• The Korean Journal of Physiology and Pharmacology
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• v.3 no.3
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• pp.263-273
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• 1999

The role of phospholipase $A_2\;(PLA_2)$ in acute lung leak induced by intestinal ischemia was investigated in association with neutrophilic respiratory burst. To induce lung leak, we generated intestinal ischemia for 60 min prior to the 120 min reperfusion by clamping superior mesenteric artery in Sprague-Dawley rats. Acute lung leak was confirmed by the increased lung leak index and protein content in bronchoalveolar fluid. These changes were inhibited by mepacrine, the non-specific $PLA_2$ inhibitor. The lung myeloperoxidase (MPO) activity denoting the pulmonary recruitment of neutrophils was increased by intestinal I/R, but decreased by mepacrine. Simultaneously, the number of leukocytes in bronchoalveolar fluid was increased by intestinal ischemia/reperfusion (I/R) and decreased by mepacrine. Gamma glutamyl transferase activity, an index of oxidative stress in the lung, was increased after intestinal I/R but decreased by mepacrine, which implicates that $PLA_2$ increases oxidative stress caused by intestinal I/R. The $PLA_2$ activity was increased after intestinal I/R not only in the intestine but also in the lung. These changes were diminished by mepacrine. In the cytochemical electron microscopy to detect hydrogen peroxide, intestinal I/R increased the generation of the hydrogen peroxide in the lung as well as in the intestine. Expression of interleukin-1 (IL-1) in the lung was investigated through RT-PCR. The expression of IL-1 after intestinal I/R was enhanced, and again, the inhibition of $PLA_2$ suppressed the expression of IL-1 in the lung. Taken together, intestinal I/R seems to induce acute lung leak through the activation of $PLA_2$, the increase of IL-1 expression associated with increased oxidative stress by neutrophilic respiratory burst.

• Childhood Kidney Diseases
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• v.10 no.1
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• pp.83-88
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• 2006

Orthostatic or postural proteinuria is a benign condition characterized by the presence of protein in urine samples collected in the upright position during the day and its absence in the supine position. Recently, nutcracker phenomenon has been documented as the source of postural proteinuria. The nutcracker phenomenon refers to compression of the left renal vein between the aorta and superior mesenteric artery, resulting in elevation of pressure in the left renal vein, leading to congestion of the left kidney and occasionally to collateral veins formation. Entrapment of the left renal vein is a cause of left-sided gross hematuria, ureteral and peripelvic varices, unexplained left flank pain and variable degrees of orthostatic proteinuria. We report the case of a 14-year-old girl with orthostatic proteinuria, diagnosed as having nutcracker syndrome by doppler sonography and MR angiography. Because daily protein excretion was more than 1.5 grams over 3 years of follow up, we decided to perform a renal biopsy which revealed moderate mesangial cell proliferation in all glomeruli.

• Journal of Chest Surgery
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• v.37 no.3
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• pp.210-219
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• 2004

Extracellular $K^{+}$ concentration ([ $K^{+}$]$_{0}$ ) can be increased within several mM by the efflux of intracellular $K^{+}$. To investigate the effect of an increase in [ $K^{+}$]$_{0}$ on vascular contractility, we attempted to examine whether extracellular $K^{+}$ might modulate vascular contractility, endothelium-dependent relaxation (EDR) and intracellular $Ca^2$$^{+}$ concentration ([C $a^2$$^{+}$]$_{i}$ ) in endothelial cells (EC). We observed isometric contractions in rabbit carotid, superior mesenteric, basilar arteries and movse aorta. [C $a^2$$^{+}$]$_{i}$ was recorded by microfluorimeter using Fura-2/AM in EC. No change in contractility was recorded by the increase in [ $K^{+}$]$_{0}$ from 6 to 12 mM in conduit artery such as rabbit carotid artery. whereas resistant vessels, such as basilar and branches of superior mesenteric arteries (SMA), were relaxed by the increase. In basilar artery, the relaxation by the increase in [ $K^{+}$]$_{0}$ to from 1 to 3 mM was bigger than that by the increase from 6 to 12 mM. In contrast, in branches of SMA, the relaxation by the increase in [ $K^{+}$]$_{0}$ to from 6 to 12 mM is bigger than that by the increase from 1 to 3 mM. $Ba^2$$^{+}$ (30 $\mu$M) did not inhibit the relaxation by the increase in [ $K^{+}$]$_{0}$ from 1 to 3 mM but did inhibit the relaxation by the increase from 6 to 12 mM. In the mouse aorta without the endothelium or treated with $N^{G}$_nitro-L-arginine (30 $\mu$M), nitric oxide synthesis blocker, the increase in [ $K^{+}$]$_{0}$ from 6 to 12 mM did not change the magnitude of contraction induced either norepinephrine or prostaglandin $F_2$$_{\alpha}$. The increase in [ $K^{+}$]$_{0}$ up to 12 mM did not induce contraction of mouse aorta but the increase more than 12 mM induced contraction. In the mouse aorta, EDR was completely inhibited on increasing [ $K^{+}$]$_{0}$ from 6 to 12 mM. In cultured mouse aorta EC, [C $a^2$$^{+}$]$_{i}$ , was increased by acetylcholine or ATP application and the increased [C $a^2$$^{+}$]$_{i}$ , was reduced by the increase in [ $K^{+}$]$_{0}$ reversibly and concentration-dependently. In human umbilical vein EC, similar effect of extracellular $K^{+}$ was observed. Ouabain, a N $a^{+}$ - $K^{+}$ pump blocker, and N $i^2$$^{+}$, a N $a^{+}$ - $Ca^2$$^{+}$ exchanger blocker, reversed the inhibitory effect of extracellular $K^{+}$. In resistant arteries, the increase in [ $K^{+}$]$_{0}$ relaxes vascular smooth muscle and the underlying mechanisms differ according to the kinds of the arteries; $Ba^2$$^{+}$-insensitive mechanism in basilar artery and $Ba^2$$^{+}$ -sensitive one in branches of SMA. It also inhibits [C $a^2$$^{+}$]$_{i}$ , increase in EC and thereby EDR. The initial mechanism of the inhibition may be due to the activation of N $a^{+}$ - $K^{+}$pump. activation of N $a^{+}$ - $K^{+}$pump.p.p.p.

• The Korean Journal of Pharmacology
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• v.26 no.1
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• pp.25-33
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• 1990

The responsiveness of various arterial smooth muscles isolated from rabbit to peptide YY (PYY) and the calcium source responsible for the muscles to contract were studied in vitro. PYY contracted the muscle strips of femoral, basilar and common iliac arteries more sensitively than renal, superior mesenteric and common carotid arteries. Common carotid and renal arteries were less sensitive to PYY $(p{\leqslant}0.05)$ than to NE; and basilar artery was more sensitive to PYY$(p{\leqslant}0.01)$ than to NE. A calcium channel blocker, verapamil and an inhibitor of intracellular calcium release, 3, 4, 5-Trime-thoxybenzoic arid 8-(diethylamino)octyl ester [TMB-8] significantly $(p{\leqslant}0.001)$ suppressed the concentration-response of the strips from femoral artery to PYY. When both verapamil and TMB-8 existed in normal PSS, the concentration-response to PYY was inhibited almost completely; and a similar suppression was observed when the muscle was incubated in calcium-free, ethyleneglycol-bis-(beta-aminoethyl ether)N,N,N',N'-tetraacetic acid [EGTA] containing PSS. The results of these experiments suggest that increased PYY activity in circulation may result in the more sensitive increase in the intracranial vascular resistance and the cerebral arterial pressure than the increased sympathetic activity and that both intra- and extracellular calcium are to be utilized for the PYY-induced contraction on arterial smooth muscle.

• Archives of Plastic Surgery
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• v.32 no.3
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• pp.369-375
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• 2005

Apoptosis is a physiologic or programmed cell death process which is controlled by genes. It is essential for the function and the appropriate development of multicellular organism. It is also thought to be one of the main mechanisms of cell death in ischemic tissues. The effect of prostaglandin $E_1$($PGE_1$) is proven to be useful in the recovery of ischemic changes by inducing vasodilation of peripheral vessels and platelet disaggregation. $PGE_1$ is also known to suppress apoptosis in human liver sinusoidal endothelial cell from ischemia-reperfusion injury. The purpose of this study is to evaluate the effects of $PGE_1$ on the apoptosis in the ischemia reperfusion injury of rat intestine. Thirty Sprague-Dawley rats were used. In control group(N=15), superior mesenteric artery was occluded for 60 minutes and after removing the vessel clamp, it was reperfused for 60 minutes and harvested. In experimental group(N=15), a jejunal flap was also made as in the control group except for the intraarterial administration of the $PGE_1$ right after clamping the artery and removing the clamp. H&E, TUNEL and immunohistochemical stains for p53, bax, and bcl-2 were performed. There were ischemic changes in gross and microscopic findings in both groups. The apoptotic index was significantly lower in the experimental group($1.29{\pm}0.82$(p=0.003)) than in the control group ($2.33{\pm}0.95$). The rat intestinal ischemia apoptosis by ischemia-reperfusion was partly related to the modulating of bcl-2, bax, and p53 expression. Our results indicate that $PGE_1$ suppresses the apoptosis in the ischemic jejunal flap and this effect is probably the result of a increase in expression of bcl-2.

• Journal of the Korean Society of Radiology
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• v.82 no.1
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• pp.237-243
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• 2021

This is a rare case of a 73-year-old male patient who presented with hematochezia and was treated using transcatheter arterial embolization following upper gastrointestinal bleeding in the third portion of the duodenum. The cause of the bleeding was not found on gastrointestinal endoscopy and CT. On the third day of hospitalization, the hemoglobin level continued to decrease. A technetium-99m-labeled red blood cell scan revealed suspicious bleeding in the diverticulum of the third portion of the duodenum. Superior mesenteric artery angiography showed active bleeding from the posteroinferior pancreaticoduodenal artery, which was embolized with N-butyl cyanoacrylate. The patient was discharged on the seventh day after embolization without re-bleeding or complication. We report a rare case of a patient with active bleeding from a duodenal diverticulum that was difficult to diagnose using routine modalities. Herein, we report a rare case of a patient with active bleeding from a duodenal diverticulum that was difficult to diagnose using routine modalities. We also conducted a relavant literature review.

• Journal of Chest Surgery
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• v.43 no.4
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• pp.345-355
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• 2010

Background: Extracellular and intracellular pH ($pH_o$ and $pH_i$), which can be changed in various pathological conditions such as hypoxia, affects vascular contractility. To elucidate the mechanism to alter vascular contractility by pH, the effects of pH on reactivity to vasocontracting agents, intracellular $Ca^{2+}$ influx, and $Ca^{2+}$ sensitivity in vascular smooth muscle were examined. Material and Method: Isometric contractions in rat superior mesenteric arteries (SMA) were observed. Intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) was recorded by microfluorometer using Fura-2/acetoxylmethyl ester in muscle cells. $pH_o$ was increased from 7.4 to 7.8 or decreased to 6.9 or 6.4. $pH_i$ was decreased by applying $NH_4^+$ or propionic acid or modulated by changing $pH_o$ after increasing membrane permeability using $\beta$-escin. Result: Decreases in $pH_o$ from 7.4 to 6.9 or 6.4 shifted concentration-response curve by norepinephrine (NE) or serotonin (SE) to the right and significantly increased half maximal effective concentration (EC50) to NE or SE. Increase in $pH_o$ from 7.4 to 7.8 shifted concentration-response curve by norepinephrine (NE) or serotonin (SE) to the left and significantly reduced EC50 to NE or SE. NE increased $[Ca^{2+}]_i$ in cultured smooth muscle cells from SMA and the increased $[Ca^{2+}]_i$ was reduced by decreases in $pH_o$. NE-induced contraction was inhibited by $NH_4^+$, whereas the resting tension was increased by $NH_4^+$ or propionic acid. When the cell membrane of SMA was permeabilized using ${\beta}$-escin, SMA was contracted by increasing extracellular $Ca^{2+}$ concentration from 0 to $10{\mu}M$ and the magnitude of contraction was decreased by a decrease in $pH_o$ and vice versa. Conclusion: From these results, it can be concluded that a decrease in $pH_o$ might inhibit vascular contraction by reducing the reactivity of vascular smooth muscle to vasoactive agents, $Ca^{2+}$ influx and the sensitivity of vascular smooth muscle to $Ca^{2+}$.

• Advances in pediatric surgery
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• v.3 no.2
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• pp.98-107
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• 1997

To determine whether bile juice exclusion can prevent the mucosal damage, and Insulin-like growth factor-I can promote mucosal regeneration in ischemia-reperfusion injury of the bowel, 39 weanling rats with 10 cm of Thiry-Vella loop were studied. Animal groups were; Control, BL(common bile duct ligation), IGF{insulin-like growth factor-I(IGF-I) infusion} and IGF-BL(combined treatment). IGF-I(1.5 mg/kg/day) was continuously delivered through a subcutaneously implanted miniosmotic pump. After 15 minutes of superior mesenteric artery clamping, a tissue specimen(P) was taken after 30 minutes of reperfusion. Intestinal continuity was restored to allow oral feeding. A specimen of main tract(M) and another of the Thiry-Vella loop(T) were collected for histomorphometry after 48 hours of reperfusion and free feeding. Villus size ratio(VSR), crypt depth(CD), crypt-depth/villus-height ratio(CVR) and injury score(IS) were measured in 15 consecutive villi. The postoperative mortalities of bile duct ligation groups(BL and IGF-BL) were higher than those of other groups. In control group, VSR of M was lower(P<0.05) than P or T, but not in the other groups. VSR of M in control was lower than those in other groups. CD of T in control, IGF and IGF-BL group were higher than those of M. CD of M and T showed gradual increments from control, IGF and IGF-BL group, respectively. CVR of M and T in IGF group were higher than those in control. CVR in IGF-BL group, T was higher than M, and M was higher than P. About IS, M of BL($20.1{\pm}2.5$) and IGF-BL($20.9{\pm}3.3$) groups were significantly lower than that of control($32.4{\pm}2.5$). These results suggest that the exclusion of bile juice reduces the severity of the reperfusion injury of the mucosa, by inability to activate pancreatic enzymes and IGF-I stimulates mucosal regeneration in injured bowel, and the effect is potentiated by bile juice exclusion.

• Tuberculosis and Respiratory Diseases
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• v.66 no.5
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• pp.365-369
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• 2009

Prompt and proper discovery of cause is important in lung cancer patients with signs and symptoms of intestinal obstruction because approach for treatment may differ according to its etiology and emergency operation can often be required to prevent more severe complications. In this report, we present two different causes of intestinal obstruction in lung cancer. Physicians need to be aware of these possibilities to differentiate the cause of intestinal obstruction in patients with lung cancer.

• Journal of Trauma and Injury
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• v.19 no.1
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• pp.14-20
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• 2006

Purpose: Although hypothermia has been used in many clinical situations, such as post cardiopulmonary resuscitation, stroke, traumatic brain injury, septic shock, and hemorrhagic shock, the mechanism by which it works has not been clearly elucidated. We aimed to evaluate the effect of hypothermia on the plasma nitric oxide (NO) concentration, lung iNOS expression, and histologic changes in intestinal ischemia-reperfusion (IR). Method: Male Sprague-Dawley rats were randomly divided into the hypothermia group (HT, n=8, $27{\sim}30^{\circ}C$) and the normothermia group (NT, n=8, $36{\sim}37^{\circ}C$). They underwent 30 min of intestinal ischemia by clamping the superior mesenteric artery, which was followed by 1.5 h of reperfusion. They were then sacrificed. The acute lung injury (ALI) score, the plasma NO concentration, and lung iNOS gene expression were measured. Results: Compared with the HT group, the NT group showed severe infiltrations of inflammatrory cells, alveolar hemorrhages, and interstitial hypertrophies in lung tissues. There were significant differences in the ALI scores between the NT and the HT groups ($8.7{\pm}1.5/HPF$ in NT vs $5.8{\pm}1.2/HPF$ in HT, p=0.008). Although the plasma NO concentration was slightly lower in the HT group, there was no significant difference between the two groups ($0.80{\pm}0.24{\mu}mol/L$ in NT vs $0.75{\pm}0.30{\mu}mol/L$ in HT, p=0.917). Lung iNOS gene expression was stronger in the NT group than in the HT group. The band density of the expression of iNOS in lung tissues was significantly increased in the NT group compared to the HT group ($5.54{\pm}2.75$ in NT vs$0.08{\pm}0.52$ in HT, p=0.002). Conclusions: This study showed that hypothermia in intestinal IR reduces inflammatory responses, ALI scores, and iNOS gene expression in lung tissues. There was no significant effect of hypothermia on the plasma NO concentration.