No abstract available.
Rabbits*

No abstract available.
Rabbits*

No abstract available.
Rabbits*

No abstract available.
Rabbits*

No abstract available.
Rabbits*

While calcium phosphate ceramics meet some of the needs for bone replacement, they have some limitation of unresorbability and fibrous encapsulation without direct bone apposition during bone remodelling. To address these problem, we developed a new ceramic, calcium metaphosphate(CMP), and report herein the biologic response to CMP in subcutaneous tissue, muscle and bone. Porous CMP blocks were prepared by condensation of anhydrous Ca(H2PO4)2 to form non-crystalline Ca(PO3)2. Macroporous scaffolds were made using a polyurethane sponge method. CMP block possesses a macroporous structure with approximate pore size range of 0.3-1mm. CMP blocks were implanted in 8 mm sized calvarial defect, subcutaneous tissue and muscle of 6 Newzealand White rabbits and histologic observation were performed at 4 and 6 weeks later. CMP blocks in subcutaneous tissue and muscle were well adapted without any adverse tissue reaction and resorbed slowly and spontaneously. Histologic observation of calvarial defect at 4 and 6 weeks revealed that CMP matrix were mingled with and directly apposed to new bone without any intervention of fibrous connective tissue. CMP blocks didn't show any adverse tissue reaction and resorbed spontaneously also in calvarial defect. This result revealed that CMP had a high affinity for bone and was very biocompatible. From this preliminary result, it was suggested that CMP was a promising ceramic as a bone substitute and tissue engineering scaffold for bone formation.
Rabbits ; Animals

No abstract available.
Rabbits ; Animals

The author carried out an experimentation to clarify a possible pathogenesis of renal papillary necrosis induced by an univisceral Shwartzman reaction. The experimental animals were healthy white rabbits in weighing between 1.7 kg and 3.0 kg. Under the condition of ureterostomy, animals were pretreated with 0.5 cc of 50% ethyl alcohol and followed by administration of 0.2 ~ 1.5 mg endotoxin (E. coli 026 : B6, bacto lipopolysaccharide B. Difco, U.S.A.) as preparation in the renal pelvis. And then sacrificed at 10 minutes, 30 minutes, 1 hour, 2 hours, 6 hours and 24 hours after intravenous injection of 0.2 mg or 0.6 mg endotoxin through the ear veins, subjection to examine light and electron microscopically. The obtained results were summarized as follows: Papillary necrosis was developed in 88% among 18 cases excluding 6 cases died before sacrification. There were two types of necrosis, namely papillary and medullary type, but the former and combined forms of both types were the most common findings. Initial main target site of injury in renal papilla induced by endotoxiin was the endothelium of vasa recta and then followed by the Henle's loop, interstitial cell and collecting tubule respectively. Vascular injuries such as swelling and detachment of endothelium were observed since 10 minutes after endotoxin injection. Henle's loop showed stratification of basement membrane without consistent features with time lapses and initially observed fatty vaculoes at 1 hour after endotoxin injection were more eminent in 24 hours group. Main changes of interstitial cells were decrease of lipid droplets while increase of fatty vacuoles; the latter were initially observed in 1 hour group and more eminent in 24 hours group. Collecting tubule showed many fatty vacuoles especially in 24 hours group. It is thought that emergence of fatty vacuoles seems to be a kind of immature lipid droplets to compensate the increased demand of PC release due to continuous ischemic condition. In conclusion, it is thought that ischemic injury due to the vascular changes is pathogenic mechanism producing renal papillary necrosis. Endotoxin induced univisceral Shwartzman reaction in the kidney may be a good experimental model in studying renal papillary necrosis.
Rabbits ; Animals

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