Most of the studies conducted have investigated the beneficial effects of ischemic preconditioning on normothermic myocardial ischemia. However, the effect of preconditioning could be attenuated through the use of multidose cold cardioplegia as practiced in contemporary clinical heart surgical procedures. The purpose of this study was to investigate whether preconditioning improves postischemic cardiac function in a model of 25℃ moderate hypothermic ischemic heart induced by cold cardioplegia in isolated rat hearts. Material and Method: The isolated Sprague-Dawley rat hearts were randomly assigned to four groups. All hearts were perfused at 37℃ for 20 minutes with Krebs-Henseleit solution before the baseline hemodynamic data were obtained. Group 1 consisted of preconditioned hearts that received 3 minutes of global ischemic preconditioning at 37℃, followed by 5 minutes of reperfusion before 120 minutes of cardioplegic arrest (n=6). Cold (4℃) St. Thomas Hospital cardioplegia solution was infused to induce cardioplegic arrest. Maintaining the heart at 25℃, infusion of the cardioplegia solution was repeated every 20 minutes throughout the 120 minutes of ischemic period. Group 2 consisted of control hearts that underwent no manipulations between the periods of equilibrium and 120 minutes of cardioplegic arrest (n=6). After 2 hours of cardioplegic arrest, Krebs solution was infused and hemodynamic data were obtained for 30 minutes (group 1, 2: cold cardioplegia group). Group 3 received two episodes of ischemic preconditioning before 30 min of 37℃ normothermic ischemia and 30 minutes of reperfusion (n=6). Group 4 served as ischemic controls for group 3 (group 3, 4: warm ischemia group). Result: Preconditioning did not influence parameters such as left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), rate-pressure product (RPP) and left ventricular dp/dt (LV dp/dt) in the cold cardioplegia group. (p=NS) However, preconditioning before warm ischemia attenuated the ischemia induced cardiac dysfunction, improving the LVSP, LVEDP, RPP, and LVdp/dt. Less leakage of CPK and LDH were observed in the ischemic preconditioning group compared to the control group (p<0.05). Conclusion: Ischemic preconditioning improved postischemic cardiac function after warm ischemia, but did not protect cold cardioplegic hearts.
Kim, Sung-hoon;Hwang, Hwa-seon;Cha, Shin-woo;Han, Sang-seop;Roh, Jung-koo
Korean Journal of Veterinary Research
/
v.33
no.3
/
pp.507-511
/
1993
The effect of captafol on the hematological value, erythrocyte membrane and plasma biochemical value was investigated using blood of SPF Sprague-Dawley male rats in vitro. For the anticoagulations, we used 0.5mg of heparin per $10m{\ell}$ of blood from vena cava. Three con-centrations($0.1{\times}10^{-4}M$, $1{\times}10^{-3}M$ and $1{\times}10^{-2}M$) captafol in ethanol were added to the each $2.5m{\ell}$ blood so that the linal concentration of ethanol was 1%. The blood contained with each concentration of captafol was incubated at $37^{\circ}C$ C for 2 hours under 5% $CO_2$ gas The whole blood and plasma were examined for hematological vaJues, erythrocyte membrane damage and biochemical values, respectively. The results obtained were summarized as follows ; 1. The number of RBC in $1{\times}10^{-2}M$ group and the concentration of MCHC in $1{\times}10^{-3}M$ group were significantly (p<0.05) decreased and increased from that of control values, respectively. The percentage of Hct was significantly (p<0.05) decreased with dose-response. 2. Erythrocyte fragility rate of $1{\times}10^{-3}M$ and $1{\times}10^{-2}M$ group were significantly (p<0.01) increased from that control with dose response. 3. Potassium ion level of $1{\times}10^{-2}M$ was significantly (p<0.05) increased from that of control. 4. The concentration of total bilirubin in the $1{\times}10^{-3}M$ and $1{\times}10^{-2}M$ groups were significantly increased from that of control. The enzyme level of creatine kinase in $1{\times}10^{-2}M$ group was significanlty (p<0.05) decreased from control value.
Background: Most of the studies conducted have investigated the beneficial effects of ischemic preconditioning on normothermic myocardial ischemia. However, the effect of preconditioning could be attenuated through the use of multidose cold cardioplegia as practiced in contemporary clinical heart surgical procedures. The purpose of this study was to investigate whether preconditioning improves postischemic cardiac function in a model of $25^{\circ}C$ moderate hypothermic ischemic heart induced by cold cardioplegia in isolated rat hearts. Material and Method: The isolated Sprague-Dawley rat hearts were randomly assigned to four groups All hearts were perfused at 37$^{\circ}C$ for 20 minutes with Krebs-Henseleit solution before the baseline hemodynamic data were obtained, Group 1 consisted of preconditioned hearts that received 3 minutes of global ischemic preconditioning at 37$^{\circ}C$, followed by 5 minutes of reperfusion before 120 minutes of cardioplegic arrest (n=6). Cold (4$^{\circ}C$) St. Thomas Hospital cardioplegia solution was infused to induce cardioplegic arrest. Maintaining the heart at $25^{\circ}C$, infusion of the cardioplegia solution was repeated every 20 minutes throughout the 120 minutes of ischemic period. Group 2 consisted of control hearts that underwent no manipulations between the periods of equilibrium and 120 minutes of cardioplegic arrest (n=6). After 2 hours of cardioplegic arrest, Krebs solution was infused and hemodynamic data were obtained for 30 minuts (group 1, 2: cold cardioplegia group). Group 3 received two episodes of ischemic preconditioning before 30 min of 37$^{\circ}C$ normothermic ischemia and 30 minutes of reperfusion (n=6) Group 4 soloed as ischemic controls for group 3 (group 3, 4: warm ischemia group). Result: Preconditioning did not influence parameters such as left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), rate-pressure product (RPP) and left ventricular dp/dt (LV dp/dt) in the cold cardioplegia group. (p=NS) However, preconditioning before warm ischemia attenuated the ischemia induced cardiac dysfunction, Improving the LVSP, LVEDP, RPP, and LV dp/dt. Less leakage of CPK and LDH were observed in the ischemic preconditioning group compared to the control group (p<0.05). Conclusion: Ischemic preconditioning improved postischemic cardiac function after warm ischemia, but did not protect cold cardioplegic hearts.
Ochratoxin A (OA) is a mycotoxin produced by Aspergillus ochraceus as well as other molds. It is a natural contaminant of mouldy food and feed. OA has a number of toxic effects, the most prominant being nephrotoxicity. Futhermore, OA is immunosuppressive, genotoxic, teratogenic and carcinogenic. OA inhibits protein synthesis by competition with phenylalanine in the phenylalanine-tRNA aminoacylation reaction. Recently, lipid peroxidation induced by OA has been reported, indicating that the lesion induced by this mycotoxin could be also related to oxidative pathway. Since it seems impossible to avoid contamination of foodstuffs by toxigenic fungi, detoxification and detoxication of OA are needed. In this study we investigated the protective effects of aspartame (Asp), phenylalanine (Phe), polyphenol 70S (PP) and aloe extract (AE) on the nephrotoxicity induced by subacute exposure to the OA. Asp and Phe are structural analogues of OA. PP, an ingredient of Green Tea and AE have been known as antioxidant and radical scavenger. Phe (40 mg/kg, i.p.) and Asp (25 mg/kg, p.o.) were administered to Sprague-Dawley rats simultaneously with OA (2.0 mg/kg, p.o.) for 2 weeks. PP (200 mg/kg, p.o.) and AE (50 mg/kg, i.v.) were pretreated before administration of OA, for 2 weeks and 3 days, respectively. Using enzymuria, BUN level, creatinemia and histophathologic examination as indices of renal damage, we observed that all of four compounds prevented the nephrotoxic effects induced by OA. It seems that structural analogues of OA such as Asp and Phe have better protective effect on the nephrotoxicity of OA than antioxidants. These results indicate that 1) formation of free radical and lipid peroxidation are likely to be involved in the nephrotoxicity of OA in vivo, 2) Asp, PP and AE might be used for prevention of renal lesions in cases of ochratoxicosis.
Laminin, a kind of multidomain glycoproteins, is mainly localized in the basement membranes of various tissues. It is known that laminin plays an important part in mammalian lung morphogenesis. The authors have undertaken this study to investigate the changes in the distribution of laminin, and to find out cells which synthesize laminin during the organogenesis and differentiation of the lung. The fetal and neoantal rats (Sprague-Dawley strain) were used as experimental animals. The immunohisto-chemical methods were employed for detection of laminin within the developing lung tissue and the immunegold cytochemical methods were performed for detection of cells which synthesize laminin according to each stage of development. The results are as follows; 1. During fetal life, strong immunoreactivity for laminin is maintained in the basement membranes of the blood vessels and the bronchioles, the extracellular matrix of the mesenchyme, and basal lamina of the alveolar septum in the fetal rat lung. 2. After birth, laminin immunoreactivity at the alveolar septum is gradually reduced. 3. During fetal life, laminin is mainly detected within the cytoplasm of the mesenchymal cells, the endothelial cells of blood vessels and the fibroblasts in fetal rat lung. 4. According to the differentiation of type I and type II pneumocyte after birth, laminin is detected within cytoplasm of the type I pneumocytes, type II pneumocytes and fibroblasts. It is consequently suggested that laminin is largely expressed in the developing lung and laminin may be also synthesized by the type II pneumonocytes at early newborn stages.
Kim, Myung-Hee;Kim, Young-Eok;Yoon, Chang-Lyuk;Ryu, Ji-Won;Ahn, Jong-Mo
Journal of Oral Medicine and Pain
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v.38
no.1
/
pp.35-51
/
2013
The aims of this study was to observed an effect of antioxidative in cardiac muscle of high fat diet induced obesity rat by treadmill exercise with intensity and time. Thirty-two Sprauge-Dawley rats which were divided into four group. Normal, Control(high fat diet induced obesity rat), Experimental I(high intensity intermittent exercise in high fat diet induced obesity rat), Experimental II(moderate intensity endurance exercise in high fat diet induced obesity rat). The results of this study were as follows: 1. In change of body weight, the outcome of each group significantly difference compared with control. Also, 1 to 3 weeks significantly different compared with pre valu experimental I and II(p<0.001). 2. In change of lipid profile, the outcome of each group significantly difference compared with control(p<0.001). Difference between experimental I and II is not significantly. 3. In change of antioxidative enzymes(SOD, CAT, GPx) in myocardium, there are significant difference between control and experimental II, and also between control and experimental I(p<0.001). 4. In change of antioxidative protein MCR-1, the outcome of each group significantly difference compared with control(p<0.01). Experimental II was most significantly difference than the other group(p<0.001). The above results suggest that treadmill exercise effectively reduced in fat. It would be considered that moderate intensity endurance exercise has an effects on improved antioxidative enzyme in cardiac muscle of high fat diet induced obesity rat.
The objective of this study was to examine the effects of vitamin C on the formation of aflatoxin $B_1$ ($AFB_1$)-DNA adduct and $AFB_1$-induing cellular oxidative damage in rat livers treated with radiation and $AFB_1$. Six-week-old male Sprague-Dawley rats were randomly divided into five groups: the control group, the $AFB_1$-treated group, the group treated with $AFB_1$ and vitamin C, the group treated with X-ray and $AFB_1$, and the group treated with X-ray and $AFB_1$ with vitamin C. On the first day of the experiment, only one dose of X-rays was exposed to the entire liver at 1,500 cGy. Next, vitamin C was injected at 10 mg/kg body weight via intraperitoneal injection, followed an hour later by the administration of 0.4 mg/kg of $AFB_1$ via intraperitoneal injection. These treatments were administered every three days for 15 days. On the 16th day, the animals were sacrificed. The $AFB_1$ contents of the rat sera were determined via indirect competitive ELISA. In the quantitative analysis of $AFB_1$ in the rat sera via ELISA, $5.17{\pm}0.34ng/mL$ of $AFB_1$ was detected in the $AFB_1$-treated groups, but the amount decreased more significantly to $3.23{\pm}0.76ng/mL$ in the groups treated with $AFB_1$ and vitamin C (p<0.01) than in the $AFB_1$-treated groups. The effect of vitamin C on $AFB_1$-DNA adduct formation was determined via ELISA. The values of $AFB_1$-DNA adduct formation were $9.38{\pm}0.41ng/mL$ in the $AFB_1$-treated groups, but the amount decreased more significantly to $5.28{\pm}0.32ng/mL$ in the groups treated with $AFB_1$ and vitamin C (p<0.01) than in the $AFB_1$-treated groups. Immunohistochemistry revealed that the accumulation of the $AFB_1$ was not observed in the normal liver tissue (G1). The $AFB_1$-positive materials were observed in the central vein and the portal vein of the liver tissue from the $AFB_1$(G2) treatment or the X-ray and $AFB_1$(G4) co-treatment, but the $AFB_1$-positive materials were observed weakly in the group treated with vitamin C (G3 and G5). These results indicate that vitamin C had ameliorating effects on the $AFB_1$ accumulation of liver tissue.
Substantial amount of caryophyllene oxide (CPO) is present in the essential oils of traditionally-used folk medicinal plants and herbal spices. The CPO, produced via chemical and/or enzymatic reaction of caryophyllene (CP), has largely being used as a flavoring component and exhibited a variety of biological activities. Now, we report the antimutagenic activity of CPO determined by Ames's preincubation test. S-9 fraction was prepared from the liver of rats treated with Arochor 1254. Anatoxin $B_1\;(AFB_1)$ and 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) were used as mutagens. Reduction of mutagenicity of $AFB_1$ or IQ for S. typhimurium TA98 and TA100 by CPO was found to be a dose-dependant manner. CPO (500 ${\mu}g/plate$) reduced mutagenicity of AEB1 for S. typhimurium TA98 and TA100 to 89% and 71%, respectively. For IQ, similar results were observed against S. typhimurium TA98 and TA100, resulting in the inhibition percentage of 77% and 51%, respectively. CP also reduced mutagenicity of AEB1 and IQ for S. typhimurium TA98 and TA100, but the reduction rate was somewhat lowered relative to that of CPO. These results indicate that CPO could be developed as a potent antimutagenic flavoring agent.
Journal of the Korean Society of Food Science and Nutrition
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v.34
no.5
/
pp.652-658
/
2005
This experimental was carried out to evaluate the clinical effects of Ophicephalus argus and Crubita moschate which have been traditionally applied to postpartum care in Korea, and compare them with the effect of Saenghwtang. Fifty Sprague-Dawley female rats weighing $250\~280$ g were divided into five groups: a normal saline-treated group (NSG), a Saenghuatang-treated group (STG), an Ophicephlus argus-treated group (OTG), and a Crubita moschate-treated group (CTG), also non-pregnant group (NPG). Except for the NPG, each extract was administered for one week to each group after delivery. We measured the WBC, RBC, serum levels of hemoglobin and hematocrit, the platelet count, serum levels of fibrinogen, albumin, thyroxine and urine levels of sodium and potassium. STG showed a significant (p<0.05) decrease of WBC count, fibrinogen content and urine levels of sodium and potassium and a significant (p<0.05) increase of RBC, hemoglobin, albumin and thyroxine in comparison with those of the NSG. OTG showed a significant (p<0.05) decrease of WBC count, fibrinogen and the significant (p<0.05) increase of albumin and thyroxine in comparison with those of the NSG. CTG showed a significant (p<0.05) increase of albumin and thyroxine in comparison with that of NSG. These results suggest that Saenghwatang is more effective than Ophicephalus argus and Crubita moschate for postpartum recuperation although they also have some effects on recuperation of deteriorative blood components after delivery. Therefore, these findings indicate that futher investigation for the other effects of Ophicephalus argus and Crubita moschate is necessary.
Background : There have been many debates about the effects of nitric oxide on the neurogenic inflammation. The role of nitric oxide in the neurogenic inflammation of airways will be required a better understanding of the localization and types of nitirc oxide synthase(NOS) activity in the neurogenic inflammation of airways. Method : To investigate the role of nitric oxide in airway neurogenic inflammation, 1) the effects of neurokinin receptor antagonist (FK224) and nitric oxide synthase inhibitor, $N^{\omega}$-nitro-L-arginine (L-NNA) on plasma extravastion were evaluated in four groups of Sprague-Dawley rats ; sham operation group(sham NANC group), electrical vagal stimulation group(NANC2 group), intravenous pretreatment groups with FK224 (1mg/kg ; FK224 group), and L-NNA(1mg/kg ; L-NNA group) 15 minutes before vagal NANC stimulation. 2) NOS activity in trachea with neurogenic inflammation was localized by immunohistochemical stain. Immunohistochemical stain was performed by antibodies specific for inflammatory cells(iNOS), brain(bNOS), and endothelium (eNOS) on trachea obtained from sham NANC, NANC2, and FK224 groups. Results : The results are that plasma extravsation in neurogenic inflammation of rat airways was inhibited by FK224, but enhanced by L-NNA pretreatment(P<0.05). There was significantly increased infiltration of inflammatory cells in subepithelium of neurogenic inflammatory trachea, but the reduction of subepithelial infiltration of inflammatory cells was observed after pretreatment with FK224(P<0.05). Immunostaining with anti-iNOS antibody showed strong reactivity only in infiltrated inflammatory cells in neurogenic rat trachea, and these iNOS reactivity was reduced by pretreatment with FK224. bNOS immunoreactivity was significantly increased only in the nerves both of neurogenic inflammatory and FK224 pretreated trachea compared with sham NANC trachea(p<0.05). eNOS immunoreactivity was not significant change in endothelium in neurogenic inflammation of rat trachea. Conclusion : These results suggest that nitric oxide released from iNOS in infiltrated inflammatory cells has main role in neurogenic inflammation of rat trachea. The presence of bNOS immunoreactivity in the nerves indicates that nitric oxide may be released from the nerves in rat trachea with neurogenic inflammation.
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