No abstract available.
Rabbits*

No abstract available.
Rabbits*

No abstract available.
Rabbits*

No abstract available.
Rabbits*

No abstract available.
Rabbits*

Ketamine hydrochloride(ketamine) is a non-barbiturate anesthetic agent chemically designated as dl-2-(0-chlorophenyl)2-(methylamino)-cyclohexanone hydrochloride. Ketamine anesthesia has been found distinctively different from that induced by conventional anesthetic agents, as it provides profound analgesia without significant impairment of respiratory function or stimulation of cardiovascular activities thus avoiding hypotension and are preserved the protective pharyngeal and laryngeal reflexes. In addition, ketamine appears to have muscle relaxation properties. This latter clinical finding, however has not been experimentally substantiated since few reports have appeared on the effect of ketamine on muscle relaxation. The present study therefore, was undertaken to determine whether this agent affects the muscle activity during d-tubocurarine block. The experiment was performed on sixteen rabbits weighing 1.8 to 2.5kg and these were divided into two groups; eight rabbits for control and eight for th study group. All animals were intubated through a tracheostomy under general anesthesia with nembutal 40mg/kg given intravenously. Respiration was controlled by means of a Harvard animal respirator. The body temperature was kept at 35 degrees C to 36 degrees C with a thermo-blanket. The common peroneal nerve and anterior tibial muscle was exposed and the nerve stimulator was applied to the nerve muscle preparation. The twhitch height of the muscle contraction was recorded on a biophysiograph through the force displacement transducer. The common peroneal nerve was stimulated supramaximally using a single twitch, square wave of 0.2 msec duration at a frequency of 0.1Hz once every 10 seconds. The degree of neuromuscular block following intravenous injection of d-tubocurarine 1mg/kg was measured in the control group. And in the study group ketamine 5mg/kg was administered intravenously when 25% of twitch height of muscle contraction was obtained spontaneously after the intravenous injection of d-tubocurarine 1mg/kg. The changes of the twitch height of muscle contraction and the time of spontaneous recovery in the study group were compared with those of the control group. The results were as follows: 1) The times and degree of maximal single twitch depression were obtained at 194.8sec and 87.3% in the control group and were at 197.5 sec and 87.8% in study group. No significant difference was observed. 2) Recovery index of the control group was 1,560.0 sec and recovery index of the study group was markedly prolonged to 2,387.5 sec(53.0% prolongation). 3) Mean decrease of single twitch height was 8.8% soon after the intravenous ketamine 5mg/kg when 25% of twitch height was obtained after the intravenous d-tubocurarine 1mg/kg in the study group.
Rabbits ; Animals

It is known that the cardiovascular system is extremely sensitive to the effect of both exogenous and endogenous opiates. In rabbits, less than 1% of the usual morphine dose necessary to produce antinociception results in significant hypotension and bradycardia. The endozenous opiate, beta-endorphin, is stored along with pitulatary adrenocorticotorphin(ACTH), and the action of stressors seems to result in the release of both peptides. Therefore it seems likely that beta-endorphin is released during stress such as shock and that it might contribute to the hypotension. In order to probe this hypothesis, hypovolemic and endotoxin shock model were produced in rabbits. If these hemorrhage and endotoxin induced hypotension were mediated through the beta-endorphin release, the blockade of beta-endorphin should reverse such hypotension. Using the specific opiate antagonist, Naloxone-HCl, these hypotensions could be reversed and prevented as following results show, 1) As compared with the saline control, the hypovolemic shock experiment had a 36.49+/-14.44% increase in mean arterial pressure(MAP) within 2 to 3 minutes and the endotoxin shock had a 52.43+/-23.66% increase in MAP within 5 to 6 minutes after naloxone treatment (0.4mg/kg). 2) AS compared with the saline control, in both hypovolemic and endotoxin shock naloxone pretreatment(0.4mg/kg) could prevent the decrease of MAP significantly. 3) No significant difference were seen in heart rate between the control and both experimental groups. And plasma bets-endorphin was measured by radioimmunoassay(RIA), using beta-endorphin kit(Immunonucler corportion, Stillwater, Minnesota, USA) and Beckman 8,000 tau-Counter, in these shock model with following results. 1) Hemorrhage and endotoxin induced shock produced a significant increase in plasma beta-endorphin to about 3 times control and reversed by naloxone treatment(0.4mg/kg) significantly as compared with saline control. 2) AS compared with the saline control, in both hypovolemic and endotoxin experiments naloxone pretreatment(0.4mg/kg) could prevent the increase of plasma beta-endorphin significantly.
Rabbits ; Animals

The authors studied the early morphologic changes of peripheral nerve, which is known as relatively radioresistant tissue to the X-ray irradiation, but recently clamied by several clinician through development of neuropathies after radiotherapy of the malignacy. Rabbits were received 1,000 or 2,000 cGy of X-ray on the knee joint areas. Sciatic nerves were extracted out 30 minutes, 1, 2, 4, 24 hours, and 3 and 7 days after irradiation. The morphologic changes were observed by light and electron microscopes. The results were summarized as follows: Light microscopically, only mild edema is noted. Electron microscopically, irregular separation and folding of myelin sheath with spherical body formation are noted. Above features were more prominent at later stages and aggregated nests of fragmented myelin were scattered 16 hours after irradiation. Schwann cell necrosis is noted after 24 hours. But above degenerative changes were scarcely present 7 days after irradiation. There is no remarkable axonal changes. The interstitial tissue revealed swelling and irregularity of surface of endothelial cells, and edema. On the basis of the results, it may be concluded that the peripheral nerve is injured by irradiation in early stages, and the main target of irradiation injury is thought to be myelin sheath and Schwann cells, which would be reversible and could be recovered promptly.
Rabbits ; Animals

Roles of the nonclipped kidney in the development and maintenance of the high blood pressure in two- kidney, one clip hypertension remain to be defined. It has been known that the pathophysiology of hypertension is different by the presence or absence of the contralateral kidney in renal hypertension. The present study was undertaken to evaluate the effects of intrarenal norepinephrine in the nonclipped kidney exposed to the high blood pressure. Experiments were performed in 7-day two-kidney, one clip Goldblatt hypertensive and sham-operated normotensive rabbits. The basal levels of renal plasma flow and urine flow, and urinary excretion of electrolytes were higher in the nonclipped kidney of two-kidney, one clip Goldblatt hypertensive than in the corresponding kidney of sham-operated normotensive rabbits. Intrarenal infusion of norepinephrine increased renal perfusion resistance, and decreased renal hemodynamics and renal excretory function in a dose-dependent manner in both hypertensive and normotensive rabbits. The renal hemodynamics and excretory responses to intrarenal norepinephrine infusion were attenuated in two-kidney, one clip Goldblatt hypertensive rabbits. The changes by norepinephrine infusion of the renal excretory function were closely correlated with those in glomerular filtration rate or renal plasma flow. These results suggest that the impaired vascular reactivity in the nonclipped kidney is one of the early changes appeared in the course of multifactorial derangements in renal hypertension and that the impairment may be an adaptive response of the kidney to high blood pressure.
Rabbits ; Animals

Renin-angiotensin system is associated with development of diabetic nephropathy. Hyperglycemia is known as a primary etiologic factor about it. Thus, we investigated the effect of high glucose on angiotensin II(ANG II) binding in the primary cultured rabbit renal proximal tubule cells(PTCs). 25 mM glucose(48 hr incubation) induces inhibition of ANG II binding. The high glucose-induced inhibition of ANG II binding was recovered by the removal of glucose, suggesting the role of glucose specificity. High glucose-induced inhibition of ANG II binding was blocked by mepacrine and AACOCF3, phospholipase A2(PLA2) inhibitors. Indomethacin, a cyclooxygenase inhibitor, significantly prevented high glucose-induced inhibition of ANG II binding. However, nordihydroguaiareic acid(NDGA), a lipoxygenase inhibitor, and econazole, a cytochrome P450 epoxygenase inhibitor, did not block the effect of high glucose. This result suggest that cyclooxygenase metabolites of arachidonic acid(AA) released by high glucose are involved in the high glucose-induced inhibition of ANG II binding. Next, we examined the involvement of PKC in the effect of high glucose. Staurosporine, bisindolylmaleimide I, protein kinase C(PKC) inhibitors, and PD 98059, a p44/42 mitogen activated protein kinase(MAPK) inhibitor, significantly blocked high glucose- induced increase of [3H]-AA release and inhibition of ANG II binding. Indeed, 25 mM glucose increased PKC activity from cytosolic to particulate fraction and phosphorylation of p44/42 MAPK. In addition, high glucose increased phosphorylation of p44/42 MAPK and its activation was significantly blocked by PKC inhibitor. In conclusion, high glucose partially inhibits ANG II binding via PKC-MAPK-PLA2 signal pathway in the PTCs.
Rabbits ; Animals