No abstract available.
Heart Failure* ; Heart*

BACKGROUND: Oxygen free radicals may play important role in coronary reperfusion resulting in cell death or dysfunction, and they believed that one specific mechanism for producing oxygen free radicals in myocardium is the xanthine oxidase system. Allopurinol, inhibitor of xanthine oxidase system, may limit myocardial dysfunction and injury produced by oxygen free radicals during coronary reperfusion. METHODS: Thirty isolated rabbit hearts undertook the retrograde nonworking perfusion for 15 minutes and followed by 15 minutes of working mode. After measurement of the hemodynamic values as baseline, all heart were arrested with cold cardioplegic solution for 60 minutes. Hearts were then revived with 15 minutes period of nonworking reperfusion, followed by 30 minutes of working reperfusion. The hemodynamic values were measured again at 20 minute of working period and expressed as percent of baseline values. Oxygen content of arterial perfusate and coronary effluent were measured and leakage of creatine kinase was measured from coronary effluent for 15 minutes of nonworking reperfusion. Wet and dry weight of the heart were obtained to determine for tissue water and water content. Animals were randomized as followings ; control(n=10), allopurinol PO(n=10, 100mg/kg before 24hr.), allopurinol IV(n=10, 10mg/kg before 1 hr.) RESULTS: 1) There were no significant differences in recovery of aortic pressure and heart rate between 3 groups. But there were significant differences in percent recovery of aortic flow, coronary flow, cardiac output and stroke volume between control group and allopurinol groups. 2) The leakage of creatine kinase following ischemic arrest was significantly lower in the allopurinol groups than the control group(control : 36.8+/-6.2IU, PO:19.7+/-3.1IU, IV : 22.2+/-4.6IU, p<0.001). 3) The allopurinol groups were significantly increased in oxygen extraction and oxygen consumption compared with the control((p<0.002, p<0.004)). 4) The tissue water and water content were significantly diminished in the allopurinol groups compared with the control group(p<0.003, p<0.001). 5) The electron micrograph showed more considerable structural damages of myocardial cell in the control group than the allopurinol groups. CONCLUSION: It is suggested from the results that allopurinol, inhibitor of xanthine oxidase, plays a inhibiting role in the production of oxygen free radicals, and improves myocardial protection during global ischemia and reperfusion in the isolating working rabbit heart model.
Allopurinol* ; Animals ; Arterial Pressure ; Cardiac Output ; Cardioplegic Solutions ; Cell Death ; Creatine Kinase ; Free Radicals ; Heart Rate ; Heart* ; Hemodynamics ; Ischemia ; Myocardial Reperfusion ; Myocardium ; Oxygen ; Oxygen Consumption ; Perfusion ; Reperfusion ; Stroke Volume ; Xanthine Oxidase

No abstract available.
Pneumonia*

BACKGROUND: Studies of human coronary plaque specimens have shown that T lymphocytes and macrophages are present in all types of lesions, from fatty streaks to advanced plaques. There is growing evidence for a pathogenic role for immune response in progression of atherosclerosis. This study was designed to investigate cytokine production by mononuclear leukocytes from patients with myocardial infarction. METHOD: We measured the kinetics of secretion of tumor necrosis factor-alpha (TNF-alpha) and interferon-r (IFN-r) by mononuclear leukocytes from 8 control subjects and 12 patients with acute myocardial infarction. Mononuclear leukocytes were isolated and incubated with plant lectin mitogen concanavalin-A for 24 and 48 hours. TNF-alpha and IFN-r secretions were measured by ELISA. RESULTS:There were no significant differences between TNF-alpha and IFN-r secretions by mononuclear leukocytes at and before 24 hours of incubation from both patients and control subjects, but TNF-alpha and IFN-r secretions at 48 hours of incubation were higher (p<0.005, p<0.05) in patients when compared with control subjects. TNF-alpha and IFN-r secretions by mononuclear leukocytes after incubation correlated with the peak level of creatine phosphokinase (CK) and CK-MB. CONCLUSION: Increased cytokine secretory capacity of mononuclear leukocytes may be due to the acute inflammatory response of myocardial infarction. Further trials may be needed to determined the effects of increase in secretory capacity of mononuclear leukocytes before myocardial infarction.
Atherosclerosis ; Creatine Kinase ; Enzyme-Linked Immunosorbent Assay ; Humans ; Kinetics ; Leukocytes, Mononuclear* ; Macrophages ; Myocardial Infarction* ; Plants ; T-Lymphocytes ; Tumor Necrosis Factor-alpha*

No abstract available.
Carcinoma, Transitional Cell* ; Cytogenetic Analysis* ; Cytogenetics* ; Urinary Bladder*

The suprapatellar plica is a synovial membrane that lies between the suprapatellar pouch and the true knee joint, but pathologic suprapatellar plica has been reported not frequently. We experienced one case of arch type of pathologic suprapatellar plica which was excised by arthroscopic technique, and report it with review of literature.
Knee Joint ; Synovial Membrane

Two collateral ligaments, accessory collateral ligaments, volar plate which prevent hyperextension of digital joints, fibrous flexor sheath which attached to volar plate, intrinsic and extrinsic muscles were contribute to the stability of the digital joints. Among them, two collateral ligaments were most important as a static stabilizer. Especially, the instability of fingers due to the rupture of ulnar collateral ligament of metacarpophalangeal joint of thumb and radial collateral ligament of index will attenuate the pinch power and maybe a cause of chronic painful limited finger motions. So, they should be repaired if ruptured completely. During the period of May 1980 to Oct. 1985, 17 cases of ruptured collateral ligaments 5 cases in thumb, 12 cases in fingers were treated surgically and followed up for average 8 weeks. The results were that normal range of digital joint motion were obtained in 14 cases and instabilities were disappeared in 16 cases and pain free in 12 cases. Therefore, careful clinical evaluation to detact therupture of collateral ligament of dig.ital joint after hand injury and then appropriate management could restore the best function of hand.
Chronic Pain ; Clinical Study ; Collateral Ligaments ; Fingers ; Hand ; Hand Injuries ; Joints ; Metacarpophalangeal Joint ; Muscles ; Reference Values ; Rupture ; Thumb

No abstract available
Constriction, Pathologic* ; Stents*

No abstract available.

This study was undertaken to clarify whether the color changes of skin in summer are remarkable or not. The skin color of abdomen, extensor and flexor of forearm, forehead, and cheek were measured in 27 health male students who had never tanned their skin intentionally during this experiment with Color and Color Difference Meter(Nippon Denshoku Kogyo Ca. CP6R 1001-DP) which represents skin color as 'L', 'a', and 'b' values. The 'L', 'a', and 'b' values mean the degree of lightness, redness, and yellowness respectively. Measurements had been performed four times repeatedly from summer(june) to auturmn(October) with intervals of 6 weeks. The obtained values were evaluated with statistical method, and the results were sumrnarized as follows: l. Abdominal skin showed no significant color changes in this experiment. 2 Extensor and flexor skin of forearm showed significant decrease in lightness from July, and the degree of decrease was more remarkable on extensor skin than on flexor skin. The lighteness had not been recovered by October on extensor skin and by September on flexor skin. There was no significant change in redness and yellowness on both places in this experiment. 3. Forehead skin showed no significant change in lightness and yellowness in this experiment, and showed transient decrease in redness in July. 4. Cheek skin showed no significant change in lighteness and redness in this experiment, and showed transient increase in yellowness in October.
Abdomen ; Cheek ; Forearm ; Forehead ; Humans ; Intention ; Male* ; Skin* ; Triacetoneamine-N-Oxyl