• Journal of the Korea Academia-Industrial cooperation Society
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• v.18 no.8
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• pp.240-247
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• 2017

The increased investigation of the cerebral arteries with magnetic resonance angiography has resulted in an increase in the identification of unruptured intracranial aneurysms (UIAs). Knowledge of the distribution and factors associated with UIAs might be helpful for understanding the pathological mechanism of unruptured aneurysms. This study examined patients who visited a health care center and had a health examination from January 2007 to December 2016. Subjects who underwent magnetic resonance angiography with a health examination at the Health Screening were enrolled in this study. The incidence and risk factors of UIAs (age, sex, hypertension, diabetes mellitus, smoking, alcohol, and coronary artery disease) were investigated by comparing the size (more than 3 mm vs. less than 3 mm) and multiple aneurysm (single vs. multiple aneurysms). The frequency of aneurysm according to the site was also analyzed. Among the 187166 subjects, who received a health examination, 18954 underwent magnetic resonance angiography. Of them, 367 (1.93%) had UIAs. A comparison of the size of more than 3 mm and less than 3 mm showed that the mean age of the more than 3 mm group of patients was significantly higher than the other size groups (more than 3 mm $57.16{\pm}8.47$ vs. less than 3 mm $55.12{\pm}8.19$; p=0.07). High-density lipoprotein was significantly higher in the more than 3 mm group than in the less than 3 mm($55.95{\pm}16.03$ vs. less than 3 mm $50.85{\pm}13.65$; p=0.007). Hypertension was significantly higher in the multiple aneurysm group (single 153 in 399 (38.3%) VS multiple 19 in 35 (54.3%); p=0.065). An aneurysm of less than 3 mm in size was frequent in the distal internal carotid artery (34.3%) and MCA-bifurcation (16.4%) (p=0.003). Aneurysms of more than 3 mm were frequent in the distal internal carotid artery (43.4%) and MCA-bifurcation (13.4%), and anterior communicating artery (13.4%) (p=0.003). The difference in size and single or multiple aneurysm revealed other risk factors. These risk factors suggest that degenerative and hemodynamic disorders may lead to the presence of aneurysms.

• Journal of Chest Surgery
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• v.39 no.4 s.261
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• pp.261-268
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• 2006

Background: Current vascular prostheses are still inadequate for reconstruction of small-diameter vessels. Autologous pericardium can be a good alternative for this purpose as it already possesses good blood compatibility and shows a mechanical behavior similar to that of natural arteries. However, the clinical use of autologous pericardial tissue as a small-diameter vascular graft has limitations due to mixed outcomes from uncertain biological behavior and difficulty to gain reliable patency results in animal experiments. To study this issue, we implanted fresh and glutaraldehyde-treated autologous pericardium as small-diameter arterial grafts in dogs, and compared their time-related changes histologically. Material and Method: As a form of 5mm-diameter arterial graft, one pair of autologous pericardial tissue was used for comparison between the glutaraldehyde-treated and the glutaraldehyde-untreated grafts in the bilateral carotid arteries in the same dog. The patency of the grafts were evaluated at regular intervals with Doppler ultrasonography. After the predetermined periods of 3 days, 2 weeks, 1 month, 3 months and 6 months, the grafts in each animal were explanted. The retrieved grafts were processed for light and electron microscopic analyses following gross observation. Result: Of 7 animals, 2 were excluded from the study because one died postoperatively due to bleeding and the other was documented as one side of the grafts being obstructed. All 10 grafts in the remaining 5 dogs were patent. Grossly, a variable degree of thromboses were observed in the luminal surfaces of the grafts at 3 days and 2 weeks, despite good patency. Pseudointimal smooth blood-contacting surfaces were developed in the grafts at f month and later. By light microscopy, mesothelial cell layers of the pericardial tissue were absent in all explanted grafts. Newly formed endothelial cell layers on the blood-contacting surface were observed in both the glutaraldehyde-treated and fresh grafts at 3 months and later. The collagen fibers became degraded by fragmentation in the fresh graft at 1 month and In the glutaraldehyde-treated graft at 3 months. At 6 months, the collagen layers were no longer visible in either the glutaraldehyde-treated or fresh grafts. By electron microscopy, a greater amount of coarse fibrin fibers were observed in the fresh grafts than in the glutaraldehyde-treated grafts and, more compact and well-arrayed layers were observed in the glutaraldehyde-treated grafts than in the fresh grafts. Conclusion: The glutaraldehyde-treated small-diameter pericardial arterial grafts showed a better endothelialization of the blood-contacting surface and a slower fragmentation of the collagen layers than the fresh grafts, although it has yet to be proven whether these differences are so significant as to affect the patency results between the groups.

• Clinical and Experimental Pediatrics
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• v.49 no.3
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• pp.317-325
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• 2006

Purpose : This study was carried out to elucidate the effects of nitric oxide synthase(NOS) inhibitor, NG-monomethyl-L-arginine(L-NMMA) and nitric oxide precursor, L-arginine(L-Arg) on cerebral hemodynamics and energy metabolism during reoxygenation-reperfusion(RR) after hypoxia-ischemia(HI) in newborn piglets. Methods : Twenty-eight newborn piglets were divided into 4 groups; Sham normal control(NC), experimental control(EC), L-NMMA(HI & RR with L-NMMA), and L-Arg(HI & RR with L-Arg) groups. HI was induced by occlusion of bilateral common carotid arteries and simultaneously breathing with 8 percent oxygen for 30 mins, and followed RR by release of carotid occlusion and normoxic ventilation for one hour. All groups were monitored with cerebral hemodynamics and cytochrome $aa_3$ (Cyt $aa_3$) using near infrared spectroscopy(NIRS). $Na^+$, $K^+$-ATPase activity, lipid peroxidation products, and tissue high energy phosphate levels were determined biochemically in the cerebral cortex. Results : In experimental groups, mean arterial blood pressure, $PaO_2$, and pH decreased, and base excess and blood lactate level increased after HI compared to NC group(P<0.05). These variables subsequently returned to baseline after RR except pH. There were no differences among the experimental groups. In NIRS, oxidized hemoglobin($HbO_2$) decreased and hemoglobin(Hb) increased during HI(P<0.05) but returned to base line immediately after RR; 40 min after RR, the $HbO_2$ had decreased significantly compared to NC group(P<0.05). Changes of Cyt $aa_3$ decreased significantly compared to NC after HI and recovered at the end of the experiment. Significantly reduced cerebral cortical cell membrane $Na^+$, $K^+$-ATPase activity and increased lipid peroxidation products(P<0.05) were not improved with L-NMMA or L-Arg. Conclusion : These findings suggest that NO is not involved in the mechanism of HI and RR brain damage during the early acute phase of RR.

• Journal of Chest Surgery
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• v.40 no.4 s.273
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• pp.264-272
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• 2007

Background: Vascular endothelial growth factor (VEGF) plays an important role in angiogenesis, including stimulating the proliferation and migration of vascular smooth muscle cells (VSMCs). It has been known that diabetes is associated with accelerated cellular proliferation via VEGF, as compared to that under a normal glucose concentration. We investigated the effects of selective blockade of a VEGF receptor by using anti-Flt-1 peptide on the formation and hyperplasia of the neointima in balloon injured-carotid arteries of OLETF rats and also on the in vitro VSMCS' migration under high glucose conditions. Material and Method: The balloon-injury method was employed to induce neointima formation by VEGF. For f4 days beginning 2 days before the ballon injury, placebo or vascular endothelial growth factor receptor-1 (VEGFR-1) specific peptide (anti-Flt-1 peptide), was injected at a dose of 0.5mg/kg daily into the OLETF rats. At 14 days after balloon injury, the neointimal proliferation and vascular luminal stenosis were measured, and cellular proliferation was assessed by counting the proliferative cell nuclear antigen (PCNA) stained cells. To analyze the effect of VEGF and anti-Flt-1 peptide on the migration of VSMCs under a high glucose condition, transwell assay with a matrigel filter was performed. And finally, to determine the underlying mechanism of the effect of anti-Flt-1 peptide on the VEGF-induced VSMC migration in vitro, the expression of matrix metalloproteinase (MMP) was observed by performing reverse transcription-polymerase chain reaction (RT-PCR). Result: Both the neointimal area and luminal stenosis associated with neointimal proliferation were significantly decreased in the anti-Flt-1 peptide injected rats, ($0.15{\pm}0.04 mm^2$ and $ 36.03{\pm}3.78%$ compared to $0.24{\pm}0.03mm^2\;and\;61.85{\pm}5.11%$, respectively, in the placebo-injected rats (p<0.01, respectively). The ratio of PCNA(+) cells to the entire neointimal cells was also significantly decreased from $52.82{\pm}4.20%\;to\;38.11{\pm}6.89%$, by the injected anti-Flt-1 peptide (p<0.05). On the VSMC migration assay, anti-Flt-1 peptide significantly reduced the VEGF-induced VMSC migration by about 40% (p<0.01). Consistent with the effect of anti-Flt-1 peptide on VSMC migration, it also obviously attenuated the induction of the MMP-3 and MMP-9 mRNA expressions via VEGF in the VSMCS. Conclusion: Anti-Flt-1 peptide inhibits the formation and hyperplasia of the neointima in a balloon-injured carotid artery model of OLETF rats. Anti-Flt-1 peptide also inhibits the VSMCs' migration and the expressions of MMP-3 and MMP-9 mRNA induced by VEGF under a high glucose condition. Therefore, these results suggest that specific blockade of VEGFR-1 by anti-Flt-1 peptide may have therapeutic potential against the arterial stenosis of diabetes mellitus patients or that occurring under a high glucose condition.

• Journal of Chest Surgery
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• v.35 no.1
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• pp.36-42
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• 2002

Background: To evaluate the efficiency of surgical treatment in patients with cardiac valvular and arterial involvement of Behcet's syndrome. Material and Method: 12 patients underwent surgical treatment due to the valvular heart diseases and the various arterial diseases associated with Behest's syndrome over 7 years; 6 with valvular heart disease, 1 with annuloaortic ectasia, 1 with ascending aortic aneurysm, 4 with pseudoaneurysms in abdominal aorta(n=2), carotid artery(n=1), and popliteal artery(n=1). All 12 patients had received valvular replacement(n=6) and the artificial(n=5) or autologous(n=1) graft interposition. We followed the results of these surgical treatments. Result: Operations were technically successful in all 12 patients and peri-operative complication was not demonstrated. However, 10 patients had recurrences; 6 with valvular dehiscence, 3 with pseudoaneurysm at anastostomosis site, and 1 with aorto-duodenal fistula. The duration of recurrence was 1 to 55 months(mean: 15.7$\pm$ 16.2 months). 7 patients underwent the second operation and among them, 4 patients showed repeated recurrences. Overall, 5 patients died 2 to 25 months after the operation(mean: 13.6 months), because of the bleeding at the anastomosis site Five patients did not present recurrence after the first(n=2) or the second operation(n=3) and their follow up duration was 5 to 60 months(mean: 45.8$\pm$41.7 months). Five patients received immune-suppressive therapy after the first(n=2) and second operation(n=3). Three did not shown recurrence for the 13, 29 and 33 months. Conclusion: Post-operative prognosis of arterial manifestation of Behcet's syndrome was not encouraging and if possible, other treatment strategy should be considered.

• The Korean Journal of Pharmacology
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• v.32 no.3
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• pp.335-345
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• 1996

A critical role of oxygen-derived free radicals has been implicated in ischemia/reperfusion (I/R)-induced brain damage. In this study, we have produced experimental I/R to the brains of Mongolian gerbil (Meriones unguiculatus) by a transient occlusion and release of the common carotid arteries. We have attempted to determine whether the oxidative stress is generated upon I/R and whether this oxidative stress is linked to the cell damage. Since hippocampus has been suggested as one of the most vulnerable regions of the brain to the oxidative stress, we analyzed samples from hippocampus in comparison with those from cortex. In addition, we have examined the expression of heat shock protein 70kD species (HSP70) in these regions in order to evaluate a possible role of this protein in I/R-induced brain damage. To determine whether the oxidative stress is produced upon I/R, we measured the glutathione oxidation, GSSG/ (GSH + 2xGSSG), as an index of oxidative stress. We found an increase of the glutathione oxidation primarily in hippocampus upon I/R. To determine whether this oxidative stress is linked to the cell damage, we measured the degree of lipid peroxidation upon I/R. We found an increase of lipid peroxidation in both regions. However, the magnitude of increases was greater in hippocampus than in cortex. In addition, we found that changes in both the magnitude and the temporal patterns of glutathione oxidation closely correlated with those of lipid peroxidation. Our study provides biochemical evidences that the oxidative stress is generated upon I/R and this oxidative stress is linked to the oxidative cell damage. Our study also provides evidences that the degree of oxidative stress as well as oxidative cell damage is greater in hippocampus than in cortex. We could not find difference in the basal level of HSP70 expression between hippocampus and cortex, indicating that the intrinsic vulnerability of hippocampus cannot be explained by the lower level of HSP70 expression. We did find, however, that the induction of HSP70 expression upon I/R was impaired in the hippocampus. This impairment appeared to be at the transcriptional level. These results suggest that the measurement of HSP70 induction may be employed as a useful predictor of differential cellular susceptibilities to the I/R-induced brain damage.

• Clinical and Experimental Pediatrics
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• v.46 no.8
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• pp.789-794
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• 2003

Purpose : We intended to evaluate the effect of hypoxia-ischemia on extracellular striatal monoamine metabolism in neonatal rat brains by in vivo microdialysis. Methods : The right common carotid arteries of five or six-day old rats were surgically ligated, and the probes for microdialysis were inserted into the right striatum with stereotaxic instrument. After stabilization for two hours, artificial cerebrospinal fluid was infused via the probe for microdialysis and samples were collected during hypoxia-ischemia and recovery periods at 20 minute intervals. The concentrations of DA(dopamine), DOPAC(3,4-di-hydroxyphenyl acetic acid), HVA(homovanillic acid), NE(norepinephrine), and 5-HIAA(5-hydroxy indole-acetic acid) were measured by HPLC(high performance liquid chromatography) and the changes were analysed. Results : The striatal levels of dopamine metabolites such as DOPAC and HVA, were significantly decreased during hypoxia-ischemia, and increased to their basal level during reoxygenation(P<0.05). Dopamine mostly increased during hypoxia but statistically not significant(P>0.05). DOPAC showed the most remarkable decrease($23.0{\pm}4.2%$, P<0.05), during hypoxia-ischemia and increase to the basal levels during reoxygenation($120.8{\pm}54.9%$, P<0.05), and HVA showed the same pattern of changes as those of DOPAC during hypoxia-ischemia($35.3{\pm}7.6%$ of basal level, P<0.05) and reoxygenation ($105.8{\pm}32.3%$). However, the level of NE did not show significant changes during hypoxia-ischemia and reoxygenation. The levels of 5-HIAA decreased($74.9{\pm}3.1%$) and increased($118.1{\pm}7.8%$) during hypoxia-ischemia and reoxygenation, respectively(P<0.005). Conclusion : Hypoxia-ischemia had a significant influence on the metabolism of striatal monoamine in neonatal rat brains. These findings suggest that monoamine, especially dopamine, and its metabolites could have a significant role in the pathogenesis of hypoxic-ischemic injury of neonatal rat brains.

• International Journal of Vascular Biomedical Engineering
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• v.4 no.2
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• pp.19-24
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• 2006

Background: Pulse wave velocity (PWV), which is inversely related to the distensibility of an arterial wall, offers a simple and potentially useful approach for an evaluation of cardiovascular diseases. In spite of the clinical importance and widespread use of PWV, there exist no standard either for pulse sensors or for system requirements for accurate pulse wave measurement. Objective of this study was to assess the reproducibility of PWV values using a newly developed PWV measurement system in healthy subjects prior to a large-scale clinical study. Methods: System used for the study was the PP-1000 (Hanbyul Meditech Co., Korea), which provides regional PWV values based on the measurements of electrocardiography (ECG), phonocardiography (PCG), and pulse waves from four different sites of arteries (carotid, femoral, radial, and dorsalis pedis) simultaneously. Seventeen healthy male subjects with a mean age of 33 years (ranges 22 to 52 years) without any cardiovascular disease were participated for the experiment. Two observers (observer A and B) performed two consecutive measurements from the same subject in a random order. For an evaluation of system reproducibility, two analyses (within-observer and between-observer) were performed, and expressed in terms of mean difference ${\pm}2SD$, as described by Bland and Altman plots. Results: Mean and SD of PWVs for aorta, arm, and leg were $7.07{\pm}1.48m/sec,\;8.43{\pm}1.14m/sec,\;and\;8.09{\pm}0.98m/sec$ measured from observer A and $6.76{\pm}1.00m/sec,\;7.97{\pm}0.80m/sec,\;and\;\7.97{\pm}0.72m/sec$ from observer B, respectively. Between-observer differences ($mean{\pm}2SD$) for aorta, arm, and leg were $0.14{\pm\}0.62m/sec,\;0.18{\pm\}0.84m/sec,\;and\;0.07{\pm}0.86m/sec$, and the correlation coefficients were high especially 0.93 for aortic PWV. Within-observer differences ($mean{\pm}2SD$) for aorta, arm, and leg were $0.01{\pm}0.26m/sec,\;0.02{\pm}0.26m/sec,\;and\;0.08{\pm}0.32m/sec$ from observer A and $0.01{\pm}0.24m/sec,\;0.04{\pm}0.28m/sec,\;and\;0.01{\pm}0.20m/sec$ from observer B, respectively. All the measurements showed significantly high correlation coefficients ranges from 0.94 to 0.99. Conclusion: PWV measurement system used for the study offers comfortable and simple operation and provides accurate analysis results with high reproducibility. Since the reproducibility of the measurement is critical for the diagnosis in clinical use, it is necessary to provide an accurate algorithm for the detection of additional features such as flow wave, reflection wave, and dicrotic notch from a pulse waveform. This study will be extended for the comparison of PWV values from patients with various vascular risks for clinical application. Data acquired from the study could be used for the determination of the appropriate sample size for further studies relating various types of arteriosclerosis-related vascular disease.

• The Korean Journal of Pharmacology
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• v.32 no.3
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• pp.323-334
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• 1996

Male Mongolian gerbils $(60{\sim}80g)$ were given DL-difluoromethylornithine (DFMO; 250mg/kg, ip) and methylglyoxal bis(guanylhydrazone) (MGBG; 50 mg/k, ip), respectively, 1 h prior to transient (7 min) occlusion of bilateral common carotid arteries (OBC7) and a daily dose of one of them for 6 days after recirculation, and the polyamine contents, activities of ornithine and S-adenosylmethionine decarboxylases (ODC and SAM-DC), and light microscopic findings of the hippocampus were evaluated. The hippocampal putrescine (PT) levels of the control gerbils treated with saline (STGr), markedly increased after OBC7, showing a peak level at 24 h after recirculation. The peak PT level was reduced in DFMO treated gerbils (DTCr) and in MGBG treated gerbils (MTGr). And 7 days after recirculation, the PT level of DTGr was decreased to about 75% of the PT level in the sham operated group (nonTGr) and to about 55% of the STGr level, respectively. The hippocampal spermidine (SD) level of STGr tended to decline, showing the lowest value at 8 h after recirculation. But the spermidine (SD) level of DTGr was somewhat higher at 8 h after OBC7 than those of STGr and MTGr The hippocampal spermine (SM) levels of all the experimental groups were little changed for 7 days after OBC. OBC7 markedly increased the hippocampal ODC activity. reaching a maximum (about 3 times higher than preischemic level) at 8 h and rapidly recovered to the control value by 24 h in STGr gerbils, and the OBC7-induced increase of ODC activity was significantly attenuated by DFMO or MGBG treatment. Whereas OBC7 induced a rapid decrease of the hippocampal SAMDC activity follwed by gradual recovery to the preischemic level, and the decrease of the SAMDC activity was slightly attenuated by DFMO or MGBG treatment. 7 Days after OBC7 the histological finding of the hippocampal complex stained with cresyl violet showed an extensive delayed neuronal damage in the CA1 region and to a lesser extent, in the dentate gyrus, sparing the CA3 region. And the neuronal death was aggevated by DFMO but significantly attenuated by MGBG. The immunochemical reactivity of hippocampus to anti-GFAP antibody was significantly increased in the CA1 region and to a lesser extent, in the dentate gyrus 7 days after OBC7, but was little changed in the CA3. And the increase of the anti-GFAP immunoreactivity was moderately enhanced by DFMO and significantly suppressed by MGBG. These results suggest that the polyamine metabolism may play a modulatory role in the ischemic brain damage.

• The Korean Journal of Physiology
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• v.15 no.1
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• pp.27-36
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• 1981

Relatively little has been done on the metabolic changes of the lung produced by the excessive alcohol ingestion to the point of the acute alcohol intoxication. In the present study, an effort was made to clarify the possible changes of the pulmonary surfactant system by the acute alcohol ingestion. The dynamic pulmonary compliance and the levels of protein and inorganic phosphorus (Pi) of both lung lavage and extract were chosen as the parameters of the pulmonary surfactant activities. The albino rats of both sexes were used, and 1.5 ml of 50% ethanol per 100 g body weight was given by oral intubation, and the experiment was performed at 1, 3, 6, 12, and 24 hours after the alcohol ingestion. The rat was sacrificed by cutting the carotid arteries, and blood sample for the determination of hematocrit(Hct) and the blood alcohol concentration was obtained. Both lungs were completely removed without dammage to the lung tissue, and the pulmonary compliance was measured by the changes of pressure-volume(P-V) curves by inflating or deflating the lung with air. Immediately after the P-V curves were recorded, the lung lavage was obtained by washing the lobes with 15ml of isotonic saline 3 times with a syringe. Next, total lungs were homogenized and filtered to obtain the lung extract. The protein and Pi levels were measured using the lung lavage and extract as the samples, and the lung/body weight ratio(L/B ratio) was also calculated. The results thus obtained were compared with the normal values and summarized as follows. The blood alcohol concentration reached the highest level of $0.71{\pm}0.02\;g\;%$ at 1 hr and gradually decreased until 24 hrs$(0.36{\pm}0.02\;g%)$ after the alcohol ingestion, but all the experimental groups showed significant increase comparing with the normal. The highest Hct value was obtained at 1hr$(64.86{\pm}2.45%)$ and significantly elevated value was continued throughout the experiment. The L/B ratio was significantly lowered from 3hrs until 24hrs after the alcohol ingestion but from 6 th hr on, a generally elevated value was observed with a significant value at 12 hrs and gradual recovery to the normal value at 24 hrs after the alcohol ingestion. The pulmonary compliance at inflation and deflation did not change appreciablly from the normal until 3 hrs after the alcohol ingestion but from 6 th hr on, a generally elevated value was observed with a significant value at 12 hrs and gradual recovery to the normal value at 24 hrs after the alcohol ingestion. The protein level of the lung lavage stowed a significantly increased value of $12.36{\pm}0.35\;mg/gm(3rd hr)$, $12.70{\pm}0.74\;mg/gm(12 th hr)$, and $12.65{\pm}0.88\;mg/gm(24 th hr)$, respectively, comparing with the normal value of $10.65{\pm}0.62\;mg/gm$, and the Pi level also showed a similar tendency of significant increase at 12th hr $(7.65{\pm}0.63\;{\mu}mol/gm)$ and 24 th hr$(6.70{\pm}0.36\;{\mu}mol/gm)$ comparing with the normal value of $5.32{\pm}0.20\;{\mu}mol/gm$. The protein level of the lung extract in the alcohol group was generally similar to the normal value with a slight decrease at 1st and 3 rd hr, tut the Pi level of the lung extract was generally increased in the alcohol group, and a significant increase was observed at 6 th hr$(17.77{\pm}1.54\;{\mu}mol/gm)$, 12 th hr$(13.92{\pm}0.78\;{\mu}mol/gm)$ and 24 th hr$(14.57{\pm}0.53\;{\mu}mol/gm)$ of the alcohol ingestion comparing with the normal value of $10.34{\pm}0.37\;{\mu}mol/gm$. From the above, it may be concluded that the acute alcohol intoxication produces the metabolic changes of the lungs by the increased surfactant activities and elevated pulmonary compliance.