BACKGROUND: Although experimental and clinical evidences suggest that endothelin-1(ET-1) may play a pathophysiological role in ischemic heart disease, it is still controversial whether ET-1 produced during myocardial ischemia and reperfusion affects the extent of necrotic myocardium. This study was performed to investigate the role of ET-1 and the effect of ET antagonists in infarct size determination. METHODS: Male Wistar rats(260-400g) were anesthetized with pentobarbital(i.p. 50mg/kg) and ventilation was assisted via tracheostomy tube. The heart was exposed by midline incision and the left anterior descending coronary artery was ligated with 6-0 silk suture. The ligature was released after 1 hour and reperfusion was performed for 2 hours. In the first set of experiment, FRI139317(ET-A antagonist) was given as bolus i.v.(3mg/kg) 10 minutes before reperfusion, followed by continuous infusion(total 24mg/kg) throughout reperfusion. In the other protocol, bosentan(ET-A/ET-B antagonist ; 10mg/kg) was given 10 minutes before coronary occlusion as i.v. bolus. At the end of reperfusion, the heart was excised and stained with Evans blue dye(1% w/v) and triphenyltetrazolium chloride(TTC;1%) to distinguish infarct region(not stained by TTC and Evans blue), ischemic but viable myocardium(stained brick-red by TTC but not stained by Evans blue) and nonischemic myocardium(dyed by Evans blue). These three regions of myocardium were separated and weighed for analysis. Infarct size(in percent) was expressed as the ratio of infarct region to ischemic myocardium(i.e. infarct region plus ischemic but viable myocardium). RESULTS: In the first protocol, infarct region was 57.0 +/-3.8% of the ischemic myocardium in control(n=9) and 58.9+/-4.9% in FR139317 group(n=7) ; The difference was not significant statistically. Likewise, ET-A/ET-B antagonist bosentan given before coronary occlusion did not reduce infarct size significantly ; the ratio was 74.2+/-3.2% in control(n=7) and 69.5+/-2.0% in bosentan group(n=7). CONCLUSIONS: ET-A antagonist FR139317, given throughout reperfusion, did not reduce myocardial infarct size in rat. Bosentan(ET-A/ET-B antagonist) given just before coronary occlusion as i.v. bolus also did not reduce myocardial infarct size in rat.
Animals ; Coronary Occlusion ; Coronary Vessels* ; Endothelin-1 ; Endothelins* ; Evans Blue ; Heart ; Humans ; Ligation ; Male ; Myocardial Infarction* ; Myocardial Ischemia ; Myocardium ; Rats* ; Reperfusion* ; Silk ; Sutures ; Tracheostomy ; Ventilation

No abstract available.
Anal Canal* ; Rectal Fistula*

No abstract available.
Stomach Neoplasms*

No abstract available.
Breast Neoplasms* ; Breast*

The PCL is the strongest ligament in the knee joint. And it gives the posterior stability to the knee joint and act on rotation of knee joint. The many authors reported the surgical approaches for PCL. But none of them was satisfactory for exposure for PCL. Authors report the approach for repair and reconstruction on PCL injury The purpose of this report is to get the more satisfactory exposure of operation field for anatomical repair of injuried PCL. 1. PCL injury combined with MCL injury. a) MCL injury at its femoral attachment area. Detach the injuried MCL from femoral attachment completely, continue with anteromedial incision, and can observe both femoral and tibial attachment of PCL and ACL. b) MCL injury at its tibial attachment area. Retract the injuried MCL, medial meniscus, joint capsule superiorly, and through between medial meniscus and tibial proximal protion, also can observe the tivial attachment of PCL. 2. Isolated PCL injury. a) at tibial attachment(avulsion fracture) Through posterior approach or straight anteromedial approach, incised the posteromedial joint capsule, and can observed the tibial attachment of PCL. b) at substance level. Detach the MCL from its femoral attachment with bone-block and apply the knee valgus force. And can observe the entire length of PCL. Also reinforce the repaired site of PCL by reconstruction using a semitendinosus tendon.
Joint Capsule ; Knee Joint ; Knee ; Ligaments ; Menisci, Tibial ; Posterior Cruciate Ligament ; Tendons

Treatment of a paralysed or flail shoulder falls into two categories; arthrodesis and reconstructive surgery. Of these the latter is preferable in view of mobility. Most authors have tried to reconstruct the paralysed abductor by transferring the trapezius muscle only. The final result of these procedures were poor in severe paralysis of the deltoid muscle or combined paralysis of the deltoid and the rotator cuff muscles. Noting the importance of the action of the rotator cuff muscles in abduction of the shoulder, Saha, in 1967, recommended simultaneous reconstruction of tne paralysed deltoid and rotator cuff muscles. We treated a case of paralysed shoulder that followed poliomyelitis by the Saha meshod, i.e., transfer of the trapezius muscle for the paralysed deltoid, transfer of the levator scapulae muscle for the supraspinatus, transfer of the pectoralis minor muscle for the subscapularis, all in one stage. Duration of the follow up was 3 months and the initial result seemed to be good in view of stability, mobility, and abductor power.
Accidental Falls ; Arthrodesis ; Deltoid Muscle ; Follow-Up Studies ; Methods ; Muscles ; Paralysis ; Poliomyelitis ; Rotator Cuff ; Shoulder ; Superficial Back Muscles

No abstract available.
Emergencies* ; Emergency Medical Technicians* ; Humans ; Military Personnel* ; Republic of Korea*

No abstract available.
Enophthalmos* ; Orbit*

No abstract available.
Colon* ; Lymphangioma, Cystic*

No abstract available.