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Biomedical subjects

K Shingu

Publications and source records attributed to K Shingu.

At least 181 records · Page 10Linked to original sources
PubMed1985

Acute tolerance to the analgesic action of nitrous oxide does not develop in rats.

The time course of nitrous oxide analgesia was studied in rats with a behavioral criterion, the tail-flick test to radiant heat. All rats were placed individually in a Plexiglas tube and exposed to either nitrous oxide, 75% in oxygen, or room air (control) for 2 hr. Analgesic potency was evaluated by prolongation of the time required to induce tail-flick. Although individual animals showed variability in the tail-flick time during exposure to nitrous oxide, no animal showed a tendency toward the development of tolerance, and a statistically significant sustained prolongation of tail-flick time was produced.

Analgesics↗
PubMed1985

Anticonvulsant actions of enflurane on epilepsy models in cats.

The effects of enflurane on three epilepsy models were studied in cats. The models used were seizures in amygdaloid kindled cats and those induced by bicuculline and penicillin. The authors found that not only a subconvulsive (1.5%) but a convulsive (3.5%) dose of enflurane suppressed the seizures in all models. There was no sign of activation by enflurane of the epileptic focal activities in the dose range studied: the penicillin-induced cortical seizure was suppressed completely, and the threshold dose of bicuculline required to induce seizure in normal cats and the threshold current required to induce seizure in amygdaloid-kindled cats were both increased by both the subconvulsive and convulsive dose of enflurane. The pattern of suppression was, however, dissimilar in each model. It was dose dependent in the case of penicillin-induced seizure, while it was biphasic in several aspects in the seizures of bicuculline-induced and amygdaloid kindled models. For the subconvulsive dose the degrees of increase in the thresholds required to induce seizure in bicuculline-induced and amygdaloid-kindled models were both greater than those for the convulsive dose of enflurane. In spite of such a definite suppression of the excitability of focus, the propagation of amygdaloid after-discharge was facilitated by the convulsive dose. The intensity of convulsion induced by suprathreshold dose of bicuculline was depressed in a dose-related manner. The intensity of the convulsion in the amygdaloid-kindled model was also suppressed when it was estimated by visual inspection of behavior and the degree of activation of the brain electrical activities. The authors conclude that there is little, if any, exacerbation by enflurane of preexisting epileptic foci, the only exception possibly being the case of certain myoclonic type epilepsies such as progressive myoclonic epilepsy and photosensitive epilepsy. This anesthetic probably can be used with a considerable degree of safety for epileptic patients.

Amygdala↗
PubMed1984

Scanning and transmission electron microscopy of cysts in the renal cortex of the macaque monkey.

Renal cysts in the cortex of the monkey kidney were observed by scanning and transmission electron microscopy, in an attempt to determine the three-dimensional structures of the epithelial cells in these cysts. The cysts were composed of a thin wall which limited a large spherical space containing a jelly-like substance and some wandering cells. Rudimentary tufts of glomerular capillaries and/or a mound-like swelling were present on the inner surface of the cyst wall, and the inner surface of the cysts was lined with an epithelium with pedicles. The epithelial cells were podocytes, whose surface structure was similar to that on the glomerular capillary in the normal renal corpuscle. The terminal foot processes were characteristically interdigitated not only on the glomerular capillaries, but also on the mound-like swelling and concave surface of the parietal portion of the cyst. A discrete, smooth-surfaced area was found on the side opposite to the glomerulus or swelling. This area was covered by squamous epithelial cells. At the peripheral zone of the smooth-surfaced area, elongated epithelial cells were demonstrated. Our findings indicate that the podocyte layer of the cyst corresponds to the internal leaflet of Bowman's capsule, and the squamous cell layer to the external leaflet. The mound-like swelling covered by podocytes is considered to represent a stage of possible evagination of the tufts of glomerular capillaries. There was no evidence of an opening of the urinary tubule in the cyst wall.

Animals↗
PubMed1984

Scanning electron microscope studies of lymphatic tissues with special reference to the structure of the reticulum.

Reticular cells of the lymph nodule in the rabbit appendix and the lymphatic pulp including the germinal center in the dog mesenteric lymph node were observed under the scanning electron microscope after removal of free cells. Three dimensional architecture and arrangement of the reticular cells varied by regions in the lymph nodule. The appendix lymph nodule encapsulated with the endothelium of lymphatic sinuses was subdivided into two regions: (1) a central region of sparsely arranged stellate cells with coarse processes and (2) a peripheral zone of densely arranged stellate cells with many delicate processes. In the lymph node, the germinal center contained a loosely formed network of delicate stellate cells. Peripheral reticular cells of the nodule were thread-like, extending concentrically around the germinal center or along the sinus wall. Many lateral bridges of the threads occurred segmentally. The reticular framework of the medullary cord formed spongy meshes by anastomoses of stellate cells. Cytoplasmic perforations were observed in the sinus wall of the medullary cord. Those may be for lymphocyte migration.

Animals↗
PubMed1983

Effects of halothane, isoflurane, enflurane, thiopental, and fentanyl on blood gas values in rats exposed to hypoxia.

In rats pretreated with phenobarbital breathing 10% oxygen, subanesthetic doses of halothane, isoflurane, enflurane, thiopental, and fentanyl caused hepatic injury. Because hypoxia per se can produce such injury, we hypothesized that the anesthetic-induced injury resulted from increased hypoxemia secondary to respiratory depression. Male Sprague-Dawley rats were pretreated with phenobarbital; half of the rats were fed and the other half were deprived of food for the 24 h before study. Isoflurane anesthesia was given for the placement of a catheter into the femoral artery. After 1 h of recovery, the rats were exposed to 10% oxygen. Control samples were obtained and halothane, isoflurane, enflurane, thiopental, or fentanyl was administered. Rats given food had higher PaCO2 and lower pH values than starved rats. Also, arterial oxygen saturation (SaO2) tended to be lower in rats given food. At concentrations of 0.15-0.2 MAC or higher, halothane, isoflurane, and enflurane slightly increased PaCO2 values relative to values for a control group exposed only to hypoxia. However, SaO2 and PaO2 did not show significant drug-induced changes. Fentanyl transiently decreased PaO2 and SaO2. Thiopental caused no changes. Thus, we conclude that subanesthetic doses of anesthetics may depress the ventilatory response to hypoxia but that this depression is inconsistent and appears to be too small to cause hepatic damage.

Anesthetics↗
PubMed1983

Hepatic injury induced by anesthetic agents in rats.

Recent studies on rats pretreated with phenobarbital indicate that anesthetic agents may produce hepatic injury even when metabolism of the anesthetic is almost negligible. This implies that anesthesia per se may cause hepatic injury. To evaluate this possibility, we determined the amount of hepatic injury produced by halothane, enflurane, isoflurane, thiopental, and fentanyl in rats pretreated with phenobarbital. Anesthetics were administered in doses ranging from 0.04-1.1 MAC (or their equivalent for thiopental or fentanyl) and were given with 10% oxygen for 2 h. Liver specimens taken 24 h later were examined microscopically for hepatic injury. At concentrations of 5-40% of MAC, all anesthetics produced more hepatic injury than did control conditions (i.e., exposure to only 10% oxygen for 2 h). There were no systematic differences among agents, nor did starvation before anesthetic exposure produce a difference among agents. Therefore, mechanisms other than anesthetic metabolism are needed to explain hepatic injury produced by anesthetic agents.

Anesthetics↗
PubMed1983

Effect of oxygen concentration, hyperthermia, and choice of vendor on anesthetic-induced hepatic injury in rats.

Although hypoxic rats exposed to anesthetics may develop hepatic injury, divergent results have been obtained. These discrepancies might be due to different levels of hypoxia, hypothermia, or choice of vendor. Male Sprague-Dawley rats purchased from Zivic-Miller were pretreated with phenobarbital for 4 days. After 24 h without phenobarbital, they were exposed to 2 h of hypoxia and halothane, enflurane, isoflurane, thiopental, or fentanyl. Rectal temperature was kept between 36.5 degrees C and 38.5 degrees C. All agents given in 10% oxygen produced more hepatic injury than did control conditions (exposure to 10% oxygen alone) (P less than 0.01). Only halothane given in 12% and 14% oxygen produced hepatic injury. No agent given in 20% or 100% oxygen demonstrated hepatotoxicity. In a separate study, rectal temperatures were kept between 32 degrees C and 34 degrees C during 2 h of exposure to 0.3 MAC halothane, enflurane, or isoflurane in 10% oxygen. Hypothermia prevented hepatotoxicity by enflurane and isoflurane, but not by halothane. Finally, although livers of rats obtained from Zivic-Miller were injured, specific pathogen-free rats from Charles River were not injured or were less injured by enflurane, thiopental, or fentanyl. Apparently, minor changes in experimental conditions can substantially affect results; hepatic hypoxia per se, anesthetic metabolism (especially that of halothane), and perhaps anesthesia itself may produce hepatic injury.

Anesthetics↗
PubMed1983

MAC values of thiopental and fentanyl in rats.

A comparison of the effects of thiopental or fentanyl with those of inhaled anesthetics requires the establishment of a comparable level of anesthetic potency. Accordingly, using the response of male Sprague-Dawley rats to tail-clamping, we determined the ED50S for thiopental and fentanyl. Half of the rats were pretreated with phenobarbital. After subcutaneous injection of various doses of thiopental or fentanyl, each rat was tested for movement in response to tail-clamping at 15-min intervals for 2 h. In untreated rats, the maximal effect of thiopental (i.e., the lowest ED50 value was 107 +/- 10 mg/kg, mean +/- SEM) occurred 75 min after injection. Although higher values were found at other times, differences from the nadir were relatively small. In rats pretreated with phenobarbital, the lowest value (130 +/- 8 mg/kg) occurred at 60 min. The lowest ED50S for fentanyl (52 +/- 7 micrograms/kg for control rats, and 73 +/- 14 micrograms/kg for pretreated rats) were found at 15 min.

Anesthesia, Intravenous↗
PubMed1982

Hypoxia per se can produce hepatic damage without death in rats.

To evaluate the importance of hypoxia itself on halothane-induced hepatic injury in the rat, the question of whether hypoxia could injure the liver without causing death was investigated. Male Sprague-Dawley rats pretreated with phenobarbital (1 mg/ml of drinking water, 4 days) and deprived of food for 24 hours were exposed to 6%, 7%, 8%, or 10% inspired oxygen with 0%, 5%, or 7.5% carbon dioxide for 2 hours. Several rats died when given 6% oxygen with 0% or 7.5% carbon dioxide, but all other rats survived. Without carbon dioxide, oxygen at a concentration of 7% or 8% produced more injury than did room air, and 6% oxygen produced the most severe damage. These results demonstrate that in rats hypoxia per se may be an important factor in causing hepatic damage.

Animals↗
PubMed1982

Hypoxia may be more important than reductive metabolism in halothane-induced hepatic injury.

To evaluate the relative importance of halothane metabolism and liver hypoxia in the occurrence of hepatic injury, the injury produced in hypoxic rats exposed to identical MAC hours of halothane but at various concentrations of halothane was compared. Groups of male Sprague-Dawley rats were pretreated with phenobarbital for 4 days, and 24 hours later they were exposed to 10 hours of 10% oxygen and concomitantly 0.2 MAC hours of halothane at the following anesthetic concentrations: 0.02% for 10 hours, 0.1% for 2 hours, 0.5% for 24 minutes, or 2.5% for 4.8 minutes. A control group received only 10% oxygen for 10 hours. Liver specimens taken 24 hours later demonstrated concentration-dependent damage; high concentrations given briefly produced more damage than lower concentrations given for long periods. As hepatic clearance of halothane by metabolism appears to be a saturable phenomenon, these results suggest that hypoxia per se may be more important than halothane metabolism in causing liver damage.

Animals↗
PubMed1981

E.E.G. activity during halothane anaesthesia in man.

The effects of i.v. administration of suxamethonium and noxious stimulation induced by skin incision on the e.e.g. were studied during halothane anaesthesia in man. These stimuli induced activation of the e.e.g. which was represented by either low-voltage fast waves or high-voltage slow waves. The low-voltage fast wave response was observed in adult patients while the high-voltage slow wave response was the predominant response in infants and children aged less than 8 yr. Suxamethonium induced the high-voltage slow wave response in 77% of cases; skin incision in 88%. The e.e.g. of four infants aged less than 60 days did not show activation with either stimulus. Both types of e.e.g. activation were associated with an increase in heart rate, increase in arterial pressure and pupillary dilatation. The possible mechanisms involved in the production of activation of e.e.g. by i.v. administration of suxamethonium are discussed.

Adolescent↗
PubMed1981

Pentobarbital-anesthetized and decerebrate cats reveal different neurological responses in anesthetic-induced analgesia.

Cats were used to assess the significance of differences in animal preparations in the study of anesthetic-induced analgesia. Comparison was made between pentobarbital-anesthetized and decerebrate non-anesthetized cats. Bradykinin dissolved in normal saline was injected into the femoral artery as a noxious stimulus, and the neural response in the spinal cord lateral funiculus was recorded using the multi-unit activity technique. The magnitude of the neural response and the changes in spontaneous firing were compared before and after cervical cord transection at C1. Before the transection, the response was greater in anesthetized than in decerebrate cats. The cord transection potentiated the response in both preparations, but the degree of potentiation was greater in decerebrate than in anesthetized cats. These studies confirmed the presence of a descending pain inhibition system acting tonically on the nociceptive neural mechanisms in the spinal cord, and indicated the susceptibility of this system to pentobarbital. We conclude that pretreatment with pentobarbital induces pharmacologically a state of partial spinal cord transection and reduces the effects of drugs acting through supraspinal CNS structures.

Animals↗
PubMed1981

Activation of the supraspinal pain inhibition system by ketamine hydrochloride.

The neurophysiologic mechanism of ketamine-induced analgesia was studied in cats under conditions of electrolytic decerebration or pentobarbital anesthesia. Injection of bradykinin into the femoral artery served as the noxious stimulus and the neural response in the lateral funiculus of the spinal cord was recorded by the multi-unit activity technique. Ketamine depressed the bradykinin-induced response more markedly in decerebrate, non-anesthetized cats than in pentobarbital-anesthetized cats. The depressant action disappeared following cervical cord transection at C1, in both decerebrate non-anesthetized and pentobarbital-anesthetized cats. Thus the analgesic action of ketamine is probably exerted mainly through activation of the supraspinal pain inhibition system and a direct action on the spinal cord nociceptive neural mechanism, if any, is slight. The excitatory action of ketamine on the supraspinal pain inhibition system is susceptible to the depressant action of pentobarbital.

Animals↗