BACKGROUND: Although hypoxic pulmonary vasoconstriction (HPC) and hypoxic coronary vasodilatation (HCD) have been recognized by many researchers, the precise mechanism remains unknown. As isolated arteries will constrict or relax in vitro in response to hypoxia, the oxygen sensor/transduction mechanism must reside in the arterial smooth muscle, the endothelium, or both. Unfortunately, much of the current evidence is conflicting, especially concerning to the dependency of HPC and HCD on the endothelium and the role of the K+ channel. Therefore, this experiment was attempted to clarify the dependency of HPC and HCD on the endothelium and the role of the K+ channel on HPC and HCD. METHODS: HPC was investigated in isolated main pulmonary arteries precontracted with norepinephrine (NE). HCD was investigated in isolated left circumflex coronary artery precontracted with prostaglandin F2 alpha. Vascular rings were suspended for isometric tension recording in an organ chamber filled with Krebs-Henseleit solution. Hypoxia was induced by gassing the chamber with 95% N2 +5% CO2, which was maintained for 15 - 25 min. RESULTS: 1)Hypoxia elicited a vasoconstriction in NE-precontracted pulmonary arteries with endothelium, but a vasodilatation in PGF 2 alpha-precontracted coronary arteries with and without endothelium. There was no difference between the amplitude of the HPC and HCD induced by two consecutive hypoxic challenges and the effect of normoxic and hyperoxic control Krebs-Henseleit solution on subsequent response to hypoxia. 2)Inhibition of NO synthesis by the treatment with Nw-nitro-L-arginine reduced HPC in pulmonary arteries, but inhibition of the cyclooxygenase pathway by treatment with indomethacin had no effect on HPC and HCD, respectively. 3)Blockades of the TEA-sensitive K+ channel abolished HPC and HCD. 4)Apamin, a small conductance Ca2+/-activated K+ (KCa) channel blocker, and iberiotoxin, a large conductance KCa channel blocker, had no effect on the HCD. 5)Glibenclamide, an ATP-sensitive K+ (KATP) channel blocker, reduced HCD. 6)Cromakalim, an K(ATP) channel opener, relaxed the coronary artery precontracted with prostaglandin F2 alpha. The degree of relaxation by cromakalim was similar to that by hypoxia and glibenclamide reduced both hypoxia- and cromakalim-induced vasodilations. 7)Verapamil, a Ca2+ entry blocker, caffeine, a Ca2+ emptying drug; and ryanodine, an inhibitor of Ca2+ release from SR, reduced HPC, respectively. CONCLUSION: HPC is dependent on the endothelium and is considered to be induced by inhibition of the mechanisms of NO-dependent vasodilation while HCD is independent of the endothelium and is considered to be induced by activation of the K(ATP) channel.
Anoxia ; Arteries ; Caffeine ; Coronary Vessels ; Cromakalim ; Dinoprost ; Endothelium ; Glyburide ; Indomethacin ; Muscle, Smooth ; Norepinephrine ; Oxygen ; Prostaglandin-Endoperoxide Synthases ; Prostaglandins F ; Pulmonary Artery ; Relaxation ; Ryanodine ; Vasoconstriction* ; Vasodilation*

The maximal stress exercise test was studied in 49 normal korean and 231 cases of various diseases. Bicycle ergometer was used in 122 cases and treadmill was used in 109 cases by modified Bruce protocol which was designed by author. The maximal heart rate, maximal work capacity, End point of maximal exercise and ST changes especially in coronary artery disease were investigated. Total 231 cases in cluded 8 cases of myocardial infarction, 46 cases of anginal pectoris, 91 cases of atypical anginal pain, 68 cases of hypertension and 18 and of diabetes mellitus. The results are as follows; 1. The maximal heart rate was markedly reduced in myocardial infarction(115/min. comparing 162/min. in normal) and slightly less reduction in angina pectoris. Also mild reductions were observed in atypical anginal pain, hypertension and diabetes mellitus. 2. The maximal work capacity was markedly reduced in myocardial infarction(93 wt comparing 180 wt in normal). It was only slightly reduced in anginal pectoris, atypical anginal pain, hypertension and diabetes mellitus which were not significantly reduced from that of normal, especially in anginal pectoris, the reduction on maximal work capacity was unremarkale comparing that of maximal heart rate. 3. The End point of maximal exercise test were exhaution in 34%, leg pain in 30%, maximal heart rate in 22%, ST depression more than 1 mm in 21%, dyspnea in 19%, anginal pain in 15% by bicycle ergometer, while by treadmill test, the End point were exhaution in 47%, dyspnea in 35%, Maximal heart rate in 22%, ST depression more than 1 mm in 19%, leg pain in 15% and anginal pain in 10%. 4. In coronary artery disease, the positive maximal exercise test(sensitivity) was 76% in treadmill test and 68% in bicycle ergometer test. 5. The ST changes among 231 patients druing the maximal exercise test occured in 47 cases(20%). In 43 cases the ST segment depressed more than 1 mm and the degree of depression ranged 1-3.5mm. The upward sloping type and horizontal depression type were equally common. There were 4 cases(1.7%) of ST elevation during exercise which returned to normal after exercise. There were 3 cases among 54 cases of coronary artery disease(5.5%) and 2 cases among 46 cases of anginal pectoris(4.3%). In one case of anginal pectoris with elevated ST segment, myocardial infarction occured in few days later. Therefore it appears that the variant angina in this study is very few.
Angina Pectoris ; Coronary Artery Disease ; Coronary Vessels ; Depression ; Diabetes Mellitus ; Dyspnea ; Exercise Test* ; Heart Rate ; Humans ; Hypertension ; Leg ; Myocardial Infarction

No abstract available.
Humans ; Spinal Cord Injuries* ; Spinal Cord* ; Urinary Tract Infections* ; Urinary Tract*

PURPOSE:Cardiovascular morbidity has recently been demonstrated to potentially reduce life expectancy in growth hormone deficiency(GHD). The aim of this study was to evaluate cardiovascular abnormalities and atherosclerotic changes in adults with childhood-onset GHD in whom GH treatment had been stopped at the achievement of final height. METHODS:Nine patients with childhood-onset GHD(7 idiopathic and 2 organic), with an age of 24.0+/-.0 year, were studied. Clinical characteristics of subjects were determined and blood pressure, body mass index(BMI), and serum concentrations of lipids were measured. Structural and functional evaluation of cardiovascular system was performed by M-mode echocardiography and linear phase array imaging transducer. RESULTS:BMI of patients was 27.3+/-.7 mg/m2, and four patients(44%) were overweight(BMI 25-30 mg/m2), but none was obese(BMI >30 mg/m2). The percentage of patients who had total cholesterol > or = 200 mg/dL, triglyceride > or = 150 mg/dL, LDL cholesterol > or = 140 mg/dL, and HDL cholesterol < or = 40 mg/dL were 56%, 44%, 33 %, and 44%, respectively. Interventricular septum thickness(IVST), left ventricular posterior wall thickness(LVPWT), left ventricular end-diastolic internal diameter (LVID), left ventricular mass index(LVMI) of patients were 6.4+/-2.1 mm(SDS -1.5+/-1.1), 6.3+/-1.2 mm(SDS -2.1+/-0.8), 44.9+/-4.3 mm(SDS -1.0+/-0.9), and 85.4+/-94.8 g/m2 (SDS -0.5+/-6.8), respectively. The number of patients whose IVST, LVPWT, LVID, and LVMI were decreased(<-2SD) were 4(44%), 5(56%), 1(11%), and 6(67%), respectively. Carotid artery intima-media thickness(IMT) was 0.86+/-0.22 mm, and it was increased(>2SD) in 3 patients(33%). Three out of four patients with IVST lower than -2SD had increased carotid artery IMT, whereas none of five patients with IVST higher than -2SD had increased carotid artery IMT. There were no differences in echocardiographic findings between groups according to sex, age, duration of disease, duration after GH discontinuation, BMI, and severity of dyslipidemia. CONCLUSION: Decreases in IVST, LVPWT, and LVMI, and an increase in carotid artery IMT were observed in a significant number of patients with childhood-onset GHD. These findings support the need of GH replacement after completion of growth and careful evaluation of cardiovascular changes in patients with childhood-onset GHD.
Adult* ; Blood Pressure ; Cardiovascular Abnormalities* ; Cardiovascular System ; Carotid Arteries ; Cholesterol ; Cholesterol, HDL ; Cholesterol, LDL ; Dyslipidemias ; Echocardiography ; Growth Hormone* ; Humans ; Life Expectancy ; Transducers ; Triglycerides

PURPOSE:Improved adult final height(FH) is a major goal in the treatment of children with short stature due to growth hormone deficiency(GHD). The purpose of this study was to evaluate final height in idiopathic and organic GHD children after long-term growth hormone(GH) treatment. METHODS:Twenty five(16 males and 9 females) patients with GHD(14 idiopathic and 11 organic GHD) were included. GHD was diagnosed by two or more GH provocation tests(peak GH level <10 ng/mL). All subjects had multiple pituitary hormone deficiencies, and aged 10.7+/-.5(5.5-14) years at the start of GH treatment. The patients were treated with GH 0.45-0.7 IU/kg/week in 3-7 divided doses for 6.9+/-.8(5.2-10) years. Treatment was ended when growth velocity reached lower than 2 cm/year and/or bone age reached 16 years. Standard auxologic measurements were performed at the start of GH treatment and at every 6 month after initial GH treatment. RESULTS:FH was 166.9+/-.8 cm, which was not significantly lower than target height(167.1+/-.9 cm) and predicted adult height(169.1+/-5 cm). FH SDS was significantly improved to -0.8+/-.5 compared with -3.4+/-.0 of height SDS at the start of GH treatment. The largest height increment was observed in the first year of GH treatment, with a gradual decrease in the following years. There was no difference in FH and FH SDS between idiopathic and organic GHD. Unwanted serious adverse events were not observed in all patients during GH therapy. CONCLUSION: Early diagnosis and continuous treatment with optimal doses of GH to near adult height improve the outcome in children with short stature due to idiopathic and organic GHD.
Adult ; Child* ; Early Diagnosis ; Growth Hormone* ; Humans ; Male

No abstract available.
Activities of Daily Living* ; Humans

No abstract available.
Humans

Primary pericardial tumors are rare than those originating within the myocardium or endocardium and, moreover, primary benign pericardial tumors are much rare in occurrence. Fine(1986) was able to collect only 43 cases of lipoma. Most cases are diagnosed only at autopsy. One fourth of the cardiac lipoma arise subepicardially, where they suggest the presence of pericardial effusion with compression or displacement of the heart. A case of primary intrapericardial lipoma simulating pericardial effusion is presented. This tumor originated in left anterior aspect of pericardium. The tumor was measured 30x30x5cm in size and 2,200mg in weight. Total excision of the mass was accomplished by posterior lateral thoracotomy incision, resulting in complete cure. This is the first case of primary benign lipoma of the pericardium in literatures in our knowledge.
Autopsy ; Endocardium ; Heart ; Lipoma* ; Myocardium ; Pericardial Effusion* ; Pericardium ; Thoracotomy

No abstract available.
Dinoprost* ; Female ; Pregnancy ; Pregnancy, Tubal*

No abstract available.
Aloe* ; Dermatitis, Allergic Contact*