Ischemia and reperfusion of skeletal muscle occurs in acute vascular occlusion and revascularization, in elective vascular surgery, in upper and lower extremity surgery by means of a tourniquet, and in free transplantation of muscle containing cutaneous flaps. During revascularization of skeletal muscle after ischemia, lipid mediators, mainly eicosanoids are released that may have a role in the pathogenesis of reperfusion injury. The exact role of eicosanoids in the imposed ischemia-reperfusion induced functional deficits in skeletal muscle is still unknown, we compared tissue edema and the changes of eicosanoids and the effects of cyclooxygenase inhibitor indomethacin in the rat right hindlimb by application of tourniquet ischemia-reperfusionn injury. After 4-hours of ischemia, reperfusion was established 4 hours by releasing tourniquet. Experimental groups comparised ischemia-reperfused animals pretreated with indomethacin 20 mg/kg. The control animals received normal saline, 4 hours of ischemia without reperfusion. To assess tissue edema, wet/dry weight ratios were determined and the concentrations of prostaglandins and thromboxane were measured by the high performance liquid chromatography with UV detector at 195 nm. Ischemia itself did not result in muscle edema and did not increase the release of cyclooxygenase metabolites, but muscle edema(52%, p<0.01), and the relase of 6-keto-PGFalpha(151%, p<0.01), thromboxane B2(98%, p<0.05), and PGE2(127%, p<0.01) were significantly increased by reperfusion. Indomethacin treatment ameliorated limb edema(35%, p<0.05 versus ischemis-reperfusion control) and decreased 6-keto-PGF1alpha(65%, p<0.05) releases. These results support view that cyclooxygenase products may play significant roles in the formation of ischemic muscle edema and suggest that nonsteroidal antiinflammatory agents and eicosanoids antagonists might be beneficial to the management of acute limb ischemia-reperfusion injury.
Animals ; Anti-Inflammatory Agents, Non-Steroidal ; Chromatography, Liquid ; Edema* ; Eicosanoids* ; Extremities ; Hindlimb ; Indomethacin ; Ischemia* ; Lower Extremity ; Muscle, Skeletal* ; Prostaglandin-Endoperoxide Synthases ; Prostaglandins ; Rats* ; Reperfusion Injury* ; Reperfusion* ; Tourniquets

No Abstract Available.
Female ; Mammaplasty*

Transient ischemic attack (TIA) often precede cerebral infarcts as a warning symptom. But the studies revealing the frequency and the correlation between preceding TIAs and following infarcts are rare. According to the western data, about one-quarter of the patients with cerebral infarct have been supposed to have the previous history of TIAs. We prospectively studied the exact frequency, clinical presentation, and presumed causes of TIAs preceding cerebral infarct. Ninety five patients diagnosed as acute cerebral infarction were interviewed whether they had had previous episodes of TIA. 4 check-list using ordinary language was used, and NINDS diagnostic criteria was applied on the consensus between several neurologists. Seventeen patients (18%) had history of preceding TIAs. Carotid territory was affected in 11 patients (65%), while vertebrobasilar in 4(24%) and undetermined in 2. Duration was less than an hour in 10 patients(59%), and attacks were multiple in about half. Time interval between the last attack and infarction was less than one week in 10 cases(59%). Incidence of recent TIA ((1 month) was 22% in large artery disease(LAD), 11% In cardioembolism(CE), 9% in small-artery disease(SAD), and 7% in mixed etiology. Conclusion, TIAs preceding cerebral infarcts are not rare, but seems to be less common in Koreans than in Caucasians. As expected, atherothrombosis of large artery is supposed to be the leading cause of TIAs.
Arteries ; Cerebral Infarction ; Consensus ; Humans ; Incidence ; Infarction ; Ischemic Attack, Transient* ; National Institute of Neurological Disorders and Stroke ; Prospective Studies

BACKGROUND & OBJECTIVE: Recent studies suggest that anticoagulation, or antiplatelet therapy is safe and effective for the prevention of cardiogenic embolic stroke. However it has not been studied in Korea how the patients with cardioembolic source were managed in practice for the prevention of stroke. This study was done to assess the current status of primary and secondary prevention of cardioembolic stroke. METHODS: Retrospective study was undertaken in 124 patients with cardiogenic embolic stroke, following items were examined, previous anticoagulation or antiplatelet therapy, previous stroke, Insight of the heart disease, and International Normalize Ratio(INR) value on arrival at the hospital. RESULTS: In 124 patients cardioembolic sources were constituted of non-valvular atrial fibrillation (NVAF) in 54, rheumatic heart disease In 40, prosthetic cardiac valve In 14, dilated cardiomyopathy(D-CMP) in 6, left ventricular akinetic segment in 7(including 3 cases of LV thrombi), recent myocardial infarction in 3. In 93 patients with no previous stroke, 44 patients had regular medical follow-up because of his/her cardiac problems and primary prevention of stroke was made only in 12 (27%) patients (8 on anticoagulation and 4 on antiplatelet therapy). The rate of primary prevention varied according to the type of cardioembolic source; 100% with mechanical prosthetic valve, 33.3% with valvular atrial fibrillation, 6.7% with NVAF, and none with D-CMP and bioprosthetic valve. Previous stroke was found in 31 patients, among whom 24 had been followed regularly. Twenty patients(83%) were under secondary prevention of cardioembolic stroke (anticoagulation in 11 and antiplatelet agents in 9). Among 19 patients who developed stroke in spite of anticoagulation, INR values were lower than 1.5 in 12(63%), between 1.5 and 2.0 in 5(26%), and above 2.0 in 2(11%). CONCLUSION: Our results suggest that cardioembolic strokes have not been prevented properly. Many physicians seem to be reluctant to anticoagulate their patients with cardioembolic source, and even with anticoaguation the dosage is frequently insufficient to prevent stroke.
Atrial Fibrillation ; Follow-Up Studies ; Heart Diseases ; Heart Valves ; Humans ; International Normalized Ratio ; Korea ; Myocardial Infarction ; Platelet Aggregation Inhibitors ; Primary Prevention ; Retrospective Studies ; Rheumatic Heart Disease ; Secondary Prevention ; Stroke*

This study intended to obtain an useful information on the prevalence of subjective symptoms, and to clarify the interrelationships between blood lead and lead related symptoms in low level lead exposure. The 93 male workers exposed to lead and 56 male nonexposed workers were examined for their blood lead (PBB), Zinc-protoporphy (ZPP), hemoglobin (HB) and personal history, and completed 15 questionnaires related to symptoms of lead absorption; also measured lead concentration in air (PBA) in the workplace. The results obtained were as follow; 1. The means of blood lead (PBB), blood ZPP and hemoglobin (HB) among workers exposed to lead were 26.1+/-8.8 microgram/dl, 28.3+/-26.0 microgram/dl and 16.2+/-1.2g/dl; whereas those of nonexposed workers were 18.7+/-5.1 microgram/dl, 20.6+/-8.7 microgram/dl and 17.3+/-1.1g/dl. The means of above three indicies between two groups showed significant difference statistically (p<0.05). 2. The means of blood lead (PBB), blood ZPP and hemoglobin of workers exposed to different lead concentration in air were as follows; When it was below 25 microgram/m3 , the indices were 24.7+/-79, 26.1+/-26.8 microgram/dl and 16.4+/-1.1 g/dl respectively; These indices were 27.1+/-8.5, 23.9+/-10.92 /dl and 16.2+/-1.3 g/dl when the lead concentration in air was 25~50 microgram/m3; and they were 3.4+/-9.3, 42.3+/-31.3 microgram/dl and 15.5+/-1.2 g/dl when the concentration of lead was above 50 microgram/m3. Although there were statistical difference in blood lead and hemoglobin among three different lead concentration in air, there was no statistical difference of blood ZPP among the three groups with different exposure levels (p>0.05). 3. The most frequently by complained symptom was "Generalized weakness and fatigue", and fewest symptom was "Intermittent pains in abdomen". 4. Only two symptoms out of fifteen symptoms checked by themselves revealed significant difference between exposed and nonexposed groups. These were "Intermittent pains of abdomen" and "Joint pain or arthralgia" (p<0.05). No positive correlation was found between the levels of blood lead and symptom groups categorized as gastrointestinal, neuromuscular and constitutional symptoms. 5. Blood lead (r=0.3995) and ZPP (r=0.2837) showed statistically significant correlation with mean lead concentration in air, whereas correlations were not demonstrated between blood lead and lead related symptoms or blood ZPP and lead related symptoms. 6. Blood lead (PBB) and ZPP showed association (r=0.2466) and the equation PBB=23.75+0.0842 ZPP was derived. 7. On stepwise multiple regression, using blood lead level as a dependent variable and ZPP, hemoglobin (HB), age, work duration (WD) and symptom prevalence as a independent variables, only ZPP significantly contributed a lot to blood lead level. 8. While the ZPP measurement was found to be a good indicator in evaluating health effect of lead absorption in low level lead exposure, lead related symptoms were not sensitive enough to evaluate of lead absorption in low level exposure.
Absorption ; Humans ; Male ; Prevalence ; Surveys and Questionnaires

BACKGROUND: Cardiogenic embolic infarction is the most preventable type of ischemic stroke. This study was under-taken to compare the infarct size, prognosis, and risk factors between cardiogenic embolic infarction (CE) and large artery atherosclerotic infarction (LAA). METHODS:We reviewed the medical records and brain computed tomography/magnetic resonance image (CT/MRI) scans of patients with CE or LAA during the period between January 1996 and May 1998. Patients with lacunar and posterior circulation infarctions were excluded. A slice of brain CT/MRI scan showing the largest lesion was selected in each patient and the area of infarction was then measured. Prognosis was determined by the Modified Rankin Disability Scale (MRDS) and was grouped as either good (MDRS 0, 1, 2) or poor (MDRS 3, 4, 5). RESULTS: The study included 103 patients : 50 with CE (NVAF in 23, VHD with or without AF in 13, prosthetic valve in 6, and others in 8) and 53 with LAA (large artery thrombosis in 29, and artery to artery embolism in 24). The infarct size of CE (23.2+/-14.7 cm2) was significantly larger than that of LAA (11.4+/-10.5 cm2) (p<0.001). The infarct size of NVAF (29.0+/-19.1 cm2) was significantly larger than that of VHD with or without AF (19.2+/-11.5 cm2) (p<0.05). Patients with CE had a worse prognosis (poor in 46%) than those with LAA (poor in 23%) (p<0.05). CONCLUSIONS Our results showed that CE led to larger lesions and worse outcomes. Therefore, we emphasize the importance of primary and secondary preventions of stroke in patients with cardiogenic embolic sources.
Arteries* ; Brain ; Embolism ; Heart Valve Diseases ; Humans ; Infarction* ; Medical Records ; Prognosis* ; Risk Factors ; Secondary Prevention ; Stroke ; Thrombosis

A series of 135 cases of pterygium observed at the Eye Dept. in the National Medical Center from April 1963 to May 1966, were treated with thio-tepa after the surgical removal and were studied clinically in regard to the incidence of the recurrence. Among the total series, only one case showed no response to the thio-tepa instillation and the recurrence persisted. There was a case of allergic response to the thio-tepa, which has not been found in any reports known. No serious local or systemic toxcity or any sequelae such as corneal damages, defective vision or the interference with wound healing could be observed.
Incidence ; Korea* ; Pterygium ; Recurrence ; Thiotepa ; Wound Healing

The mechanisms involved in brain neuronal damage in ischemia are related to the elevation of cytosolic calcium concentration and calcium antagonist is considered as a promising drug that may alleviate ischemic neuronal damage. Using transient global ischemia model of Mongolian gerbil, we studied the effect of nimodipine, a cerebroselective calcium antagonist, on ischemic brain edema. We treated each gerbil intraperitoneally with nimodipine (lmg/kg) or the same amount of saline 30 minutes prior to ischemia, and transient global ischemia was induced by means of clipping both common carotid arteries either for 10 minutes or for 45 minutes. Three hours after reperfusion, the animals were decapitated and the water content of the bain was determined by oven dry method. With 10 minute ischemia the brain water content in nimodipine pretreatment group (78.6 +/- 0.2%) was lower than that in saline pretreatment group (79.1 +/- 0.4%) significantly (p<0.05). But with 45 minute ischemia nimodipine pretreatment did not reduce the postischemic increase of water content compared with saline pretreatment (79.8 +/- 0.4% and 79 6 +/- 0.4%, respectively; not significant). Our results suggest that nimodipine pretreatment may suppress the development of ischemic brain edema and its effect depends largely on the extent of brain ischemia.
Animals ; Brain Edema* ; Brain Ischemia ; Brain* ; Calcium ; Carotid Artery, Common ; Cytosol ; Gerbillinae* ; Ischemia ; Neurons ; Nimodipine* ; Reperfusion

BACKGROUND AND PURPOSE: Current therapy for acute ischemic stroke is highly focused on neuroprotective agents, and many ion channel blockers have been challenged for experimental models. In this study, we tried to reveal the neuroprotective effect of lamotrigine, a voltage-sensitive sodium channel blocker, for transient global ischemia of Mogolian gerbil. METHODS: Lamotrigine (50mg/kg) was administered via gastric tube 30 minutes before and after global ischemia (for 10 min) under body temperature monitoring. Sham-operated and non-treated ischemia group were compared. Seven days after reperfusion, gerbils were killed with perfusion/fixation technique and representative sections were cut through the hippocampus. Hematoxylin-Eosin staining was done for microscopic examination and number of viable neurons in CA1 area was counted. RESULTS: Neuronal density was different between sham-operated (n=11), non-treated ischemic (n=11), and lamotrigine-treated (n=26) group (107.8+13.1/mm vs. 21.5+23.0/mm vs. 82.0+13.1/mm, p<0.01). Both pre-(n=17) and post-treated group (n=9) showed significant neuroprotective effect compared with non-treated group. Neuronal density of pre-treated group was slightly higher than in post-treated group, though statistically not significant (84.6+13.0/mm vs. 77.3+12.7/mm, p=0.13). CONCLUSION: These results show that lamotrigine may have some effects reducing the delayed neuronal death in transient global ischemia. Considering the mechanism of action, we suggest that activation of voltage-sensitive sodium channel and release of glutamate at early phase of ischemia may be related to the delayed neuronal death.
Body Temperature ; Cerebral Infarction ; Gerbillinae ; Glutamic Acid ; Hippocampus ; Ion Channels ; Ischemia* ; Models, Theoretical ; Neurons ; Neuroprotective Agents* ; Reperfusion ; Sodium Channels ; Stroke

No abstract available.
Guillain-Barre Syndrome* ; Pregnancy*