Anesthetic agents are useful in inducing the anesthesia for surgical operations and various biological experiments, but they can disturb the body homeostasis and cause the stress in animal. Much efforts have been directed on reducing such side effects of anesthesia. In this work, we measured the serum ACTH, corticosterone and glucose concentration in rabbits to compare the degree of stress induced by two commonly-used anesthetics, ketamine, xylazine, and the combination of xylazine and ketamine. 1. The anesthesia was induced in about 10 min in the rabbits treated with xyalzine, ketamine and xylazine-ketamine. The duraion of complete loss of righting reflex were 12, 13 and 115 min in the groups treated with xylazine, ketamine and xylazine-ketamine, respectively. 2. Serum ACTH concentrations in all treatment groups were gihger than those in control group. At 30 min after the administration of the drugs, serum ACTH levels in ketamine-treated group were significantly higher than those in control, xylazine- and xylazine-ketamine-treated groups. However, at 1, 2, 5 and 9 hours after the drug administration, serum ACTH levels in xylazine-treated-group were gihger than those in control. 3. Serum corticosterone levels in xylazine- and xylazine-ketamine-treated groups were lower than those in control or ketamine=treated groups at 0.5 and 1 hour after the administration. However, at 5 and 9 hours after the administration, serum corticosterone levels inxylazine- and xylazine-ketamine-treated groups were significantly higher than those in ketamine-treated group or control. 4. Serum glucose levels transiently increased to 3 tives of the pre-injection levels at 0.5 and 1 hours after the administration in xylazine or xylazine-ketamine-treated groups, but were not changed in control and ketamine-treated group. These results indicate that xylazine-induced stress lasts longer than ketamine-induced, suggesting that the difference in stress-related hormone levels during anethesia could be due to the differences in modes of actions of individual drugs used and the depth of anesthesia.

Hemal nodes and hemolymph nodes are lymphoid organs which share morphologic and functional characteristics of lymph nodes and spleens. Hemal nodes and hemolymph nodes are normally present in Korean native goats. Hemal nodes had extensive subcapsular and deep sinuses distended by a great number of erythrocytes, and no typical cortex and medulla were observed. Blood vessels commonly occurred, but lymph vessel was not observed in the hemal node. Hemolymph nodes had distince cortex and medulla, and also had afferent and efferent lymph vessels. The aim of the present study was to obtain new informationon the distinct morphological structures of hemal nodes and hemolymph nodes according to ages, and have the basic data for their functions. Goats are divided into 5 groups, consisting of 3 animals aged 1, 3, 6, 10, and 12 momths. The morphological studies of the organs were carried out by groww anatomy, light microscopy and immunohistochemistry. During aging, there was an increase in the size of the organs, while there were no significant changes of their numbers, locations and colors. As the goat got older, the lymphatic nodules of hemal nodes were more developed, and the number of macrophage containing phagocytosed erythrocytes was more increased. As the goat was younger,the lymphatic tissues of hemolymph nodes were less developed. There was no difference in distribution of T-and B-lymphocytes according to ages.

A six-month-old, male mongrel dog presented with wet ventral abdominal skin hairs and a short prepuce with penis. In physical examination, the penis was underdeveloped with fusion failure of the prepuce and the urethral opening was in the transitional area between os penis and perineal region. the radiological shape of urinary bladder was normal in positive contrast cystography and there was no any other routes except the observed urethral opening. Cryptochidism was also shown. It was diagnosed as hypospadia.

Anatomical and histological changes were studied in the dorsal, ventral, third and splenic lobes of the pancreas of the chicken embryos (8 days of incubation, 10 days of incubation to hatching). From 13 days of incubation, all four pancreatic lobes, namely, dorsal, ventral, third and splenic lobes were observed. Histologically, the pancreas of 10-14 days of incubation were consisted of mesenchymal tissue, exocrine acini and pancreatic islets. But mesenchymal tissues were disappeared from 15 days of incubation. The pancreatic ducts were observed from 14 days of incubation. The dark and light typed pancreatic islets were observed in splenic lobe from 13 days of incubation, in the third lobe from 11 days of incubation, and in the dorsall lobe from 13 days of incubation. But no dark typed islets were observed in the ventral lobes.

Renal failure is one of the main causes of economic impacts in the poultry industry and complex syndrome with different severity of clinical signs caused by multiple nephropathogenic factors such as infectious bronchitis viral infection and excess salt and calcium in diet. To evaluate the correlation between severity of renal failure and the causative nephropathogenic factors, one-day-old specific patogen free chicks were treated with either single causative factor or multiple causative factors described as above. Each group was designed as control for non-treated control, IB for infectious bronchitis virus (IB virus) infectio, IBHNa for IB virus infection with high diet salt, IBHCa for IB virus infectio with high diet calcium, IBHNC for IB virus infection with high diet salt and calcium, HNa for high diet salt, HCa for high diet calcium and HNC for high diet salt and calcium. Chickens were inoculated with IB virus at 1-day-old and remained on their respective diets until 21 day of age. The high dietary salt feeding groups such as IBHNa, IBHNC, HNa, HNC increased water intake, watery diarrhea, general subcutaneous edema and the high dietary calcium feeding groups such as IBHCa and IBHNC showed severe visceral gout. Two more than treated groups caused high mortality in comparison with the single treated groups. In virus exposure significantly increased urate deposition and lymphocytic interstitial nephritis. Espcecially urate deposition dramatically increased when excess diet calcium was combined together. In excess diet salt treated groups enlarged edematous kidneys were observed and hypertrophy of glomeruli were showed. These results suggest that IB virus enhanced the incidence and severity on chicken renal failure clearly related to the quantity of salt and calcium.

The purpose of this study is to assess the suitability of the statistical techniques employed in papers published in the Korean Journal of Veterinary Research from March 1997 to March 1999 and it is hoped that the critical assessment may be of help to other researchers preparing their works for publication. Of the 246 original papers 94 were inclluded in the analysis. of 62 papers with the measure of central location and dispersion of data 34(54.8%) used them correctly:9 (39.1%) of 23 for t-test; 1 (33.3%) of 3 for correlation analysis; 7 (43.8%) of 16 for analysis of variance (ANOVA); 5 (62.5%) of 8 for chi-square test; 44 (71%) of 62 for description of p-value. A number of papers employed ANOVA did not perform subsequent analysis of multiple comparison. Compared to the results of others, relatively higher proportion of papers in the present study was evaluated as appropriate analysis. The reason is that papers described insufficiently on the study design were not included, and evaluation items were restricted to the cases violated seriously ingerent assumptions for each statistical technique. Statistical misuse or abuse appeared in the study is due to lack of knowledge on statistics and short of its importance for improvement the quality of paper. Because an inappropriate analysis can lead the readers to misunderatand on findings, observed statistical analyses must be valid,and correctly undertaken. It is suggested that more intensive statistical refereeing are needed,and the communication should be allowed for the controversial points.

Magnesium (Mg2+) plays an important role in the regulation of a range of intracellular processes. Regulation of extracellular Mg2+ contents was studied in the anesthetized Sprague-Dwley (SD) rats. Animals were injected intraperitoneally with sodium nitrite (NaNO2), and circulating Mg2+([Mg2+]c) was observed in animals injected with NaNO2 at a dose of 10mg/kg or higher. Pretreatment with methylene blue preventd the NaNO2-induced increse in [Mg2+]c.[Mg2+]c displayed an inverse linear correlation with hemoglobin and exponential correlation during NaNO2 injection. Injection of KCN or rotenone also induced an increase in [Mg2+]c. An increase in [Mg2+]c was observed when respiration rate was reduced from 100/min (140ml/min) to 10/min (14ml/min) during 30 min. These results indicate that changes in [Mg2_]c inversely reflect alteration of ATP in a model of metabolic inhibition

Previous studies suggested that the inhibition of thyroxine (T4) release by alpha1-adrenoceptor and muscarinic receptor stimulation results in activated protein kinase C (PKC) from mouse and guinea pig thyroids. In the present study, the effect of carbachol, methoxamine, phorbol myristate acetate (PMA), and R59022 on the release of T4 from the mouse, rat, and guinea pig thyroids was compared to clarify the role of PKC in the regulation of the release of T4. The thyroids were incubated in the medium containing the test agents, samples of the medium were assayed for T4 by EIA kits. Forskolin, an adenylate cyclase activator, chlorophenylthio-cAMP sodium, a membrane permeable analoge of cAMP, and isobutyl-methylxanthine, a phospho-diesterase inhibitor, like TSH (thyroid stimulating hormone), enhaced the release of T4 from the mouse, rat, and guinea pig thyroids. Methoxamine, an alpha1-adrenoceptor agonist, inhibited the TSH-stimulated release of T4 in mouse, but not rat and guinea pig thyroids. In contrast, carbachol, a muscarinic receptor agonist, inhibited the release of T4 in guinea pig, but not mouse and rat thyroids. These inhibition were reversed by prazosin, an alpha1-adrenoceptor antagonist or atropine, a muscarinic antagonist or M1- and M3- muscarinic antagonists, in mouse or guinea pig thyroids. In addition, staurosporine, a PKC inhibitor, reversed methoxamine or carbachol inhibition of TSH stimulation. Furthermore, PMA, a PKC activator, and R59022, a diacylglycerol (DAG) kinase inhibitor, inhibited the TSH-stimulated release of T4 in mouse, rat, and guinea pig thyroids. These inhibition were blocked by staurosporine. these findings suggest that the activation of receptor or DAG inhibits TSH-stimulated T4 release through a PKC-dependent mechanism in thyroid gland.

A four-year-old female Jindo dog was admitted to the hospital because of bilaterally symmetrical alopecia and inappentence. Systemic abnomalities detected on physical examination were obesity,bradycardia, exercise intolerance, mental dullness and hypothermia. Dermatologically symmetrical alopecia, exercise intolerance, mental dullness and hypothermia. Dermatologically symmetrical alopecia on the back, trunk and dorsal tail, and ventral hyperpigmentation were observed. Also face was very tragic. The level of basal T4 was 0.01 micro gram/dl. In TSH stimulation test fT4 value was 0.08ng/dl. After treatment was initiated with L-thyroxine the dog's general condition was improved at 4 weeks.

The present experiments were performed to examine the effects of acetylcholine (ACh) and carbachol (CC) on thyroxine (T4) release and any possible relation between inhibition of T4 relese and sighaling pathway in guinea pig thyroids. The thyroids were incubated in the medium containing the test agents, samples of the medium wer assayed for T4 by EIA kits. ACh and CC inhibited the TSH-stimulated T4 release. These inhibition were reversed by atropine, but not by d-tubocurarine. The ingibitory effects of ACh on T4 release were prevented by M1- and M3-muscarinic antagonists and its inhibition was also slightly reversed by M2- and M4- muscarinic antagonists. R59022, like ACh and CC, also inhibited the TSH-stimulated T4 release. This inhibition was reversed by protein kinase C inhibitor and Ca2+ channel blocker. The present study suggests that cholinergic inhibition of T4 release from thyroids can be induced mainly by ctivation of the M1- or M3-receptors and that it is mediated throught the muscarinic receptor-stimulated protein kinase C activation