• Journal of Chest Surgery
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• v.27 no.6
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• pp.455-459
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• 1994

We experienced 20 cases of acquired aortic diseases during last 1 year [Sep. 1992-Aug. 1993] with newly developed surgical strategies. There were 13 cases[65%] of aortic dissections, 5 cases[25%] of aortic aneurysms and 2 cases of Takayasu arteritis with mean age of 56 + 16 years[range:5-78].In ten cases of patients requiring ascending aortic replacement, femoral artery and femoral vein &/or RA auricle were used as cannulation site. With deep hypothermic circulatory arrest and retrograde cerebral perfusion of cold oxygenated blood via SVC, we can replace the ascending aorta and part of arch if necessary. The mean duration of circulatory arrest was 30 minutes[17-45 min]. In 5 cases of patients who requiring descending and thoracoabdominal aorta replacement, we used simple aortic crossclamping under normothermia with no heparin. The mean duration of aortic crossclamping was 37 minutes[25-50 min].The results of operation were as follow:Operative mortality[2 cases, 10%], delayed cerebral infarct[1], low extremity weakness[1] and intraoperative myocardial infarct[1]. There are no delayed complication or mortality as yet.

• Biomolecules & Therapeutics
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• v.7 no.3
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• pp.234-241
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• 1999

The present study assessed the cerebroprotective effect of platelet-activating factor(PAF) antagonists in transient cerebral ischemia of rats. Right middle cerebral artery (MCA) of Sprague-Dawley rats was occluded for 2 hours using an intraluminal filament technique, and was reperfused for 6 hours following cerebral ischemia. The infarct area of seven coronal brain slices was measured morphometrically following stain ing in the 2% 2,3,5-triphenyltetrazolium chloride solution. The changes in regional cerebral blood flow (rCBF) and pial arteriolar diameter were measured by laser-Doppler flowmetry and by a videomicroscopy, respectively. The infarct size was significantly reduced by PAF antagonists, BN 52021 and CV-6209, which were administered i.p. 10 min before MCA occlusion. Pretreatment with PAF antagonists significantly restored the changes in pial arterial diameter as well as those in rCBF during the period of cerebral ischemia-reperfusion. PAF antagonists significantly inhibited the inducible nitric oxide synthase activity in the pial arteries ipsilateral to ischemia. These results suggest that PAF antagonists exert a cerebroprotective effect against ischemic brain damage through an improvement of postocclusive cerebral blood flow.

• Korean Journal of Audiology
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• v.23 no.3
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• pp.167-172
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• 2019

Differentiating central vestibulopathy from more common vestibular disorders is crucial because it often necessitates different treatment strategies, and early detection can help to minimize potential complications. Isolated nodular infarct is one of the central brain lesions that can mimic peripheral vertigo. We present a case of isolated nodular infarct that had been misdiagnosed as vestibular neuritis on the contralateral side at the initial evaluation. The patient was successfully treated with anticoagulants and antihyperlipidemic agents. Clinicians should keep in mind that some causes of central vertigo mimic peripheral vestibulopathy at the early stage.

• Journal of Audiology & Otology
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• v.23 no.3
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• pp.167-172
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• 2019

Differentiating central vestibulopathy from more common vestibular disorders is crucial because it often necessitates different treatment strategies, and early detection can help to minimize potential complications. Isolated nodular infarct is one of the central brain lesions that can mimic peripheral vertigo. We present a case of isolated nodular infarct that had been misdiagnosed as vestibular neuritis on the contralateral side at the initial evaluation. The patient was successfully treated with anticoagulants and antihyperlipidemic agents. Clinicians should keep in mind that some causes of central vertigo mimic peripheral vestibulopathy at the early stage.

• The Journal of Korean Medicine
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• v.22 no.1
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• pp.10-21
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• 2001

Objective : This study was performed to investigate the protective effect of Stephania tetrandra(ST) against ischemic brain damage after a middle cerebral artery(MCA) occlusion. The effect was evaluated using histological tests, neurobehavioral tests, and biochemical tests. Methods : Rats(Sprague-Dawley) were divided into four groups : sham operated group, MCA occluded group, post MCA occlusion Stephania tetrandra administrated (7.6mg/l00g) group, and normal group. The MCA was occluded by intraluminal method. Stephania tetrandra was administrated orally twice at 1 and 4 hours after MCA occlusion. The neurobehavioral test was performed at 3, 6, 9 and 24 hours after MCA occlusion by posture reflex test and swimming behavioral test. All groups were sacrificed then. The brain tissues were stained with 2% triphenyl tetrazolium chloride(TTC) or 1 % cresyl violet solution, to examine infarct size, volume and cell number. Tumor necrosis $factor-{\alpha}$ level was measured from sera using Enzyme-Linked Immunoabsorbent Assay(ELISA). The mRNA expression level of inflammatory cytokines and related receptor type I and II, $IL-1{\beta}$, IL-6, and IL-10 6hours after MCA occlusion were also studied by reverse transcriptase polymerase chain reaction(RTPCR). Results : The results showed that : Stephania tetrandra (1) reduced infarct size and total infarct volume by 52.2% compared to the control group; (2) attenuated significantly in neuronal death, which was shown by a decrease in cell number(P<0.01) and size(P<0.01) in the boundary area of the infarction; (3) significantly reduced serum $TNF-{\alpha}$ level, and increased the mRNA level of IL-10 in the cortex region(P<0.01). However, there was no significant effect on motor deficit in swimming behavioral test. Conclusions : In conclusion, Stephania tetrandra has protective effects against ischemic brain damage at the early stage of ischemia.

• Journal of Chest Surgery
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• v.47 no.6
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• pp.510-516
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• 2014

Background: Acute cerebral infarction is a major risk factor for postoperative neurologic complications in cardiac surgery. However, the outcomes associated with acute silent cerebral infarction (ASCI) have not been not well established. Few studies have reported the postoperative outcomes of these patients in light of preoperative Diffusion-weighted magnetic resonance imaging (DWI). We studied the postoperative neurologic outcomes of patients with preoperative ASCI detected by DWI. Methods: We retrospectively studied 32 patients with preoperative ASCI detected by DWI. None of the patients had preoperative neurologic symptoms. The mean age at operation was $68.8{\pm}9.5$ years. Five patients had previous histories of stroke. Four patients had been diagnosed with infective endocarditis. Single cerebral infarct lesions were detected in 16 patients, double lesions in 13, and multiple lesions (>5) in three. The median size of the infarct lesions was 4 mm (range, 2 to 25 mm). The operations of three of the 32 patients were delayed pending follow-up DWI studies. Results: There were two in-hospital mortalities. Neurologic complications also occurred in two patients. One patient developed extensive cerebral infarction unrelated to preoperative infarct lesions. One patient showed sustained delirium over one week but recovered completely without any neurologic deficits. In two patients, postoperative DWI confirmed that no significant changes had occurred in the lesions. Conclusion: Patients with preoperative ASCI showed excellent postoperative neurologic outcomes. Preoperative ASCI was not a risk factor for postoperative neurologic deterioration.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2001.11a
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• pp.85-85
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• 2001

Sam-Hwang-Sa-Shim-Tang(SHSST), a traditional Chinese medicine, composed of Rhei rhizoma, Scutellaria radix, and Coptidis rhizoma were used in the several disease including hypertension, constipation, and hemorrhage. In the present study, we investigated the neuroprotective effects of SHSST and its ingredients on the ischemia/ reperfusion-induced brain injury was evaluated in the rat brain. Ischemia was induced by intraluminal occlusion of the right middle cerebral artery for 120 min and reperfusion was continued for 22 h. SHSST (450 mg/kg), Rhei rhii oma (100 mg/kg), Coptidis rhizoma (100 mg/kg), and Scutellaria radik (100 mg/kg) were orally administered twice, promptly prior to reperfusion and 2 h after the repefusion. Total infarction volume in the ipsilateral hemisphere of ischemia/ reperfusion rats was significantly lowed by the treatments of SHSST (39.2%) and Scutellaria radix (66.5%). However, Coptidis rhizoma did not show any significant effects on the total infarct volume. The inhibiting effect of Scutellaria radix on the total infarct volume was more potent than that of SHSST. In addition, Scutellaria radix significantly inhibited myeloperoxidase (MPO) activity, an index of neutrophil infiltration in ischemic brain tissue. However, there was marked mismatch between total infarct volume and MPO activity in the Scutellaria radix-treated rats. Our findings suggest that Scutellaria radix as an ingredient of SHSST plays a protective role in ischemia-induced brain injury by inhibiting neutrophil infiltration. The effects of Rhei rhizoma on transient brain ischemia-induced neuronal injury are under study.

• Biomedical Science Letters
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• v.11 no.3
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• pp.355-363
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• 2005

This study aimed to investigate the cerebroprotective effect of vascular endothelial growth factor (VEGF) on permanent focal cerebral ischemia in Sprague-Dawley rats. Right middle cerebral artery (MCA) was occluded for 6 and 24 hours by an intraluminal monofilament technique. An open cranial window was made on the right parietal bone for determination of continuous changes in regional cerebral blood flow (rCBF) by laser-Doppler flowmetry. The infarct size was morphometrically determined using the 2,3,5-triphenyltetrazolium chloride technique. Brain edema was determined by measuring brain water content. In normal rats, rCBF was significantly increased by intravenous infusion of VEGF for 10 minutes. The VEGF-induced increase in rCBF was significantly inhibited by pretreatment with suramin, a heparin-binding growth factor inhibitor as well as $N^{\omega}-nitro-L-arginine$, a nitric oxide synthase inhibitor. In focal cerebral ischemic rats, the amplitude of decrease in rCBF during ischemic period was significantly less in VEGF-treated group, compared with that in vehicle-treated group. The cerebral infarct size was reduced by VEGF in a dose-dependent manner. The brain edema formation was dose-dependently reduced by VEGF in 24-hour MCA occlusion group but not in 6-hour MCA occlusion group. It is suggested that VEGF not only improves the rCBF during cerebral ischemic period but also reduces the brain edema formation, and thereby exert a protective effect on focal cerebral ischemia in rats.

• Nutrition Research and Practice
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• v.8 no.4
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• pp.391-397
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• 2014

BACKGROUND/OBJECTIVE: Myocardial cell death due to occlusion of the coronary arteries leads to myocardial infarction, a subset of coronary heart disease (CHD). Dietary fiber is known to be associated with a reduced risk of CHD, the underlying mechanisms of which were suggested to delay the onset of occlusion by ameliorating risk factors. In this study, we tested a hypothesis that a beneficial role of dietary fiber could arise from protection of myocardial cells against ischemic injury, manifested after occlusion of the arteries. MATERIALS/METHODS: Three days after rats were fed apple pectin (AP) (with 10, 40, 100, and 400 mg/kg/day), myocardial ischemic injury was induced by 30 min-ligation of the left anterior descending coronary artery, followed by 3 hr-reperfusion. The area at risk and infarct area were evaluated using Evans blue dye and 2,3,5-triphenyltetrazolium chloride (TTC) staining, respectively. DNA nicks reflecting the extent of myocardial apoptosis were assessed by TUNEL assay. Levels of cleaved caspase-3, Bcl-2, and Bax were assessed by immunohistochemistry. RESULTS: Supplementation of AP (with 100 and 400 mg/kg/day) resulted in significantly attenuated infarct size (IS) (ratio of infarct area to area at risk) by 21.9 and 22.4%, respectively, in the AP-treated group, compared with that in the control group. This attenuation in IS showed correlation with improvement in biomarkers involved in the apoptotic cascades: reduction of apoptotic cells, inhibition of conversion of procaspase-3 to caspase-3, and increase of Bcl-2/Bax ratio, a determinant of cell fate. CONCLUSIONS: The findings indicate that supplementation of AP results in amelioration of myocardial infarction by inhibition of apoptosis. Thus, the current study suggests that intake of dietary fiber reduces the risk of CHD, not only by blocking steps leading to occlusion, but also by protecting against ischemic injury caused by occlusion of the arteries.

• Biomedical Science Letters
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• v.11 no.2
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• pp.201-209
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• 2005

This study aimed to investigate the cerebroprotective effect of nociceptin on transient focal cerebral ischemia in Sprague-Dawley rats by determining the changes in regional cerebral blood flow (rCBF) and the infarct size. Right middle cerebral artery (MCA) was occluded for 2 hours, and thereafter was followed by reperfusion by an intraluminal monofilament technique. An open cranial window was made on the right parietal bone for determination of continuous changes in rCBF by laser-Doppler flowmetry. The infarct size was morphometrically determined using the 2,3,5-triphenyltetrazolium chloride technique. In normal rats, nociceptin ($0.01\~100\;nmol/kg$, Lv.) increased rCBF and decreased cerebral arterial resistance in a dose-dependent manner. Systemic arterial blood pressure was little affected by nociceptin at the doses of 0.01 and 0.1nmol/kg, but dose-dependently reduced at the doses of 1 nmol/kg or more. In transient cerebral ischemic rats, nociceptin ($0.01\~0.1$ nmol/kg, i.p.) significantly attenuated the postischemic cerebral hyperemia, and progressively increased rCBF. The improving effect of nociceptin on the postischemic rCBF response was markedly blocked by pretreatment with $[Nphe^1]nociceptin(1-13)NH_2$ (1 nmol/kg, i.p.), a selective nociceptin receptor antagonist, but not by naloxone ($3{\mu}mol/kg$, i.p.), a selective opioid receptor antagonist. The cerebral infarct size was significantly reduced by nociceptin ($0.01\~0.1$ nmol/kg) administered i.p. 5 min after MCA occlusion in transient cerebral ischemia of 2-hour MCA occlusion and 22-hour reperfusiion. It is suggested that nociceptin improves the postischemic cerebral hemodynamics and thereby has a cerebroprotective effect in transient focal cerebral ischemia.