Objectives : This study was designed to investigate the effects of acupuncturing $PC_8$ used perpendicular needling method determine the mechanism of action of acupuncturing $PC_8$ by measuring the changes of regional cerebral blood flow (rCBF) and mean arterial blood pressure (MABP) in normal rats. Methods : This study also investigated the effects of acupuncturing $PC_8$ on the change of rCBF in cerebral ischemic rats, and revealed the mechanism of its action. In addition, the effects of acupuncturing $PC_8$ on focal ischemic brain injury was studied in cerebral ischemic rats. Results : 1. Acupuncturing $PC_8$ significantly increase rCBF but decreased MABP in normal rats. 2. Acupuncturing $PC_8$ increased of rCBF was significantly inhibited by pretreatment with indomethacin (1mg/kg, i.p.), an inhibitor of cyclooxygenase in normal rats. 3. Acupuncturing $PC_8$ increased of rCBF was significantly inhibited by pretreatment methylene blue (10 ${\mu}g$/kg, i.p.), an inhibitor of guanylate cyclase in normal rats. 4. Acupuncturing $PC_8$ was significantly improved the rCBF than control group increased unstable in cerebral ischemic rats. 5. Acupuncturing $PC_8$ was not significantly improved the rCBF than control group by pretreatment with indomethacin (1mg/kg, i.p.), an inhibitor of cyclooxygenase in cerebral ischemic rats. 6. Acupuncturing $PC_8$ was significantly increased the rCBF than control group by pretreatment methylene blue ($10{\mu}g$/kg, i.p.), an inhibitor of guanylate cyclase in cerebral ischemic rats. Conclusions : In conclusion, our study suggested that acupuncturing $PC_8$ can increase rCBF in normal state, and improve stability of rCBF in ischemic state. In addition, we suggested that mechanisms related with acupuncturing $PC_8$ was involved in the guanylate cyclase pathway.
Proceedings of the Korean Society of Applied Pharmacology
/
1994.04a
/
pp.335-335
/
1994
Possibility whether lead ingestion can cause selective toxicity to central serotonergic nervous system in rats was tested. Three groups of wistar rats; 1)Control, 2) Low dose and 3) High dose groups, were prepared. In prenatally lead-exposed rats, until parturition from dams, rat pups were intoxicated via placenta of mother rats having received drinking water containing either 0%(control ), 0.05%(low dose) or 0.2%(high dose) of lead acetate respectively, In postnatally lead-exposed rats, right after parturition from dams rat pups received drinking water containing either 0% (control), 0.05%(low dose) or 0.2%(high dose) of lead acetate. At 2, 4, 6 and 8 weeks of age, tryptophan hydroxylase (TPH) activity and Na$\^$+//K$\^$+/-ATPase activity were measured in 4 areas of rat brain; Telencephalon, Diencephalon, Midbrain and Pons/Medulla. TPH activities were assayed by modified method of Beevers et al. (1983) using L-(5-$^3$H)-tryptophan as substrate. TPH activity was determined as a criterion of lead poisoning to central serotonergic nervous system and Na$\^$+//K$\^$+/-ATPase activity as a criterion of non specific lead poisoning to any kinds of tissues. Selective toxicity of lead poisoning to central serotonergic nervous system was evaluated by the changes of TPH activities without concomitant changes of Na$\^$+//K$\^$+/-ATPase activities. In prenatally lead-exposed rats. this selectivity was found in Telencephalon (2 weeks of age), Diencephalon/Midbrain (2 weeks of age), Midbrain (4 and 6 weeks of age), Pons/Medulla (2, 4 and 6 weeks of age) In rats exposed to low dose of lead and Pons/Medulla (2 weeks of age) to high dose of lead. In postnatal Iy lead-exposed rats, this selectivity was found in Telencephalon (8 weeks of age), Diencephalon(8 weeks of age), Pons/Medulla (6 and 8 weeks of age) in rats exposed to low dose of lead and Pons/Medulla (8 weeks of age) to high dose of lead. These results suggest that lead poisoning may exhibit selective toxicity to central serotonergic nervous system.
Our previous study demonstrated that dietary taurine or glycine supplementation significantly lowered plasma and hepatic cholesterol and triglyceride concentrations in rats fed a cholesterol-free diet. In the present study, the effect of long term dietary taurine or glycine supplementation, for the purpose of preventing and/or treating of hyperlipidemia and other known biological functions, on plasma and hepatic free amino acid concentrations and profiles were evaluated in rats. Three groups of male rats(110-130g) were fed a control diet(CD), taurine-supplemented diets(TSD ; CD+ 1.5% taurine) or glycine-supplemented diet(GSD ; CD+1.5% glycine) for 5 weeks. Plasma and hepatic free amino acid concentrations were determined by an automated amino acid analyzer based on ion-exchange chormatography. The feeding of TSD for 5 weeks yielded a 444% higher plasma taurine concentration , and the feeding GSD for the same period resulted in a 143% higher plasma glycine level in rats compared to those fed DB. Hepatic taurine concentration was significantly higher in rats fed TSD(145% increase) compared to the control rats. However, hepatic glycine concentration was not influenced by dietary glycine supplementation , which implies that the massive dose of glycine entering the body was more rapidly metabolized or excreted than taurein. Dietary taurine or glycine supplementation resulted in similar changes in plasma free amino acid concentrations, except in levels of taurine and glycine. Plasma levels of histidine, lysine, phenylalanine , alanine, proline, hydroxypoline, $\alpha$-aminogutyric acid, cystathionine and ethanolamine were significantly higher in rats fed TSD or GSD than those fed GD. Glycine supplementation did not change hepatic free amino acid concentrations as compared to CD. Concentrations of most hepatic free amino acids were not influenced by dietary taurine supplementation with the exception of significantly higher levels of asparate and tyrosine(56-63% increase) and lower levels of histidine and glutamate(33-34% decrease) compared to the control rats. These results suggest long-term dietary taurine or glycine supplementation resulted in increases in most plasma free amino acid levels, but did not cause a characteristic change in plasma aminogram pattern compared to rats fed CD.
This study was performed to investigate the effect of dietary protein level on renal senescence. Male rats of 337.8$\pm$5.7g body weight were underlateral nephrectomy or shamoperation. The rats were divided into high protein(40% casein), normal protein(15% casein) and low protein(8% casein)diets and fed experimental diets ad libitum for 24 weeks. The results are summarized as follows. There was a hypertophy of the remnant kidney of uninephrectomized rats of 40% or 15% protein group, coming up to the comparable weights of both kidneys of sham-operated rats. However, the hypertrophic effect was not seen in uninephrectomized rats of 8% protein group. Serum albumin was lower in uninephrectomized rats. With increasing dietary protein level blood urea nitrogen was increased, whereas, urinary urea nitrogen excretion was decreased. Urinary solute excretion was higher in uninephrectomized group than in sham-operated group. However, effect of dietary protein level on urinary solute excretion varied dpending on th solutes tested. GFR and urinary protein excretion, throughout experiment, increased with feeding period and with dietary protein level. Proteinuria was most severe in uninephrectomized rats fed 40% casein diet. Maximum urine concentration ability measured after dehydration was not different among the experimental groups. Light microscopic examination showed focal segmental glomerulosclerosis and mild increas of glomerular mesangial matrix in uninephrectomized rats fed 40% and 15% protein diet, however, which was not observed in uninephrectomized rats fed 8% protein diet and in sham-operated rats fed 40% diet. Immunofluorescence studies revealed segmental deposits of albumin in the mesangium and capillary loops in high protein and uninephrectomized groups. Minimal granular deposition of IgG was noted in the mesangium of all experimental groups. In conclusion, high protein intake accelerated deterioration of renal function and it was correlated with morphological change. Low protein intake was effective in preventing these changes.
The effect of morphine on food intake on freely fed Sprague - Dawley rats was examined Opiate receptor binding assay was used to investigate the possibility of the opioid system involved in food intake regulation of normal rats. When rats were treated with 5mg morphine per kg body weight, subcutaneously, the food intake of the rats for the first 2 hours was increased 125% of the control rats. The effect of morphine on food intake of male and female rats were greater when the morphine was injected at 10 : 00 a.m than that in the rats administered the morphine at 4 : 00 p.m. The morphine effect was not significant in older rats and female was more responsive than male rats. In morphine treated rats, opioid receptor density has exhibited 33% reduction as measured by the $^{3}H-naloxone$ binding assay with whole brain homogenate. These results indicate that the increase of food intake by morphine for 2 hours after the injection may be mediated through the opioid system in rat brain.
Pulmonary edema is a disease involving the principal symptoms: dyspnea, bloody phlegm, asthma, cough, etc. According to oriental medical references, Jeomglyukdaejosapaetang (J.D.T) was efficacious for dropsy, cough, dysnea, etc, so it was thought to be used for remedy of pulmonary edema. Therefore experimental study was performed to investigate the effects of J.C.T on pulmonary edema of the rats induced by the herbicide, paraquat.Thus the survival rats, respiratory rats, lung weights and histopathological view of the lungs of rats were studied. The results are as follows. 1. The survival rates at 72hours of the rats injected with paraquat and treated with J.D.T increased in B group(J.D.T + Cortex Lycii Radicis + Cortex mori). The others were not different with the control. 2. The respiratory rates of the rats which survived 72hours later significantly decreased in B group(J.D.T + Cortex Lycii Radicis + Cortex mori). 3. The lung weights of the rats which survived for 72hours later significantly decreased in B group(J.B.T + Cortex Lycii Radicis + Cortex mori). 4. The histopathological views of the lungs of rats induced by paraquat were seen severe hemorrhage, edema and some broken alveoli in control group. But B group(J.D.T + Cortex Lycii Radicis + Cortex mori) were seen little hemorrhage and interstitial hyperplasia. According to the above results, J.D.T + Cortex Lycii Radicis + Cortex mort is effective on the remedy for pulmonary edema of rats induced by paraquat.
Growing evidence indicates that enhanced generation or actions of nitric oxide (NO) are implicated in the pathogenesis of hypertension in spontaneously hypertensive rats and diabetic nephropathy in streptozotocin (STZ)-induced diabetic rats. We investigated whether inducible nitric oxide synthase (iNOS) expression in STZ-induced diabetic rats is responsible for the alterations of vascular reactivity. Diabetic state was confirmed 28 days after injection of STZ (i.p) in rats by measuring blood glucose. In order to evaluate whether short term (4 weeks) diabetic state is related with altered vascular reactivity caused by iNOS expression, isometric tension experiments were performed. In addition, plasma nitrite/nitrate (NOx) levels and expression of iNOS in the lung and aorta of control and STZ-treated rats were compared by using Griess reagent and Western analysis, respectively. Results indicated that STZ-treated rats increased the maximal contractile response of the aorta to phenylephrine (PE), and high $K^+,$ while the sensitivity remained unaltered. Endothelium-dependent relaxation, but not SNP-mediated relaxation, was reduced in STZ-treated rats. Plasma nitrite/nitrates are significantly increased in STZ-treated rats compared to controls. The malondialdehyde (MDA) contents of liver, serum, and aorta of diabetic rats were also significantly increased. Furthermore, nitrotyrosine, a specific foot print of peroxynitrite, was significantly increased in endothelial cells and smooth muscle layers in STZ-induced diabetic aorta. Taken together, the present findings indicate that enhanced release of NO by iNOS along with increased lipid peroxidation in diabetic conditions may be responsible, at least in part, for the augmented contractility, possibly through the modification of endothelial integrity or ecNOS activity of endothelium in STZ-diabetic rat aorta.
Pulmonary arterial hypertension (PAH) is a progressive disease characterized by vascular remodeling of pulmonary arteries (PAs) and increased vascular resistance in the lung. Monocrotaline (MCT), a toxic alkaloid, is widely used for developing rat models of PAH caused by injury to pulmonary endothelial cells; however, characteristics of vascular functions in MCT-induced PAH vary and are not fully understood. Here, we investigated hypoxic pulmonary vasoconstriction (HPV) responses and effects of various vasoconstrictors with isolated/perfused lungs of MCT-induced PAH (PAH-MCT) rats. Using hematoxylin and eosin staining, we confirmed vascular remodeling (i.e., medial thickening of PA) and right ventricle hypertrophy in PAH-MCT rats. The basal pulmonary arterial pressure (PAP) and PAP increase by a raised flow rate (40 mL/min) were higher in the PAH-MCT than in the control rats. In addition, both high $K^+$ (40 mM KCl)- and angiotensin II-induced PAP increases were higher in the PAH-MCT than in the control rats. Surprisingly, application of a nitric oxide synthase inhibitor, L-$N^G$-Nitroarginine methyl ester (L-NAME), induced a marked PAP increase in the PAH-MCT rats, suggesting that endothelial functions were recovered in the three-week PAH-MCT rats. In addition, the medial thickening of the PA was similar to that in chronic hypoxia-induced PAH (PAH-CH) rats. However, the HPV response (i.e., PAP increased by acute hypoxia) was not affected in the MCT rats, whereas HPV disappeared in the PAH-CH rats. These results showed that vascular contractility and HPV remain robust in the MCT-induced PAH rat model with vascular remodeling.
The purpose of this study was to investigate the effects of a butanol fraction of fraction of Alisma canaliculatum All. Braun et Bouche (Ac), and of selenium (Se), on plasma gllucose and lipid levee in streptozotocin (STD-induced diabetic rats. Male Sprague-Dawley rats, fed the AIN-93 recommended diet, were divided into five groups: a non-diabetic control group (no STZ treatment), and four 572-induced diabetic groups which consisted of a diabetic-control group, an Ac-treated group, an Ac-Se treated group, and a Se-treated group. Diabetes was induced in the rats by an injection of STZ into the tail vein at a dose of 45 mg/kg body weight. The butanol (BuOH) fraction of Ac was orally administered at a rate of 400 mg/kg body weight for 21 days to both the Ac and Ac-Se groups. The supplementation of selenium in the Se and Ac-Se groups was achieved by adding (freshly, every day) 2 mg of Se as Na$_2$SeO$_3$ per kg of feed. The rats'body weights and hematocrit (Hct) levels were measured, along with plasma levels of glucose, insulin, cholesterol, HDL-cholesterol, triglyceride (TG), and free fatty acids (FFA). Aminotransferase activities were also analyzed. The non-diabetic rats gained weight, while the diabetic rats lost weight - except in the Ac-Se group, which maintained their initial weight. The blood glucose levels of the Ac group and the Se group were significantly lower than for the diabetic-control group. The plasma triglyceride levels were lowered when both Ac and Se were administered to diabetic rats. The concentrations of plasma FFA in the Ac-Se group were significantly lower compared with the diabetic-control group. Plasma cholesterol levels and alanine aminotransferase activity in the Ac, Ac-Se, and Se groups were significantly lower when compared with the diabetic-control group. Aspartate aminotransferase activity was significantly lower in the Se group compared to the other diabetic groups. These data show that treatment with a butanol fraction of Ac in combination with Se has no synergistic effect. Plasma glucose levels tended to be low when Se was administered to diabetic rats. Supplementation of Se in diabetic rats did not elicit a significant increase in plasma insulin levels or result in hypolipemic effects.
The effects of dietary Ca and Na levels on lipid metabolism in hyper lipidemic/hypercholesterolemic rats were examined. In Expt. 1, normal rats were divided into six groups and fed high fat(15%, w/w)/cholesterol(1%, w/w) diet containing two levels of Na, low (0.05) or high(1.5%) and three levels of Ca, low(0.1%), normal (0.5%), or high(1.5%) for 8 weeks. In Expt. 2, hyperlipidemia / hypercholesterolemia rats were induced by feeding high fat / cholesterol diet for 4 weeks. They were divided into four groups and fed the high fat / cholesterol diet, containing two levels of Na, low or high and two levels of Ca, low or high for 4 weeks. In Expt. 1, total lipid and total cholesterol contents in serum and liver were significantly lower in rats fed high Ca diet than in rats fed normal or low Ca diet regardless of dietary Na levels. Serum TG was the highest in rats fed low Ca and low Na diet. In Expt. 2, Serum total lipid, TG, and total cholesterol levels decreased by 24, 35, 26% respectively in rats fed high Ca diet regardless of dietary Na levels. Serum total lipid level tended to increased in rats fed low Na diet. The total lipid and TG contents in liver slightly decreased in rats fed high Ca diet. Another observation was that high Ca intake significantly faciliated the fecal lipid and cholesterol excretion regardless of dietary Na levels. There results suggest that the hypolipidemidc/hypocholesterolemic effects of high Ca diet could be partly due to increase in lipid and cholesterol excretion and these effects may be independent of dietary Na levels.
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