• 대한본초학회지
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• 제28권3호
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• pp.7-15
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• 2013

Objectives : Interruption and subsequent restoration of blood flow into the kidney result in renal injury. As an approach to preventing the renal injury, we determined the optimal conditions and the underlying mechanisms by which supernatant of hot water extract of ground Triticum aestivum L. (extract) attenuated ischemia/reperfusion (I/R) injury. Methods : One hour after administration of the extract (400 mg/kg) by intraperitoneal injection, renal I/R injury was generated by clamping the left renal artery in rats after surgical removal of the right kidney, followed by reperfusion. The maximal difference between the vehicle-treated and the extract-treated group under ketamine/xylazine or enflurane anesthetization was assessed at varying periods of ischemia (30-45 min) and reperfusion (3-48 hr), based on the renal function assessed with serum creatinine levels, tissue injury with hematoxylin/eosin staining, and apoptosis with terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling staining. Results : Enflurane anesthetization with 40 min of ischemia and 24 hr of reperfusion was identified to be the optimal condition, under which condition serum creatinine levels and tubular damage in the extract-treated group were significantly reduced compared with those in the vehicle-treated group ($1.3{\pm}0.2$ versus $2.7{\pm}0.3$ mg/dL, P < 0.01, and average score $1.8{\pm}0.1$ versus $3.5{\pm}0.3$, P < 0.01, respectively). These beneficial effects were mediated by inhibition of apoptotic cascades through attenuation of renal tissue malondialdehyde levels, Bax/Bcl-2 ratio and caspase-3 levels. Conclusions : The extract conferred renal protection against ischemia/reperfusion injury in rats by scavenging reactive oxygen species and consequently blocking apoptotic cascades, plausibly augmented by enflurane protection.

• Journal of Yeungnam Medical Science
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• 제12권1호
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• pp.96-104
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• 1995

여러가지 색전물질이 조직내에서 어떤 변화를 야기시키며 또한 시간경과에 따라 어떤 변화를 보이게 되는지를 알아보기 위해 EVAL, Histoacryl, Ivalon을 이용하여 토끼의 신동맥을 통해 색전을 실시하였으며 시간경과에 따라 조직학적으로 검사하여 다음과 같은 결과를 얻었다. EVAL은 1주일이내의 초기단계에는 혈관 내에서 별다른 조직변화를 일으키지 않았으나 2주일 이내의 중기단계에는 혈관벽의 비후를 나타냈다. Histoacryl은 1주일이내의 초기단계에 벌써 심한 섬유소양 변성을 보여 심한 조직변화를 일으킨다는 것을 알 수 있었고 실험 예의 반수에서 신동맥의 폐쇄에 의한 경색을 볼 수 있어 강한 조직유착성을 시사해 주었으며 실제 환자에 적용함에 있어 주의를 환기시켜 주었고 혈류가 빠르거나 누공등이 있는 경우에 더욱 적절히 사용될 수 있음을 알 수 있었다. Ivalon은 초기에는 혈관염의 소견을, 중기에는 이물질반응에 의한 거대세포를, 후기에는 심한 섬유화의 소견을 보여 주었고 수술을 대신하는 치료적인 목적보다는 혈류를 줄여 수술을 보다 용이하게 해주는 등 수술의 보조적인 이용에 바람직할 것으로 기대된다.

• Childhood Kidney Diseases
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• 제1권2호
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• pp.166-169
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• 1997

The nutcracker syndorme refers to compression of the left renal vein between the aorta and the superior mesentric artery which results in renal vein, left gonadal vein varices, hematuria and left sided flank pain. We report this experience of 11yr-11mon of girl has typical Nutcracker syndrome with persistent proteinuria and without typical hematuria. According to the renal biopsy for persistent proteinuria, biopsy shows pathologic findings similar to minimal change nephrotic syndrome. All symtpoms relieved without any specific treatments but she had no response to steroid treatment for persistent proteinuria. Now she was followed up through OPD base without symptom and consideration of surgical intervention.

• 대한약리학회지
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• 제5권1호
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• pp.57-64
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• 1969

Acetylsalicylic acid, administered intravenously in a dose of 120 mg+250 mg/h, markedly decreased the urinary excretion of sodium and chloride, and slightly depressed potassium excretion, so that the ratio of urinary concentrations of potassium to sodium increased after ASA. Osmolar and free water clearances also diminished during water diuresis, and free water reabsorption $(T^cH_2O)$ decreased after ASA during mannitol diuresis. Glomerular filtration rate and urine flow rate changed little. When infused directly into a renal artery, ASA exhibited identical action on both kidneys, indicating that the renotropic action is mediated by some endogenous humoral agents or by some metabolites of ASA. A dose of 100 mg i.v. of spironolactone, a aldosterone antagonist, slightly reversed the renal reflect when given during maximum action of ASA. Ethacrynic acid could display its full diuretic action unhindered during maximum ASA action. Above observations lead to the suggestion that acetylsalicylic acid might release aldosterone and the action on electrolyte excretion may be mediated by the mineralocorticoid.

• 대한핵의학회:학술대회논문집
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• 대한핵의학회 1977년도 제16차 학술대회
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• pp.97.2-97.2
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• 1977

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 2002년도 창립10주년기념 및 국립독성연구원 의약품동등성평가부서 신설기념 국재학술대회:생물학적 동등성과 의약품 개발 전략을 위한 국제심포지움
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• pp.233-233
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• 2002

• Journal of Chest Surgery
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• 제23권2호
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• pp.333-341
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• 1990

aortoiliac pattern, Group II; femoropopliteal pattern and Group g; tibioperoneal pattern. A majority of patients belonged to group I [27 cases], 8 patients came under group II .and none in group g. Thirty patients underwent bypass operation with autogenous saphenous vein or synthetic graft with or without concomitant lumbar sympathectomy. Remaining 5 patients were operated on with sympathectomy only, Bypass procedures were anatomic bypass in 22 cases: aortoiliac artery bypass in 11 cases, femoropopliteal artery bypass in 10 cases, sequential femoropopliteal artery bypass in one case and extra-anatomic bypass in 8 cases, axillary-bifemoral artery bypass in one case and femorofemoral artery bypass in 7 cases. Postoperative complications which mainly composed of superficial wound infection[5 cases] which were treated without any significant sequel in all cases and thrombosis[2 cases]. Three patients died whose causes of death were acute renal failure in 2 cases and myocardial infarction in other, The overall patency, rate was 70Zo in 5 years. In conclusion, the clinical pattern and operative outcome were similar to he western pattern and all cases of death did not related to operative procedures and ischemic symptoms were relieved by bypass operations except several cases. I think and recommend that all patients suffering chronic arterial insufficiency by atherosclerosis obliterans ought to be managed with urgent and adequate operative procedure.

• Journal of Chest Surgery
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• 제19권1호
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• pp.58-67
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• 1986

Aggressive revascularization of the ischemic lower extremities in atherosclerotic, occlusive diseases or acute embolic arterial occlusion due to cardiac valvular disease by thromboembolectomy or an arterial bypass operation has been advocated by some authors. We have performed 68 first time vascular operations, including thromboembolectomies on RR patients with ischemic lower extremities, within an 11-year-and-6-month period, from January 1974 to June 1984. We have reviewed and analyzed our vascular operative procedures and post operative results. The patients upon whom thromboembolectomies were performed were 42 males and 13 females ranging from 5 to 72 years of age. The major arterial occlusive sites were common iliac artery in 20 cases, femoral artery in 21 cases, popliteal artery in 8 cases, common iliac artery and femoral artery in 4 cases, and femoral artery and popliteal artery in 3 cases. The underlying causes of arterial occlusive disease were atherosclerosis obliterans in 34 cases; Buerger`s disease in 3 cases; emboli due to cardiac valvular disease in 13 cases; and vascular trauma in 4 cases, including cardiac catheterization in I of those cases. Arterial bypass operations with autogenous or artificial vascular prosthesis were done in 31 cases. Amputations were done on 2 patients carrying out any more vascular operative procedures would have been of no benefit to them. Our bypass operations for ischemic lower extremities were classified as follows: those done between the abdominal aorta and the femoral artery in 17 cases, including those done between the aorta and the bifemoral arteries with a Y graft in four of those cases and long ones done from the axillary to the femoral artery in 4 cases. Five patients died in the hospital following vascular surgery for ischemic lower extremities, the causes of death were not directly related to the vascular reconstructive operative procedures. The leading causes of death were respiratory failure due to metastatic lung carcinoma: renal failure due to complications from atherosclerosis obliterans; sepsis from open, contaminated fractures of the tibia and fibula; and myocardial failures due to open heart surgery in one case and reconstructive surgery of the ascending aorta in another.

• The Korean Journal of Physiology
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• 제24권1호
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• pp.67-76
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• 1990

The contractile mechanisms of serotonin were investigated in the renal artery of a rabbit. The helical strips of isolated renal artery were immersed in the normal or $Ca^{2+}$-free tris-buffered Tyrode's solution, which was equilibrated with 100% $O_{2}$ at $35^{\circ}C$. The contraction by serotonin or norepinephrine (NE) began at $1{\times}10^{-7}\;M$ and reached the maximal contraction at $1{\times}10^{-5}\;M$. The maximal contraction by serotonin corresponded to $58.1{\pm}4.2%$ of maximal contraction by NE. Cyproheptadine, a serotonin receptor blocker, shifted the concentration-response curve to the right without any reduction in the maximum response but shifted that of NE to the right with reduction in maximum response. And phentolamine, an ${\alpha}-receptor$ blocker, shifted the concentration-response curve of serotonin or NE without any reduction in maximum responses. The $pA_{2}$ values for cyproheptadine against serotonin and NE were $10.35{\pm}0.04$ and $8.45{\pm}0.13$, respectively. The $pA_{2}$ values for phentolamine against serotonin and NE were $6.87{\pm}0.04$ and $8.14{\pm}0.08$, respectively. after the pretreatment with 6-hydroxydopamine, the contraction induced by 100 mM $K^{+}$, tyramine and serotonin reduced to $83.0{\pm}2.0$, $26.8{\pm}6.2$ and $82.0{\pm}3.5%$ of control, respectively. The contraction by serotonin in the $Ca^{2+}$-free Tyrode's solution was increased and sustained with the addition of $Ca^{2+}$ extracellulary. The serotonin-sensitive intracellular $Ca^{2+}$ pool was depleted completely by the pretreatment with NE, but the NE-sensitive intracellular $Ca^{2+}$ pool was depleted partially by the pretreatment with serotonin. From the above results, it is suggested that the contraction induced by serotonin in the renal artery of a rabbit may be due to mechanisms in which serotonin acts directly on specific serotonin receptors and also acts indirectly on ${\alpha}-adrenoceptors$ by displacing NE from neuronal stores.

• The Korean Journal of Physiology and Pharmacology
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• 제4권6호
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• pp.471-477
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• 2000

In the rabbit renal artery, acetylcholine $(ACh,\;1\;nM{\sim}10\;{\mu}M)$ induced endothelium-dependent relaxation of arterial rings precontracted with norepinephrine $(NE,\;1\;{\mu}M)$ in a dose-dependent manner. $N^G-nitro- L-arginine$ (L-NAME, 0.1 mM), an inhibitor of NO synthase, or ODQ $(1\;{\mu}M),$ a soluble guanylate cyclase inhibitor, partially inhibited the ACh-induced endothelium-dependent relaxation. The ACh-induced relaxation was abolished in the presence of 25 mM KCl and L-NAME. The cytochrome P450 inhibitors, 7- ethoxyresorufin $(7-ER,\;10\;{\mu}M),$ miconazole $(10\;{\mu}M),$ or 17-octadecynoic acid $(17-ODYA,\;10\;{\mu}M),$ failed to inhibit the ACh-induced relaxation in the presence of L-NAME. 11,12-epoxyeicosatrienoic acid $(11,12-EET,\;10\;{\mu}M)$ had no relaxant effect. The ACh-induced relaxation observed in the presence of L-NAME was significantly reduced by a combination of iberiotoxin $(0.3\;{\mu}M)$ and apamin $(1\;{\mu}M),$ and almost completely blocked by 4-aminopyridine (5 mM). The ACh-induced relaxation was antagonized by $P_{2Y}$ receptor antagonist, cibacron blue $(10\;and\;100\;{\mu}M),$ in a dose-dependent manner. Furthermore, 2-methylthio-ATP (2MeSATP), a potent $P_{2Y}$ agonist, induced the endothelium-dependent relaxation, and this relaxation was markedly reduced by either the combination of iberiotoxin and apamin or by cibacron blue. In conclusion, in renal arteries isolated from rabbit, ACh produced non-NO relaxation that is mediated by an EDHF. The results also suggest that ACh may activate the release of ATP from endothelial cells, which in turn activates $P_{2Y}$ receptor on the endothelial cells. Activation of endothelial $P_{2Y}$ receptors induces a release of EDHF resulting in a vasorelaxation via a mechanism that involves activation of both the voltage-gated $K^+$ channels and the $Ca^{2+}-activated\;K^+\;channels$. The results further suggest that EDHF does not appear to be a cytochrome P450 metabolite.