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Biomedical subjects

K Shimoji

Publications and source records attributed to K Shimoji.

At least 145 records · Page 8Linked to original sources
PubMed1989

Tolerance to N2O-induced alterations in somatosensory evoked potentials.

The effect of nitrous oxide (N2O) on somatosensory evoked potentials from the cortical (CEP) and spinal cord (SCP) regions in response to forepaw stimulation was studied in ketamine-anesthetized and mechanically ventilated rats. The CEP was recorded from the skull over the contralateral somatosensory area; the SCP was recorded from the supraspinous ligament at C57-6 and L1-2 levels of the spine. Rats were exposed to 70% N2O for 5 h, whereupon N2O was withdrawn for 2 h. Thereafter, the rats were re-exposed to N2O for 10 min. The N13-P21 component of the CEP, the slow positive wave (P2) of the segmental SCP, and the heterosegmental positive cord dorsum potential (HSP) were significantly suppressed by N2O, while the large negative (N1) component of the segmental SCP remained unchanged. A partial recovery of the CEP and HSP was observed during the 5 h of N2O anesthesia, while significant recovery of the P2 component of the SCP was not observed. The withdrawal from N2O following 5 h exposure caused an augmentation of the CEP (When compared to the control values). Re-exposure of rats to N2O again caused the suppression of these potentials as in the initial exposure. The results suggest that the phenomenon of tolerance to N2O in terms of evoked potentials develops within 5 h in the brain but not in the spinal cord.

Journal Article↗
PubMed1989

[Two case reports of septic shock due to Vibrio vulnificus with liver cirrhosis].

We have recently experienced a case of Vibrio vulnificus septicemia which occurred in a patient with hepatic cirrhosis, and as we were able to give early antibiotic treatment, the patient survived. We would like to report this case here together with another case experienced 2 years ago. Case 1 was a 58-year-old male who was attending our hospital as an outpatient for hepatic cirrhosis. At 5:30 pm on August 8, 1987, he consumed abalone and giant clam and at 9 pm complained of high fever with shaking chills. He was admitted to our department as an emergency case. Cefoperazone was administered resulting in a decline of fever on the following day. During the course of treatment he fell transiently into pre-DIC, but due mainly to the administration of antibiotics his condition was subsided. Case 2 was a 53-year-old male who was under medical care in our hospital for grave hepatic cirrhosis. On October 11, 1985, he consumed sushi and two days later suffered chills and pyrexia. A blood culture revealed Vibrio vulnificus. His condition improved transiently with administration of Cefazolin, but oliguria, hypotension and ascites occurred subsequently, and finally the patient died on the 22nd day.

Humans↗
PubMed1989

[Death after delayed recovery and respiratory failure following injection sclerotherapy in a small infant under general anesthesia].

A 12 month old boy weighing 6.4kg with esophageal varices caused by congenital biliary hypoplasia was scheduled for emergency sclerotherapy under general anesthesia. Anesthesia was induced with thiamylal sodium 3mg.kg-1 i.v. and then maintained with nitrous oxide, oxygen and a low concentration of enflurane, paralysed with pancuronium bromide. As soon as a small dose of sclerosant (5% ethanolamine oleate) was injected, transient moderate bradycardia and hypotension occurred. As his spontaneous breathing was very weak and the movements of extremities convulsive and his consciousness drowsy, prophylactic respiratory care was carried out. He had pneumonia and manifestation of DIC 4 days after sclerotherapy. He died of a massive tracheal hemorrhage. The cause of the patient's death seemed largely due to the several toxicities of sclerosant itself. We stress that although this therapy is effective for the child with portal hypertension, the incidence of complications might be high in patient with severely damaged liver function. Therefore, anesthetic and postoperative management in injection sclerotherapy should be performed very carefully.

Anesthesia, General↗
PubMed1989

Hypoxia in brain slices.

The effects of hypoxia on hippocampal CA1 neurones in tissue slices of the rat brain were studied in vitro by intracellular recording. In response to superfusion of a hypoxic medium equilibrated with 95%N2-5% CO2, a majority of the neurones showed a transient depolarization followed by a hyperpolarization of 5-15 mV in amplitude and 4-12 min in duration. The hyperpolarization was, in turn, followed by a slow depolarization which within 20 min of hypoxic exposure reached a plateau level of about 25 mV above the prehypoxic resting potential. Both the initial hyperpolarization and subsequent depolarization were associated with a reduction in membrane resistance. The hyperpolarization reversed in polarity at a membrane potential of -83 mV. There was an almost linear relationship between amplitude of the hyperpolarization and membrane potential. The hyperpolarization was markedly enhanced in potassium-free media and was depressed in high-potassium solution. Superfusion of ouabain (5-7 microM)-containing medium in normoxic conditions produced hyperpolarizing and depolarizing responses similar to those elicited by hypoxic exposure. The slow depolarization was also mimicked by elevation of the extracellular potassium concentration to 10-20 mM. Evoked i.p.s.p.s were abolished within 4 min of hypoxic exposure while evoked e.p.s. p.s were maintained for about 20 min of hypoxic superfusion. Soma spikes of the neurones elicited by a depolarizing pulse were also well preserved. Their threshold was, however, raised, concomitant with a decrease in the peak amplitude. In a minority of the neurones the slow depolarization was suddenly followed by a rapid depolarization, after which the neurones showed no functional recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Three case reports of relapsing polychondritis and their immunopathological analysis].

Three cases of relapsing polychondritis are reported. They all complained of dyspnea, which derived from tracheal involvement. Other clinical manifestations were saddle nose (3 cases), painful swelling of ear (2 cases), arthralgia (1 case) ophthalmodynia (1 case). The pathological examination of biopsied cartilage of the pinnae showed loss of basophils with cellular infiltration, fibrosis and breakdown of the matrix. We also performed PAP (Peroxidase-Anti-Peroxidase) staining of biopsied cartilage, which showed the deposition of IgG, C3, C4 and fibrinogen. The results suggested that the pathogenesis of RP might be related to the autoimmune mechanism.

Aged↗
PubMed1989

The effect of alpha-interferon on the liver in a patient with hairy cell leukemia: light and electron microscopic studies.

A daily dose of 3 x 10(6) or 6 x 10(6) units of alpha-interferon was given during two 4- to 6-month periods to a 65-yr-old male patient with hairy cell leukemia, reducing splenomegaly and decreasing the number of hairy cells. Liver biopsy specimens taken during treatment revealed predominantly decreased hairy cell infiltration in the dilated sinusoids and enlarged or vacuolar nuclei of hepatocytes, compared with those in the liver before treatment. The ultrastructure of hepatocytes in specimens taken during treatment showed cytoplasmic vacuoles, weakly stained glycogen particles, and conspicuously decreased endoplasmic reticulum. Liver tests revealed decreased serum cholinesterase and total cholesterol levels in the early stage of treatment, low levels of total protein and albumin during treatment, and a very low value in the [13C]aminopyrine breath test. No clinical reports have been made on the decreased microsomal function during treatment with interferon. alpha-Interferon damaged the endoplasmic reticulum of hepatocytes, although it was effective for the reduction of hairy cells in the liver of hairy cell leukemia.

Aged↗
PubMed1988

Changes in spontaneous firing patterns of rat hippocampal neurones induced by volatile anaesthetics.

1. The effects of the volatile anaesthetics, halothane, isoflurane and enflurane, on rat hippocampal CA1 and CA3 neurones in in vitro preparations were studied by intracellular recording methods. 2. The three anaesthetics, at concentrations similar to those used clinically (0.2-1.2 mM), initially increased and then subsequently decreased the spontaneous firing of CA1 neurones without affecting the resting membrane properties or the EPSPs evoked by focal stimuli. 3. The anaesthetics at these concentrations depressed both the fast after-hyperpolarization of the soma spike and the post-tetanic hyperpolarization induced by repetitive stimulation. They also decreased the IPSPs evoked by focal stimuli. 4. The threshold for spike generation was gradually elevated by as much as 4-6 mV during application of the anaesthetics at these concentrations. The subthreshold potential oscillations (which are likely to be associated with periodic alterations in non-inactivating Ca2+ and Na+ currents) were enhanced in the low concentrations (0.2-0.5 mM), but were depressed in the high concentrations (0.8-1.2 mM). 5. The results suggest that the transient increase in the firing frequency was caused by a depression of both the spike after-hyperpolarization and the post-tetanic hyperpolarization, and that the reduction of spontaneous firing was mainly due to an elevated threshold for spike generation. 6. The three anaesthetics altered the pattern of spontaneous spike-firing in CA3 neurones from solitary spiking to burst firing without affecting the resting membrane properties. 7. The effects of the anaesthetics on the active membrane properties and the postsynaptic potentials in CA3 neurones were similar to the effects in CA1 neurones. 8. In the majority of CA3 neurones, soma spikes elicited by depolarizing current pulses were followed by a Ca2+-dependent after-depolarization, which was in turn followed by a prolonged after-hyperpolarization (post-burst hyperpolarization). The anaesthetics facilitated the after-depolarizing potential, while they depressed the post-burst hyperpolarization. Combination of the two effects would give rise to the highly stereotyped burst (about 1 Hz in frequency) in the presence of the volatile anaesthetics.

Action Potentials↗
PubMed1988

Lesions of spinal and trigeminal dorsal root entry zone for deafferentation pain. Experience of 35 cases.

Spinal and trigeminal dorsal root entry zone destruction (DREZ-tomy) was performed on 35 patients with deafferentation pain of various types. Overall, satisfactory pain relief was obtained in 65.5% of spinal DREZ-tomy cases in the follow-up observation. The result in the brachial plexus avulsion group was the best (82.4% improved), followed by the limb pain group without root avulsion (50.0%), but the truncal or visceral pain group showed the worst result (33.3%). Two patients with postherpetic trigeminal neuralgia were completely relieved of pain in the average follow-up period of 32 months, while in 2 patients with postrhizotomy facial pain, pain recurred 4 months after the operation in 1, and, in the other, pain in the medial part of the face remained unchanged. Complications were seen in about 60% of the patients, which were, however, all mild, except for 2 cases of death due to gastrointestinal disease.

Adult↗
PubMed1988

Effects of propranolol and nitroglycerin on cephalad collateral venous flow in patients with cirrhosis: evaluation using transesophageal real-time two-dimensional Doppler echography.

We used transesophageal real-time two-dimensional Doppler echography (TE2DD) to assess the effects of propranolol (n = 18, 6 mg each) and nitroglycerin (n = 18, 0.5 mg each) on blood flow in the intercostal veins, azygos vein, thoracic aorta, and esophagogastric varices. The primary disease in all of the patients was liver cirrhosis. Propranolol infusion markedly reduced the flow velocity in the varices, intercostal vein, azygos vein, and thoracic aorta (-24%, -41%, -34%, and -24%, respectively). It also significantly reduced the blood flow volume index (BFVI), defined as mean velocity in cm/sec X the square of the diameter in cm2 of both the azygos vein and the aorta (-34%, -21%, respectively). Nitroglycerin infusion did not cause significant changes in the hemodynamics of the above vessels, because the hemodynamic responses to the drug differed from individual to individual. The BFVI of the azygos vein correlated well with the azygos venous flow measured by the conventional thermodilution technique (r = 0.79, p less than 0.01). TE2DD appears to be a useful method for studying the hemodynamics of ascending collaterals in patients with portal hypertension.

Aged↗
PubMed1988

[In vitro susceptibilities of clinical isolates of Staphylococcus aureus].

In vitro susceptibilities of 350 strains of Staphylococcus aureus to ampicillin (ABPC), methicillin (DMPPC), cloxacillin (MCIPC), cefazolin (CEZ), cefmetazole (CMZ), cefmenoxime (CMX), latamoxef (LMOX) and 5 non-beta-lactam antimicrobial agents were determined according to the standard method of Japan Society of Chemotherapy. Frequencies of the appearance of resistant organisms (MIC greater than or equal to 12.5 micrograms/ml) to beta-lactam antibiotics were 45% for ABPC, 27% for DMPPC, 11% for MCIPC, 24% for CEZ, 15% for CMZ, 36% for CMX and 51% for LMOX. To non-beta-lactam antimicrobial agents, resistant strains appeared at 31% to gentamicin, 15% to amikacin, 0.6% to minocycline (MINO), 1% to norfloxacin (NFLX) and 65% to fosfomycin (FOM). More than 80% of DMPPC-resistant strains were also resistant to LMOX, CMX, ABPC, FOM, and CEZ, but most of those were susceptible to MINO and NFLX. Incidence of DMPPC-CEZ resistant S. aureus was 23% of the 350 strains tested. As stated above, multiply resistant strains of S. aureus are present throughout different hospitals in Okinawa.

Ampicillin↗
PubMed1988

[Effects of halothane and isoflurane on the canine duodenal paraneurons].

Administration of amino acid solution (50 mM tryptophane and phenylalanine in saline) into the canine duodenum is known to cause an increase in pancreatic secretion. This response is mediated by the excitation of duodenal endocrine cells, paraneurons, which release cholecystokinin (CCK) into the systemic circulation in response to intraluminal amino acid stimuli. Pancreatic secretory cells are then evoked by the CCK in the blood to secrete the juice into the duodenum. The authors investigated the effects of two general anesthetics, halothane and isoflurane, on this response. Nine mongrel dogs were subjected to this study. Each dog underwent laparotomy under nitrous oxide (75%)-oxygen (25%) anesthesia with pancuronium (GO-Pb). The duodenal loop was exposed and two polyethylene cannulae (18Fr) were introduced into the loop. Proximal cannula was for the administration of the amino acid solution into the loop, and distal one was for drainage of the solution. The pancreatic duct was inserted with a polyethylene catheter, through which pancreatic juice was collected and measured for the volume and protein output by spectrophotometry. After these surgical procedures, the pancreatic secretory response to intraluminal amino acid stimuli was examined under GO-Pb (Control). Then halothane (1.0%) (Group 1, four dogs) or isoflurane (2.0%) (Group 2, five dogs) was administered for 30 min and the same response was tested. The pancreatic secretory response to intraluminal amino acid stimulus was suppressed by the surgical concentrations of both halothane (1.0%) and isoflurane (2.0%). Neither halothane nor isoflurane suppressed the pancreatic secretory response evoked by intravenous CCK infusion (10 Ivy Dog Units.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Effects of pentobarbital and ketamine on brain injury-induced anti-ischemic activity.

Survival rates following incomplete brain ischemia induced during pentobarbital anesthesia were significantly higher in mice with a minor brain injury, inflicted one week before, than in those given a sham operation. Improvement of the survival rates in mice with brain injury, however, became insignificant when brain ischemia was imposed during ketamine anesthesia, suggesting that the actions of certain factors or protective mechanisms against brain ischemia, developed by brain injury, are antagonized by ketamine and/or potentiated by barbiturate anesthesia.

Anesthesia↗
PubMed1987

Effects of hypoxia on rat hippocampal neurones in vitro.

1. The effects of hypoxia on the rat hippocampal CA1 neurones in tissue slices of the rat brain were studied in vitro by intracellular recording. 2. In response to superfusion of a hypoxic medium equilibrated with 95% N2-5% CO2, a majority of the neurones showed a hyperpolarization of 5-15 mV in amplitude and 4-12 min in duration. The hyperpolarization was, in turn, followed by a slow depolarization which within 20 min of hypoxic exposure reached a plateau level of about 25 mV above the pre-hypoxic resting potential. Both the initial hyperpolarization and subsequent depolarization were associated with a reduction in membrane resistance. 3. The hyperpolarization reversed in polarity at a membrane potential of -83 mV. There was an almost linear relationship between amplitude of the hyperpolarization and membrane potential. The hyperpolarization was markedly enhanced in potassium-free media and was depressed in high-potassium solutions. 4. The hyperpolarization was not significantly affected by low-chloride or low-sodium medium or by solution containing tetraethylammonium (10 mM), 4-aminopyridine (1.5 mM) or caesium (3 mM). Moreover, intracellular injection of ethyleneglycol-bis-(beta-aminoethylether)N,N-tetraacetic acid (EGTA) did not alter the hyperpolarization. On the other hand, barium (0.5 mM)-containing medium reduced the amplitude of the hyperpolarization by 20-40%. 5. Superfusion of ouabain (5-7 microM)-containing medium in normoxic conditions produced hyperpolarizing and depolarizing responses similar to those elicited by hypoxic exposure. The slow depolarization was also mimicked by elevation of the extracellular potassium concentration to 10-20 mM. 6. Evoked i.p.s.p.s were abolished within 4 min of hypoxic exposure while evoked e.p.s.p.s were maintained for about 20 min of hypoxic superfusion. Soma spikes of the neurones elicited by a depolarizing pulse were also well preserved. Their threshold was, however, raised, concomitant with a decrease in the peak amplitude. 7. When the slice was reoxygenated after 20-40 min of hypoxic exposure, the neurones immediately began to repolarize and showed a transient hyperpolarization of 5-10 mV in amplitude and 1-2 min in duration. The membrane potential, input resistance and action potential returned to the pre-hypoxic levels after 15-20 min of reoxygenation. The amplitude of the reoxygenation-induced hyperpolarization was not significantly changed when the membrane was hyperpolarized or depolarized. The hyperpolarization was eliminated by potassium-free medium or solution containing ouabain (1 microM).(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗