• Childhood Kidney Diseases
• /
• 제3권1호
• /
• pp.20-26
• /
• 1999

목 적 : 스트레스 유발 고혈압을 일으키는데 말초성 benzodiazepine수용체가 중요한 역할을 하리라 추정되어 왔다. 반복적 부동화 스트레스에 의한 신장의 말초성 benzodiazepine수용체의 변화 양상을 Sprague-Dawley rats와 boderline hypertensive rats의 두 실험동물군에서 비교, 관찰하여 고혈압을 유발하는데 신장의 말초성 benzodiazepine 수용체의 병태생리학적 기능을 규명하고자 하였다. Benzodiazepine수용체의 변화 양상은 방사성 동위원소를 사용한 수용체 결합 반응으로 검색하였으며 elevated plus maze검사로 각 실험동물의 불안도를 측정하여 각 군간의 결과를 비교, 관찰하였다. 방 법 : 불안도를 보기 위하여 측정한 plus-maze performance에서 percent open crosses는 Sprague-Dawley rats ($34.7{\pm}2.2$)에 비해 boderline hypertensive rats ($16.2{\pm}1.7$)가 유의하게 낮았고(P<0.05), percent time in open도 Sprague-Dawley rats ($22.5{\pm}1.0$)에 비해 boderline hypertensive rats ($12.1{\pm}1.2$)가 유의하게 낮아 불안도가 높은 상태임을 나타내었다(P<0.05). 스트레스를 주지 않은 Sprague-Dawley rats의 신장 말초성 benzodiazepine수용체의 수(Bmax: $5.5{\pm}0.6$pmol/mg protein)에 비하여 boderline hypertensive rats의 수용체의 수($3.1{\pm}0.7$pmol/mg protein)는 유의하게 낮았다(P<0.05). 하루 2시간씩 14일간 부동화 스트레스를 부하하였을 때, Sprague-Dawley rats와 boderline hypertensive rats에서 신장의 말초성 benzodiazepine 수용체의 수($7.4{\pm}0.7$ 및 $5.9{\pm}1.2$ pmol/mg protein)는 스트레스를 주지 않았을 때보다 증가하였으며(P<0.05), 스트레스에 노출된 boderline hypertensive rats는 스트레스에 노출된 Sprague-Dawley rats에 비하여 신장 말초성 benzodiazepine수용체의 수가 여전히 낮은 수준임을 관찰할 수 있었다(P<0.05). 결 론 : 이상의 결과로부터 신장의 말초성 benzodiazepine수용체는 스트레스 조절작용을 매개하며, 본 수용체의 수적 감소는 스트레스에 의한 고혈압 발생에 중요한 역할을 할 것으로 생각되었다.

• 환경위생공학
• /
• 제14권1호
• /
• pp.88-96
• /
• 1999

The effect of acute cadmium-neuropathy on phospholipid metabolism in rat sciatic nerve was investigated. An animal model of cadmium neuropathy was induced by feeding diet containing cadmium to Sprague-Dawley rat for two weeks. Four weeks aged Sprague-Dawley rats were divided into four groups : normal control group, 10ppm-cadmium treated group, 100ppm-cadmium treated group, 1000ppm-cadmium treated group, reference drug, myo-inositol-treated group. All rats were sacrificed at the end of two weeks. The rate of incorporation of 2-[3H]myo-inositol into polyphosphinositide was significantly decreased while the rates of incorporation into phospholipid of titratedserine, ethanolamine and choline were unchanged in sciatic nerve obtained from cadmium-treated rat. Continuously the activities of three enzymes concerned with inositol phospholiped metabolism were measured in homogenates of rat sciatic nerves. Cystidine diglyceride transferase and phophatidylinositol kinase showed significantly decreased activities while phosphatidylinositol-4-phosphate kinase did not show any significant change in activity by cadmium treatment. However these deficits of inositol phospholipid metabolism were ameliorated by myo-inositol administration and these effectiveness were more potent in lower dose cadmiumtreated rats than higher dose cadmium-treated rats. These results suggest that cadmium intoxicated peripheral nerve with perturbation of the ployphosphoinositide metabolism and alteration of the enzyme activity which concerned with myo-inositol metabolism.

• 환경위생공학
• /
• 제11권2호
• /
• pp.21-26
• /
• 1996

In our previous studies, we reported that lead intoxicated nerve cell by inhibition of the Na$^{+}$-K$^{+}$ ATPase activity and reduction of myo-inositol in nerve cell. As the second series of experiments, in order to understand toxic mechanism of lead for nerve cell, the characteristics of myo-inositol transport system and the effect of lead on its system have been studied in the sciatic nerves of control and lead-treated rats. A lead intoxicated animal model was induced by feeding diet containing lead to Sprague-Dawley rat for two weeks. Four weeks aged Sprague-Dawley rats were divided into three group : normal control group, 10ppm-lead treated group, 100ppm-lead treated group. All rats were sacrified at the end of two weeks. The rate o myo-inositol transport by sciatic nerve isolated from lead-treated rat was significantly decreased compared with that of control rat. This deficit results from that myo-inositol transport system which is carrier mediated and sodium-potassium dependent was inhibited by the lead treatment (both 10ppm and 100ppm) due to increase of the Km value without affecting Vmax value for myo-inositol carrier. These observations suggest that the toxic mechanism of lead on nerve myo-inositol transport system might be a change of affinity without change of maximum transport velocity for carrier.

• 환경위생공학
• /
• 제10권3호
• /
• pp.45-55
• /
• 1995

This study was carried out to elucidate the toxic mechanism of cadmium in peripheral nerve. An animal model of cadmium neuropathy was induced by feeding diet containing cadmium to Sprague- Dawley rat (or two weeks. Four weeks aged Sprague- Dawley rats were divided into four groups : normal control group, 10ppm- cadmium treated group, 100ppm- cadmium treated group, 1000ppm- cadmium treated group, reference drug- treated group. All rats were sacrificed at the end of two weeks for assessing the development of cadmium neuropathy, These results obtained were summarized as follows : 1. Cadmium reduced peripheral flow of both acetylcholinesterase and cholinesterase in rat sciatic nerve. 2. The toxic mechanism of cadmium might be the result of an reduction of myo-inositol concentration in peripheral nervous system 3. Reduction in myo-inositol content of peripheral nerve resulted from the inhibition of sodium- Potassium ATPase activity, which is responsible for myo-inositol transport, by cadmium 4. Oral administration of myo-inositol improved the flow of both acetylcholinesterase and cholinesterasenerve in cadmium intoxicated rat. These results suggest that mild cadmium neuropathy might be diagnosed by checking nervous myo-inositol content and oral administraion of myo-inositol might prevent the development of severe cadmium neuropathy with special reference to detective axonal transport.

• Biomolecules & Therapeutics
• /
• 제16권4호
• /
• pp.299-305
• /
• 2008

Active cardiovascular anaphylactic response was induced in ovalbumin-sensitized, pithed Sprague-Dawley and Wistar rats. On intravenous administration of the antigen, ovalbumin, marked tachycardia and pressor responses were immediately elicited. Thereafter, a delayed long-lasting severe hypotensive response was observed. These anaphylactic cardiovascular responses were maximal 2-3 weeks after the sensitization, and the response was slightly diminished 6 weeks after sensitization. The immediate pressor response was blocked by a non-selective serotonin antagonist methysergide at a dose-dependent manner, but not by histamine receptor antagonists mepyramine (pyrilamine) or cimetidine. The delayed hypotension was reduced either by histamine $H_1$ receptor antagonist mepyramine or $H_2$ receptor antagonist cimetidine, both in a dose-dependent manner. The tachycardic response was not influenced by serotonin or histamine receptor antagonists examined in this study. Differently from the cardiovascular responses, there was no observable bronchial contraction in Sprague-Dawley rat trachea in contrast to Wistar rat where the trachea contracted to in vitro antigen challenge. The cardiovascular anaphylactic model seems to be useful for studying cardiovascular events that occur exclusively in peripheral heart-blood vessel systems. The involvement of two major anaphylactic mediators, serotonin and histamine, is partially demonstrated.

• 한국독성학회:학술대회논문집
• /
• 한국독성학회 2002년도 Current Trends in Toxicological Sciences
• /
• pp.68-68
• /
• 2002

To investigate the disease and recovery process of pneumoconiosis induced by welding-fume exposure, a lung fibrosis model was established by building a stainless steel arc welding fume generation system and exposing male Sprague-Dawley rats for 90 days.(omitted)

• 한국응용약물학회:학술대회논문집
• /
• 한국응용약물학회 1993년도 제2회 신약개발 연구발표회 초록집
• /
• pp.54-54
• /
• 1993

Two strains of genetically epilepsy-prone rats (GEPRs) have been derived from Sprague Dawley stock. One strain, known by the acronym GEPR-9, has a more pronounced epileptic condition than the other strain, known by the acronym GEPR-3. Only a small fraction of commercially available Sprague Dawley rats exhibits evidence of epilepsy. GEPRS are similar to most humans with epilepsy in that their general behaviors appear normal . GEPRS also share other traits with their non-epileptic counterparts. They are susceptible to forebrain and brainstem seizures produced by convulsant drugs and electrical currents. Because GEPRs and normal rats share these seizure non-epileptic brain rather than to an understanding of epilepsy. However, humans wi th epilepsy, the GEPR and other mammal inn models of genetic epilepsy are distinctive because they are characterized by seizure predisposition.

• 환경위생공학
• /
• 제18권2호
• /
• pp.60-66
• /
• 2003

This study was carried out to elucidate the preventive mechanism of molybdenum on lead-induced neuropathy, An animal model of lead neuropathy was induced by feeding diet containing lead to Sprague-Dawley rat for three weeks. Four weeks aged Sprague-Dawley rats were divided into four groups : normal control group, 10ppm-lead treated group, 1mg/kg-molybdenum treated group, 10ppm-lead and 1mg/kg-molybdenum treated group. The parameters on neuropathy were examined by measuring concentration of myo-inositol and myo-inosito uptake in sciatic nerve. In the lead-treated rats, myo-inositol concentration and myo-inositol uptake rate were reduced by from 54% to 33% respectively. This deficit results from that myo-inositol uptake system which is carrier mediated and sodium-potassium dependent was inhibited by the lead treatment. However, the molybdenum administration significantly eliminated the impairment and maintained myo-inositol concentration to about 82% of normal level. These results suggest that lead-induced neurotoxicity was significantly reduced by administration of molybdenum and the mechanism might be partly normalization of myo-inositol uptake system in sciatic nerve.

• 대한간호학회지
• /
• 제40권4호
• /
• pp.580-588
• /
• 2010

Purpose: The purpose of this study was to examine effects of decreased locomotor activity on mass, Type I and II fiber cross-sectional areas of ipsilateral and contralateral hindlimb muscles 21 days after establishing the Parkinson's disease rat model. Methods: The rat model was established by direct injection of 6-hydroxydopamine (6-OHDA, 50 ${mu}g$) into the left substantia nigra after stereotaxic surgery. Adult male Sprague-Dawley rats were assigned to one of two groups; the Parkinson's disease group (PD; n=17) and a sham group (S; n=8). Locomotor activity was assessed before and 21 days after the experiment. At 22 days after establishing the rat model, all rats were anesthetized and soleus and plantaris muscles were dissected from both ipsilateral and contralateral sides. The brain was dissected to identify dopaminergic neuronal death of substantia nigra in the PD group. Results: The PD group at 21 days after establishing the Parkinson's disease rat model showed significant decrease in locomotor activity compared with the S group. Weights and Type I and II fiber cross-sectional areas of the contralateral soleus muscle of the PD group were significantly lower than those of the S group. Conclusion: Contralateral soleus muscle atrophy occurs 21 days after establishing the Parkinson's disease rat model.

• 한국식품위생안전성학회지
• /
• 제6권1호
• /
• pp.13-26
• /
• 1991

간의 부분적 절제수술을 하지 않고 새로운 발암성 검색법을 찾고자, 화학물질에 민감한 신생암첫 Sprague-Dawley 랫드를 이용하여 diethylnitrosamine(DENA)으로 암을 유발시킨 후, 제1군에는 강력한 촉진제로서 2-acetylaminofluorene(2-AAF)을 사료하여 0.01%가 되게 섞어 투여하였고, 제2군은 약한 촉진제인 phenobarbital을 암수에 0.05% 농도로 녹여 토여하였으며, 제 3군은 대조군으로 DENA만을 1회 투여하였다. 그리고 발암성 평가는 glutathione S-transeferase placental form을 사용하여 검색하였다. 그 결과 체중에 대한 간의 무게비는 이유후 4주째 (7주)에 제2군이 제3군인 대조군에 비해 유의성 있게 (p<0.01)높았으며, 이유후 8주째(11주)에는 제1군과 제 2군이 대조군에 비해 각각 유의성 있게 (p<0.01, p<0.001)높았다. 그리고 이유후 4주(7주)째에 GST-P 양성병변을 이용한 전암병변의 면적을 비교해본바 제 1군과 제2군이 각각 유의성있게 (p<0.01, p<0.05)높게 나타났다. 이상의 결과에서 신생 랫드를 이용한 발암성 실험은 간의 부분적 절제수술을 하지 않고도 화학물질의 발암성을 좀더 이른 시기에 검색할 수 있음을 알 수 있었다. 그러므로 신생동물을 이용한 발암성 실험은 많은 화학물질들의 발암성을 검색하는데 매우 유용한 방법으로 사료된다.