to investigate whether Ang-(1-9) improves pulmonary vascular remodeling in monocrotaline (MCT)-induced pulmonary hypertensive rats. Sprague-Dawley rats received Ang-(1-9) ($576{\mu}g/kg/day$) or saline via osmotic mini-pumps for 3 weeks. Three days after implantation of osmotic mini-pumps, 50 mg/kg MCT or vehicle were subcutaneously injected. MCT caused increases in right ventricular weight and systolic pressure, which were reduced by co-administration of Ang-(1-9). Ang-(1-9) also attenuated endothelial damage and medial hypertrophy of pulmonary arterioles as well as pulmonary fibrosis induced by MCT. The protective effects of Ang-(1-9) against pulmonary hypertension were inhibited by Ang type 2 receptor ($AT_2R$) blocker, but not by Mas receptor blocker. Additionally, the levels of LDH and inflammatory cytokines, such as $TNF-{\alpha}$, MCP-1, $IL-1{\beta}$, and IL-6, in plasma were lower in Ang-(1-9) co-treated MCT group than in vehicle-treated MCT group. Changes in expressions of apoptosis-related proteins such as Bax, Bcl2, Caspase-3 and -9 in the lung tissue of MCT rats were attenuated by the treatment with Ang-(1-9). These results indicate that Ang-(1-9) improves MCT-induced pulmonary hypertension by decreasing apoptosis and inflammatory reaction via $AT_2R$.

• 한국임상수의학회지
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• 제39권5호
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• pp.240-245
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• 2022

A 15-year-old, neutered male, Shih-Tzu, was presented at the Chonnam National Veterinary Medical Teaching Hospital for evaluation of acute onset of persistent coughing, exercise intolerance, and abnormal heart sound. On thoracic auscultation, a split-second heart sound and a wheezing sound were detected on both sides of the chest walls. On physical examination, the dog's body condition score (BCS) was 7/9, and had stenotic nares. Thoracic radiographs revealed right-sided enlargement of the cardiac silhouette (vertebral heart score (VHS) 11.2; reference interval = 8.9-10.1), mild main pulmonary artery (MPA) bulging, mild interstitial infiltration, and hepatomegaly. The electrocardiogram showed right axis deviation, suggesting right ventricular hypertrophy. The echocardiographic study showed moderate pulmonary hypertension and moderate tricuspid regurgitation. There were no findings of a tracheobronchial disease, pulmonary thromboembolism, congenital shunt, left heart disease, or parasitic disease. Based on clinical signs and diagnostic findings, the dog was diagnosed with pulmonary hypertension secondary to brachycephalic syndrome. To rectify respiratory exacerbating factors, the dog was recommended weight control by restricting dietary intake and managing concurrent Cushing's syndrome. Treatments included sildenafil, pimobendan, furosemide, and ramipril. After five months of taking medications and weight control, the severity of pulmonary hypertension improved from moderate to mild. The clinical signs of the patient, including coughing and exercise intolerance, improved a lot. For 5 months of follow-up, the patient has not reported further recurrence of respiratory distress.

• Journal of Chest Surgery
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• 제43권6호
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• pp.627-634
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• 2010

배경: 조직판막의 내구성은 심장 판막 수술에서 기계판막과 조직판막을 선택하는 중요한 기준이 된다. 본 연구는 조직판막이 사용된 대동맥판막치환술의 중기성적을 분석해 보았다. 대상 및 방법: 이 연구는 1990년 3월부터 2009년 3월까지 조직판막을 이용하여 대동맥판막치환술을 시행한 380명의 환자들을 대상으로 하였다. 술 후 평균 관찰 기간은 $46.7{\pm}40.8$월(0~196개월)이었으며 외래 경과 기록과 의무기록을 통하여 후향적으로 분석하였다. 결과: 총 380명의 환자에서 389예의 수술이 시행되었으며 환자들의 평균 연령은 $69{\pm}9$세, 남녀 비는 227 : 162였다. 조기 사망은 15명 (3.9%)이었다. 1년, 5년, 10년 생존율은 92.3%, 78.1%, 54.2%였다. 재수술의 l년, 5년, 10년 회피율(Freedom from reoperation)은 98.4%, 97.1%, 91.7%였으며 구조적 판막 손상 1년, 5년, 10년의 회피율(Freedom from structural valvular deterioration)은 96.1%, 92.3%, 88.0%였다. 수술 전 위험인자의 다변량 분석에서 젊은 나이 (p<0.001)가 재수술의 위험인자였으며 수술 후 판막 부하 최고속도(p=0.034)와 젊은 나이(p=0.029)가 구조적 판막 손상의 위험인자였다. 고령(p=0.001), 장시간의 심폐기사용(long bypass time) (p=0.035), 관상동맥 우회술을 동시에 실시한 경우(concomitant CABG) (p=0.003), 술 전 중등도 이상의 좌심실 기 능부전(Left ventricular ejection fraction, LVEF<40%) (p=0.003)이 조기 사망의 위험인자였으며 술 전 신기능저하(estimated glomerular filtration rate, eGFR<60 mL/min) (p=0.025)와 지속적인 좌심실비대(persistent left ventricular hypertrophy, LVH) (p=0.032)가 만기 사망의 위험인자였다. 결론: 이 연구를 통해 조직판막을 이용한 대동맥판막치환술은 재수술과 구조적 판막 손상 회피율 등의 측면에서 만족할 만하다고 할 수 있으며, 향후 더 많은 환자에서 보다 장기적인 연구가 필요할 것으로 생각된다.

• 한국가금학회지
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• 제33권2호
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• pp.159-164
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• 2006

본 연구는 사료와 음수에 함유된 염분 수준이 육계 초기 병아리에 미치는 영향을 조사하기 위하여 실시하였다. 1일령 초생추(Hubbard)를 공시하여 14일 동안 시험을 수행하였다. 시험 1에서, 사료내 염분 함량은 0, 0.25, 0.5, 0.75, 1.0, 2.0, 3.0, 4.0%로 조절하여 8처리구 처리구당 3반복, 반복당 12수씩 총 288수에 급여하였고, 시험 2에서, 음수내 염분 함 량은 0, 0.1, 0.2, 0.5, 1.0%로 조절하여 5처리구 처리구당 3반복, 반복당 12수씩 총 180수에 공급하였다. 시험 1의 경우에, 사료 섭취량과 증체량은 사료내 염분 함량이 증가할수록 감소하는 경향이었다. 특히 4% 처리구에서 각각 481 g과 168 g으로 가장 낮았으며, 폐사율은 75%로 가장 높았다. 시험 2의 경우에는, 음수 1% 처리구에서 사료 섭취량과 증체량은 각각 427 g과 162 g이었고, 폐사율은 77.8%로 가장 높았다. 염 중독 증상을 나타낸 닭들은 갈증, 식욕부진, 기립불능, 졸림, 경련 등을 나타내었고, 부검 소견에서는 복수증, 심낭수종, 심비대, 각종 장기의 출혈 등이 나타났다. 이상의 결과로 육계 초기에서 사료내 염분 함량이 3%, 음수내 염분 함량은 1% 이상에서 뚜렷한 생산성의 저하는 물론 생리 해부학적인 염분중독 증상이 나타남을 알 수 있다.

• The Korean Journal of Physiology and Pharmacology
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• 제20권1호
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• pp.9-14
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• 2016

Adenosine 3',5'-cyclic monophosphate (cAMP) participates in the regulation of numerous cellular functions, including the $Na^+-K^+$-ATPase (sodium pump). Ouabain, used in the treatment of several heart diseases, is known to increase cAMP levels but its effects on the atrium are not understood. The aim of the present study was to examine the effect of ouabain on the regulation of atrial cAMP production and its roles in atrial endothelin-1 (ET-1) secretion in isolated perfused beating rabbit atria. Our results showed that ouabain ($3.0{\mu}mol/L$) significantly increased atrial dynamics and cAMP levels during recovery period. The ouabain-increased atrial dynamics was blocked by KB-R7943 ($3.0{\mu}mol/L$), an inhibitor for reverse mode of $Na^+-Ca^{2+}$ exchangers (NCX), but did not by L-type $Ca^{2+}$ channel blocker nifedipine ($1.0{\mu}mol/L$) or protein kinase A (PKA) selective inhibitor H-89 ($3.0{\mu}mol/L$). Ouabain also enhanced atrial intracellular cAMP production in response to forskolin and theophyline ($100.0{\mu}mol/L$), an inhibitor of phosphodiesterase, potentiated the ouabain-induced increase in cAMP. Ouabain and 8-Bromo-cAMP ($0.5{\mu}mol/L$) markedly increased atrial ET-1 secretion, which was blocked by H-89 and by PD98059 ($30{\mu}mol/L$), an inhibitor of extracellular-signal-regulated kinase (ERK) without changing ouabain-induced atrial dynamics. Our results demonstrated that ouabain increases atrial cAMP levels and promotes atrial ET-1 secretion via the mitogen-activated protein kinase (MAPK)/ERK signaling pathway. These findings may explain the development of cardiac hypertrophy in response to digitalis-like compounds.

• Korean Circulation Journal
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• 제53권7호
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• pp.425-451
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• 2023

Most patients with heart failure (HF) have multiple comorbidities, which impact their quality of life, aggravate HF, and increase mortality. Cardiovascular comorbidities include systemic and pulmonary hypertension, ischemic and valvular heart diseases, and atrial fibrillation. Non-cardiovascular comorbidities include diabetes mellitus (DM), chronic kidney and pulmonary diseases, iron deficiency and anemia, and sleep apnea. In patients with HF with hypertension and left ventricular hypertrophy, renin-angiotensin system inhibitors combined with calcium channel blockers and/or diuretics is an effective treatment regimen. Measurement of pulmonary vascular resistance via right heart catheterization is recommended for patients with HF considered suitable for implantation of mechanical circulatory support devices or as heart transplantation candidates. Coronary angiography remains the gold standard for the diagnosis and reperfusion in patients with HF and angina pectoris refractory to antianginal medications. In patients with HF and atrial fibrillation, longterm anticoagulants are recommended according to the CHA₂DS₂-VASc scores. Valvular heart diseases should be treated medically and/or surgically. In patients with HF and DM, metformin is relatively safer; thiazolidinediones cause fluid retention and should be avoided in patients with HF and dyspnea. In renal insufficiency, both volume status and cardiac performance are important for therapy guidance. In patients with HF and pulmonary disease, beta-blockers are underused, which may be related to increased mortality. In patients with HF and anemia, iron supplementation can help improve symptoms. In obstructive sleep apnea, continuous positive airway pressure therapy helps avoid severe nocturnal hypoxia. Appropriate management of comorbidities is important for improving clinical outcomes in patients with HF.