No abstract available.
Humans* ; Leprosy*

No Abstract Available.
Anisometropia*

BACKGROUND: The action of the volatile anesthetics on various organs in the body is not well known. Since Furchgott (1980) discovered endothelium derived relaxing factor (EDRF) from endothelium, many studies have been tried. Many investigators were studied about the relationship between the EDRF and the effect of the volatile anesthetics on blood vessels too. But the effect of volatile anesthetics and the site of action on the blood vessel were still controversial. In this study, we evaluated that the effect and the action site of halothane and isoflurane on isolated aortic rings of the rabbit. METHODS: Each of obtained thoracic aorta from rabbits (1.5~2.5 Kg) was divided into 3~5 mm sized rings, and a half of that were denuded. All of the aortic rings were preconstricted with phenylephrine 1.5 10-7 Mole in warm organ bath filled with modified Krebs' solution, and then LNAME (inhibitor of nitric oxide synthase, 3 10-4Mole) was administered to one group of aortic rings. MB (inhibitor of soluble guanylate cyclase, 2 10-5Mole) was administered to another one group and neither of LNAME nor MB was administered to the other group. And then isoflurane or halothane was administered (1~4%) to all of aortic rings. The polygraph recorded the changes of tension of aortic ring which was transmitted through the force transducer. RESULTS: It was proved that basal EDRF was released from endothelium by the fact that intact aortic rings were more constricted after LNAME or MB administration. The intact aortic rings were constricted in all concentration of isoflurane and both intact and denuded rings were relaxed in 4% concentration of halothane. CONCLUSION: It is concluded that isoflurane in all concentrations has an endothelium -mediated vasoconstriction and 4% halothane produced vascular relaxation directly independent of existence of the endothelium of vessel.
Anesthetics ; Aorta, Thoracic ; Arginine* ; Baths ; Blood Vessels ; Endothelium ; Endothelium-Dependent Relaxing Factors ; Guanylate Cyclase ; Halothane* ; Humans ; Isoflurane* ; Methylene Blue ; Nitric Oxide Synthase ; Phenylephrine ; Rabbits ; Relaxation ; Research Personnel ; Transducers ; Vasoconstriction

BACKGROUND: Exogenously administered epinephrine under enflurane anesthesia was known to have mild myocardial sensitizing effect. And N2O activates the sympathetic nervous system mildly. We planed this study to confirm cadiovascular effects of clinically administered epinephrine for hemostasis under the enflurane-N2O anesthesia during tonsillectomy. METHODS: Eighty children scheduled to have tonsillectomy were selected randomly and divided into 2 groups as follows; Group E: 1:100,000 epinephrine 2ug/kg and Group EL: 1:100,000 epinephrine containing 1% lidocaine 2 g/kg. Blood pressure, heart rate, and the occurrence of arrhythmia were evaluated before injection, at injection, 1 min, 2 min, 3 min, 5 min and 10 min after injection and 1 min after operation start. RESULTS: In both groups, systolic and diastolic blood pressure and heart rate are increased. But there are no significant statistical differences in each group and between groups. One min after operation, there are significant increases in systolic and diastolic blood pressure and heart rate in both groups (p<0.05), but there is no significant difference between groups. CONCLUSION: Under the enflurane-N2O anesthesia of children, 1:100,000 epinephrine 2ug/kg used for hemostasis could be used comparatively safe without any significant hemodynamic changes. But because there is always the possibility of myocardial sensitization, careful observation is necessary during epinephrine injection under the enflurane-N2O anesthesia.
Anesthesia* ; Arrhythmias, Cardiac ; Blood Pressure ; Child ; Enflurane ; Epinephrine* ; Heart Rate ; Hemodynamics ; Hemostasis* ; Humans ; Lidocaine ; Sympathetic Nervous System ; Tonsillectomy*

BACKGROUND: Desflurane is a new inhaled anesthetic with the lowest blood/gas partition coefficient and enflurane is one of the major anesthetics in these days. But the effect of volatile anesthetics and the site of action on the blood vessel are still controversial. Since Furchgott (1980) discovered endothelium derived relaxing factor (EDRF) from endothelium, many investigators have studied about the relationship between the EDRF and the effect of the volatile anesthetics on blood vessels. In this study, we evaluated that the effect and the action site of enflurane and desflurane on isolated aortic rings of the rabbit. METHODS: Each of obtained thoracic aorta from rabbits (1.5~2.5 kg) was divided into 4~6 mm rings, and a half of that were denuded. All of the aortic rings were preconstricted with phenylephrine 1.5 10-7 Mole in warm organ bath filled with modified Krebs' solution, and then LNAME (inhibitor of nitric oxide synthase, 3 10-4Mole) was administered to one group of aortic rings. MB (inhibitor of soluble guanylyl cyclase, 2 10-5Mole) was administered to another one group and neither of LNAME nor MB was administered to the other group. And then enflurane (1%, 2%, 3%, 4%) or desflurane (6%, 9%, 12%) was administered to all of aortic rings. The polygraph recorded the changes of tension of aortic ring which was transmitted through the force transducer. RESULTS: It was proved that basal EDRF was released from endothelium by the fact that intact aortic rings were more constricted after LNAME or MB administration. The intact aortic rings were constricted in all concentration of enflurane and both intact and denuded rings were maintained from control tension in all concentrations of desflurane. CONCLUSION: It is concluded that enflurane in all concentrations has an endothelium-mediated vasoconstriction effect and desflurane in all concentrations has no effect on isolated aortic rings of rabbit.
Anesthetics ; Aorta, Thoracic ; Arginine* ; Baths ; Blood Vessels ; Endothelium ; Endothelium-Dependent Relaxing Factors ; Enflurane* ; Guanylate Cyclase ; Humans ; Nitric Oxide Synthase ; Phenylephrine ; Rabbits ; Research Personnel ; Transducers ; Vasoconstriction

No abstract available.
Animals ; Hindlimb Suspension* ; Hindlimb*

No abstract available.
Anencephaly* ; Autopsy*

Minoxidil is a potent direct-acting peripheral vasodilator indicated in the management of severe or refractory hypertension. Well-known adverse effects include reflex tachycardia, fluid retention and hypertrichosis. This drug has also been reported to cause pericardial effusion in about three percent of nondialyzed patients with compromised renal function and to cause cardiac tamponade less frequently. Many studies have reported that the mean duration of therapy that caused pericardial effusion was about 8 months (range 1 month-53 months). We report a case of cardiac tamponade in nondialyzed patient with chronic renal failure receiving minoxidil for 10 years. A 58-year-old female was admitted to our hospital with dyspnea of NYHA III. She was a chronic renal failure patient without dialysis treatment and received kidney transplantation from cadaver donor and was dignosed chronic rejection in 1994. Minoxidil 10mg has been used for past 10 years. Lasix has been used for past 2 years, with dosage of 40mg to 240mg. On admission, blood pressure was 90/60mm Hg. Cardiomegaly was seen on chest radiograph. The two-dimensional echocardiogram showed a large amount of pericardial effusion. Emergency treatment with pericardiocentesis removed 2500ml of straw- colored pericardial fluid and resulted in marked improvement of dyspnea and stabilized blood pressure. The minoxidil was discontinued. The evidence of pericardial effusion was not seen for 12 months after minoxidil had been discontinued.
Blood Pressure ; Cadaver ; Cardiac Tamponade* ; Cardiomegaly ; Dialysis ; Dyspnea ; Emergency Treatment ; Female ; Furosemide ; Humans ; Hypertension ; Hypertrichosis ; Kidney Failure, Chronic* ; Kidney Transplantation ; Middle Aged ; Minoxidil* ; Pericardial Effusion ; Pericardiocentesis ; Radiography, Thoracic ; Reflex ; Tachycardia ; Tissue Donors

To study factors related to release of atrial natriuretic polypeptide(ANP) in human subjects, instracardiac pressure and plasma ANP concentration in peripheral and central circulation were measured in patients with various heart disease (18 valvular heart disease, 4 congenital heart disease, 2 cardiomyopathy). 1) The concentration in peripheral venous plasma were increased in 14 patients with New York Heart Associaion (NYHA) functional class III-IV (87+/-38 pg/ml) as compared with that in 10 patients with NYHA functional class I-II (39+/-21 pg/ml, P<0.005)and 15 normal subjects (51+/-21 pg/ml, P<0.01). 2)The concentration of plasma ANP in inferior vena cava, right ventricle, pulonary artery, left ventricle and aorta were markedly increased in patient with NYHA functional class III-IV, elevated mean right atrial pressure (MRAP> or =8 mmHg) elevated mean pulmonary capllary wedge pressure (MPCWP> or =15 mmHg) and/or elevated pulminary artery systolic pressure (PASP> or =35 mmHg), as compared with those in patients with NYHA functional class I-II and/or lower intracardiac pressure (MRAP<8 mmHg, MPCWP<15 mmHg, and/or PASP<35 mmHg). 3) A step up in ANP concentration between inferior vena cava and right atrium was seen in patients with elevated MRAP (81+/-28pg/ml, 137+/-60pg/ml, P<0.05), MPCWP (74+/-37pg/ml,112+/-62pg/ml, P<0.05) and/or PASP (75+/-29 pg/ml,119+/-64 pg/ml, P<0.05). But there were no differences among intracardiac ANP concentrations from right atrium though aorta. 4) Plasma concentrations in right atrium, pulmonary artery, left ventricle and aorta correlated with MRAP (r=0.82, 0.63, 0.56, p<0.005 and r=0.52, P<0.01, respectively), MPCWP (r=0.86, 0.75, 0.73 and 0.72 respectively, P<0.005 in all) and PASP (r=0.73, 0.57, 0.68 and 0.59 respectively P<0.005 in all). 5) Left atrial diameter correlated with plasma ANP concentration in peripheral plasma (r=0.55, P<0.01), inferior vena cava (r=0.51, P<0.025), right atrium (r=0.45, P<0.05), right ventricle (r=0.55, P<0.01), pulmonary artery (r=0.52, P<0.01), left ventricle (r=0.55, P<0.01) and aorta (r=0.56, P<0.005). These results suggest that the heart secrets atrial natriuretic polypeptide into right atrium in response to increased mean right atrial pressure, mean pulmonary capillary wedge pressure, pulmonary artery systolic pressure and/or left atrial distention.
Aorta ; Arteries ; Atrial Natriuretic Factor ; Atrial Pressure ; Blood Pressure ; Heart ; Heart Atria ; Heart Defects, Congenital ; Heart Diseases* ; Heart Valve Diseases ; Heart Ventricles ; Humans ; Plasma* ; Pulmonary Artery ; Pulmonary Wedge Pressure ; Vena Cava, Inferior

No abstract available.
Colon* ; Rectum*