1.The Pulmonary Hemodynamic Effects of Nitric Oxide Inhalation on Hypoxic Pulmonary Vasoconstriction.
Hae Jeong JEONG ; Seong Kee KIM ; Chung Su KIM ; Jeon Jin LEE ; Sung Deok KIM
Korean Journal of Anesthesiology 1997;33(5):811-821
BACKGROUND: Nitric Oxide (NO) has been discovered to be an important endothelium-derived relaxing factor. The exogenous inhaled NO may diffuse from the alveoli to pulmonary vascular smooth muscle and produce pulmonary vasodilation, but any NO that diffuses into blood will be inactivated before it can produce systemic effects. To examine the effects of NO on pulmonary and systemic hemodynamics, NO was inhaled by experimental dogs in an attempt to reduce the increase in pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) induced by hypoxia in dogs. METHODS: Eight mongrel dogs were studied while inhaling 1)50% O2 (baseline), 2)12% O2 in N2 (hypoxia), 3)followed by the same hypoxic gas mixture of O2 and N2 containing 20, 40 and 80 ppm of NO, respectively. RESULTS: Breathing at FIO2 0.12 nearly doubled the pulmonary vascular resistance from 173 56dyn sec cm-5 to 407 139dyn sec cm-5 and significantly increased the mean pulmonary artery pressure from 16 3mmHg to 22 4mmHg. After adding 20~80 ppm NO to the inspired gas while maintaining the FIO2 at 0.12, the mean pulmonary artery pressure decreased (p<0.05) to the level when breathing oxygen at FIO2 0.5 while the PaO2 and PaCO2 were unchanged. The pulmonary vascular resistance decreased significantly and the right ventricular stroke work index returned to a level similar to breathing at FIO2 0.5 by addition of NO into the breathing circuit. Pulmonary hypertension resumed within 3~5 minutes of ceasing NO inhalation. In none of our studies did inhaling NO produce systemic hypotension and elevate methemoglobin levels. CONCLUSIONS: Inhalation of 20~80 ppm NO selectively induced pulmonary vasodilation and reversed hypoxic pulmonary vasoconstriction without causing systemic vasodilation and bronchodilation. Methemoglobin and NO2 were within normal limit during the study.
Animals
;
Anoxia
;
Dogs
;
Endothelium-Dependent Relaxing Factors
;
Hemodynamics*
;
Hypertension, Pulmonary
;
Hypotension
;
Inhalation*
;
Methemoglobin
;
Muscle, Smooth, Vascular
;
Nitric Oxide*
;
Oxygen
;
Pulmonary Artery
;
Respiration
;
Stroke
;
Vascular Resistance
;
Vasoconstriction*
;
Vasodilation
2.Antiatherogenic Effect of Naringin Independent of Lipid-Lowering Action in Hypercholesterolemic Rabbits.
Seong Choon CHOE ; Hyo Soo KIM ; Tae Sook JEONG ; Song Hae BOK ; Young Bae PARK
Korean Circulation Journal 1998;28(11):1873-1881
BACKGROUND: Naringin, one of the flavonoids in citrus fruit peels, is known to have antioxidant and hepatotonic effects in animal studies. We evaluated the effect of naringin on 1) blood lipid profiles, 2) regression of fatty streak of aorta, and 3) liver toxicity in diet-induced hypercholesterolemic rabbits. METHODS: New Zealand White Rabbits (2.0 - 2.5 Kg) were divided to three groups; group without treatment, group treated with 100 mg/kg/d or 500 mg/kg/d naringin, and group treated with 1 mg/kg/d or 20 mg/kg/d lovastatin. They were fed on 0.25% or 1.0% cholesterol-containing diet for 8 weeks and then sacrificed. Blood samples were collected for measurement of total cholesterol, HDL-cholesterol, triglyceride, serum GOT and GPT. Aortas and livers were harvested for evaluation of fatty streak and pathologic examination. RESULTS: 1)Feeding of 1% cholesterol diet for eight weeks significantly increased the cholesterol level upto 20 folds. Neither lovastatin nor naringin did lower these marked hypercholesterolemia. But both naringin (500 mg/kg/d) and lovastatin (1 mg/kg/d) significantly reduced the area of fatty streak by 75% and 58%, respectively. Naringin was more effective in inhibition of fat infiltration into liver than lovastatin which showed hepatotoxicity as increase of serum GPT level (p=0.01). 2)Feeding of 0.25% cholesterol diet for eight weeks significantly increased the cholesterol level upto 17 folds. Total cholesterol and triglyceride levels tended to decrease by treatment with naringin (500 mg/kg/d) and lovastatin (20 mg/kg/d), but this decreases were not statistically significant. However, areas of fatty streak significantly decreased by treatment with naringin and lovastatin by 64 and 82%, respectively (p<0.05). Microscopic analysis revealed that foam cell infiltration into intima was significantly reduced by naringin and lovastatin. In contrast to lovastatin, naringin significantly reduced the level of serum GPT (p<0.05). CONCLUSION: Like lovastatin, naringin has strong antiatherogenic action which may not be associated with its very mild lipid lowering action. In contrast to lovastatin, naringin does have hepatoprotective effect.
Animals
;
Aorta
;
Cholesterol
;
Citrus
;
Diet
;
Flavonoids
;
Foam Cells
;
Hypercholesterolemia
;
Liver
;
Lovastatin
;
Rabbits*
;
Triglycerides
3.The Effect of Serum Uric Acid in Generating Idiopathic Benign Paroxysmal Positional Vertigo
Journal of the Korean Balance Society 2010;9(1):27-31
BACKGROUND AND OBJECTIVES: The causative role of serum uric acid has been controversial in Benign paroxysmal positional vertigo (BPPV). The aim of this study was vto determine the role of serum uric acid in developing idiopathic BPPV. MATERIALS AND METHODS: We recruited 168 consecutive patients with a confirmed diagnosis of idiopathic BPPV. The patients comprised 116 women (age range: 29~70 years, mean+/-SD: 55.8+/-9.7 years) and 52 men (age range: 32~70 years, mean+/-SD: 55.2+/-10.9 years). The serum uric acid levels of the patients were compared with those of 194 controls (age range: 20~70 years, mean+/-SD: 55.5+/-7.8 years) without a history of dizziness. RESULTS: The serum uric acid levels were decreased in patients with BPPV compared with those in normal controls (4.8+/-1.3 vs 5.3+/-1.3, p=0.001). However, multiple logistic regression analyses adjusted for age, sex, alcohol, smoking, hyperphosphatemia and osteopenia/osteoporosis did not demonstrate that the hypouricemia is an independent risk factor for BPPV. CONCLUSION: This study suggests that serum uric acid level is not a risk factor for developing idiopathic BPPV.
Dizziness
;
Female
;
Humans
;
Hyperphosphatemia
;
Logistic Models
;
Male
;
Risk Factors
;
Smoke
;
Smoking
;
Uric Acid
;
Vertigo
4.Diagnosis and Differential Diagnosis of Migrainous Vertigo
Journal of the Korean Balance Society 2012;11(2):45-50
Migrainous vertigo is one of common recurrent vestibular disorders. Because the diagnostic criteria have not been yet settled internationally, we have a difficulty in both diagnosis and research in migraineurs with vertigo. Literature about the diagnostic criteria of migrainous vertigo and its differential diagnosis were reviewed. Until now, the criteria proposed by Neuhauser et al. is regarded as most adequate in diagnosis of migrainous vertigo. Differential diagnosis of migrainous vertigo should be guided by distinction of vestibular symptoms and nonvestibular dizziness and consider the common causes of recurrent vertigo. Just like migraine itself, migrainous vertigo is diagnosed on the basis of history and exclusion of other vestibular disorders mimicking migrainous vertigo. Therefore, delicate history taking is the most important in diagnosis and management of patients with migrainous vertigo.
Diagnosis, Differential
;
Dizziness
;
Humans
;
Migraine Disorders
;
Vertigo
6.The Effect of Venous Extension on the prognosis of Renal Cell Carcinoma.
Seong Jin JEONG ; Jeong Hyun KIM ; Cheol KWAK ; Eun Chan PARK ; Hae Won LEE ; Sang Eun LEE
Korean Journal of Urology 2000;41(6):731-740
No abstract available.
Carcinoma, Renal Cell*
;
Prognosis*
7.The Effect of Venous Extension on the prognosis of Renal Cell Carcinoma.
Seong Jin JEONG ; Jeong Hyun KIM ; Cheol KWAK ; Eun Chan PARK ; Hae Won LEE ; Sang Eun LEE
Korean Journal of Urology 2000;41(6):731-740
No abstract available.
Carcinoma, Renal Cell*
;
Prognosis*
8.A Case of Acardiac Twin.
Seong Yun JEONG ; Hae Hyeog LEE ; Seok Min LEE ; Hwan Sung JAE ; Kye Hyun NAM ; Im Soon LEE ; Kwon Hae LEE ; Dong Won KIM
Korean Journal of Perinatology 2000;11(2):221-227
No abstract available.
Humans
9.Diagnosis and Management of Malignant Pleural Effusion.
Hae Seong NAM ; Jeong Seon RYU
Korean Journal of Medicine 2011;81(2):167-173
Malignant pleural effusions (MPEs) are an important clinical problem in patients with neoplastic disease. They can occur as the initial presentation of cancer, a delayed complication in patients with previously diagnosed malignancies, or the first manifestation of cancer recurrence after therapy. Common cancer types causing MPEs include lymphomas, mesotheliomas, and carcinomas of the breast, lung, and ovaries. However, almost all tumor types have been reported to cause MPEs. Regardless of the etiology, the median survival from clinical recognition is 4 months. New imaging modalities assist the evaluation of patients with a suspected MPE. However cytologic or tissue confirmation of malignant cells is necessary to establish a diagnosis. Management of an MPE remains palliative. Managements are directed toward removing pleural fluids and when appropriate, performing pleurodesis or initiating long-term drainage to prevent fluid reaccumulation. Talc pleurodesis is still the choice of treatment although concerns about its safety remain. Several factors such as performance status, expected survival, lung re-expansion following pleural fluid drainage and co-morbidities should be considered before the treatment.
Breast
;
Drainage
;
Female
;
Humans
;
Lung
;
Lymphoma
;
Mesothelioma
;
Ovary
;
Pleural Effusion
;
Pleural Effusion, Malignant
;
Pleurodesis
;
Recurrence
;
Talc
10.Vascular Reactivity by Purinoceptor Activation in Rat Inferior Vena Cava.
Boo Soo LEE ; Hae Sook CHUNG ; Kyu Sang PARK ; In Deok KONG ; Seong Woo JEONG ; Joong Woo LEE
Korean Circulation Journal 2000;30(9):1156-1164
BACKGROUND: Extracellular ATP, released from platelets and nerve endings, plays significant roles in the regulation of circulation. The effects of ATP depend on the location of the vessels and the species of experimental animals. Until now, studies were limited to arteries, so we compared the effects of ATP in rat vena cava with those in the aorta and attempted to identify the characteristics of their receptors. METHODS: Vascular rings were isolated from the rat inferior vena cava and descending thoracic aorta. Endothelial cells were preserved or removed by gentle rubbing. The isometric contractions were recorded on polygraph using a force transducer. RESULTS: In the vena cava ring precontracted by 100 nM norepinephrine (NE), ATP elicited relaxations in a dose-dependent manner. These effects were abolished by removal of the endothelium or pretreatment with a nitric oxide synthase inhibitor. Relaxations to ATP in the vena cava (EC50 :9.9 microM) were less potent than those in the aorta (1.7 microM). The relative order of potencies was ADP>ATP>AMP>adenosine, but the maximal relaxation to ADP was smaller than to ATP. ATP-induced vasorelaxation was blocked by suramin, a nonselective antagonist for P2 purinoceptor and reactive blue-2, a P2Y blocker. At basal tension, ATP contracted the vena cava dose-dependently and these effects were potentiated by endothelium-removal. Contractions in the vena cava were also less potent than in the aorta, and the order of potencies was alpha, beta-MeATP>UTP>ATP>ADP>AMP=adenosine. ATP-induced vasoconstriction was blocked by suramin and alpha, beta-MeATP, a desensitizing antagonist of P2X purinoceptor, and potentiated by pretreatment with UTP. CONCLUSION: These results suggest that ADP and ATP acts on P2Y1- and P2Y2-purinoceptor in the endothelium, respectively and induces vasorelaxation of the vena cava, which is mediated by nitric oxide. Since ATP and UTP induced vasoconstriction in endothelium-denuded condition, it may be mediated by the activation of the P2X and P2Y4, 6 purinoceptor on smooth muscles, respectively.
Adenosine Diphosphate
;
Adenosine Triphosphate
;
Animals
;
Aorta
;
Aorta, Thoracic
;
Arteries
;
Endothelial Cells
;
Endothelium
;
Isometric Contraction
;
Muscle, Smooth
;
Nerve Endings
;
Nitric Oxide
;
Nitric Oxide Synthase
;
Norepinephrine
;
Rats*
;
Receptors, Purinergic P2
;
Receptors, Purinergic P2X
;
Receptors, Purinergic*
;
Relaxation
;
Suramin
;
Transducers
;
Uridine Triphosphate
;
Vasoconstriction
;
Vasodilation
;
Vena Cava, Inferior*