A case of sudden death after gingival injection of a therapeutic dose of lidocaine: distribution of lidocaine in whole blood and various tissues

We report a case of sudden death after gingival injection of lidocaine, which made us suspect overdosing or anaphylactic shock. Using liquid chromatography-mass spectrometry (LC-MS), we measured the lidocaine concentrations in whole blood and tissues including the gingivae. The lidocaine concentration in blood (0.70 μg/ml) was lower than the therapeutic level. Lidocaine levels distributed to various organs were also low. Among them, the lung showed the highest level, followed by the liver, brain, and spleen. The concentrations in the gingivae with and without pus were 938 μg/g and 1048 μg/g, respectively. Together with the above analytical data, we made histopathological examinations, and tryptase and immunoglobulin E (IgE) assays as markers of anaphylactic shock. Macroscopically, myocardial ischemic changes were observed over relatively large areas. In such cardiac areas, there were focal necrosis, disarrangement of cardiac muscles, and stromal edema microscopically. The tryptase value was within the normal range. By carefully considering all data obtained from the victim, we diagnosed that the victim died of heart failure under the stress of the dental treatment.     

Kinetics of sequential metabolism from D-leucine to L-leucine via alpha-ketoisocaproic acid in rat.

D-Leucine is considered to be converted into the L-enantiomer by two steps: oxidative deamination to form alpha-ketoisocaproic acid (KIC) and subsequent stereospecific reamination of KIC. We investigated the pharmacokinetics of leucine enantiomers and KIC in rats to evaluate how deamination of D-leucine, reamination of KIC, and decarboxylation of KIC were affected to the overall extent that converted D-leucine into the L-enantiomer. After intravenous administrations of D-[(2)H(7)]leucine, L-[(2)H(7)]leucine, or [(2)H(7)]KIC, their plasma concentrations together with endogenous L-leucine and KIC were determined by gas chromatography-mass spectrometry. The rapid appearances of [(2)H(7)]KIC and L-[(2)H(7)]leucine were observed after administration of D-[(2)H(7)]leucine, whereas no detectable amount of D-[(2)H(7)]leucine was found after administrations of [(2)H(7)]KIC or L-[(2)H(7)]leucine. The fraction of conversion from D-[(2)H(7)]leucine into [(2)H(7)]KIC (F(D-->KIC)) was estimated by using the area under the curve (AUC) of [(2)H(7)]KIC on the D-[(2)H(7)]leucine administration [AUC(KIC(D))] and that of [(2)H(7)]KIC on the [(2)H(7)]KIC administration (AUC(KIC)) to yield 70.1%. The fraction of conversion from [(2)H(7)]KIC to L-[(2)H(7)]leucine (F(KIC-->L)) was 40.2%. The fraction of conversion from D-leucine to the L-enantiomer (F(D-->L)) was considered to be the product of F(D-->KIC) and F(KIC-->L), indicating that 28.2% of D-[(2)H(7)]leucine was metabolized to L-[(2)H(7)]leucine via [(2)H(7)]KIC. These results suggested that the relatively low conversion of D-leucine into the L-enantiomer might depend on irreversible decarboxylation of KIC. Regardless of [(2)H(7)]KIC, F(D-->L) was also calculated directly using AUC(L(D)) and AUC(L) to yield 27.5%. There were no differences between the two F(D-->L) values, suggesting that almost all of the formation of L-[(2)H(7)]leucine from D-[(2)H(7)]leucine occurred via [(2)H(7)]KIC as an intermediate.     

A case of cranial polyneuropathy presenting with prominent facial diplegia, elevated serum Borrelia burgdorferi antibody and lymphocytic pleocytosis

A 54 year-old male patient developed acute cranial polyneuropathy including prominent facial diplegia and radicular++-neuritis. He was proven to have lymphocytic pleocytosis, and elevated serum Borrelia burgdorferi antibody to X800 (normal; less than X200). A diagnosis of typical early neuro-borreliosis was made after these clinical and laboratory findings. This case is the first neuro-borreliosis showing the triad of neurological manifestations (meningitis, cranial neuritis, radicular++-neuritis) in Japan. It is concluded that neuro-borreliosis should be considered to be a cause of acute cranial polyneuropathy, particularly of facial diplegia, even if the patient has no apparent history of a tick bite.     

Evidence for uptake of basement membrane by differentiating ameloblasts in the rat incisor enamel organ

Demonstration of type-IV collagen and acid phosphatase (ACPase) was carried out in the rat incisor enamel organ after the animals were fixed by perfusion with periodate-lysine-paraformaldehyde. Their incisors were dissected out, demineralized with EDTA, and prepared into 6-microns-thick frozen sections. The sections, which had been treated by means of antibody incubation for type-IV collagen, were washed with a Trismaleate buffer, incubated in Novikoff's medium for acid phosphatase (ACPase), and then incubated in a 3, 3'-diaminobenzidine solution. After osmification, the sections were embedded in epoxy resin for electron microscopy. The plasma membranes of the distal ends of the inner-enamel-epithelial cells were relatively even and were lined with a basement membrane. Type-IV collagen was localized both in the lamina densa and in the filaments attached to the lamina densa. In differentiating ameloblasts, the remarkably undulating distal plasma membranes formed irregular shallow and deep invaginations, and small cytoplasmic processes that penetrated the basement membrane. Coated pits occurred in various parts of these undulating plasma membranes. Positive reaction to type-IV collagen was observed in the invaginations and coated pits. ACPase-positive granules, present in inner-enamel-epithelial cells, increased in number and sometimes appeared close to both shallow and deep invaginations of differentiating ameloblasts. These results indicate that type-IV collagen in the basement membrane of the enamel organ is removed and degraded by differentiating ameloblasts by means of their engulfing system.     

Immunoelectron microscopic analysis of the distribution of tyrosine kinase receptor B in olfactory axons

To determine the morphological basis for the neurotrophic effects of brain-derived neurotrophic factor (BDNF) in the primary olfactory pathway (POP), tyrosine kinase receptor B (TrkB), a membrane-bound receptor for BDNF, was identified and localized in axons of olfactory receptor cells (ORC) of neonatal rat olfactory mucosa using immuno-histochemical and-cytochemical techniques. Initially, the immunospecificity of an anti-TrkB antibody that had been used as a specific antibody for full-length TrkB was confirmed in the olfactory mucosa. Then, a combination of a reduced osmium-LR-White and post-embedding immunogold technique was applied to ORC axons in the lamina propria just beneath the olfactory epithelium. Immunogold particles, which indicate TrkB immunoreactivity, were noted either in close association with the plasma membranes of ORC axons, and designated plasma-lemmal (PL), or within their cytoplasm, and designated cytoplasmic (CP). Most PL particles were seen in the CP portion of the axonal plasma membranes, suggesting that the anti-TrkB antibody binds to the membrane-inserted TrkB that acts as a functional receptor. Some CP particles were on vesicular structures. Quantitative analysis demonstrated that the ratio of CP to PL particles was 7∶3, and this ratio was constant between animals examined (n=5). Because membrane proteins are wrapped in vesicles and transported within the axonal cytoplasm and inserted into the plasma membrane to function there, the present study suggests that TrkB is transported within the cytoplasm of ORC axons and is positioned as a functional receptor for BDNF in their membranes.     

Application of gypsum-bonded investment containing niobium carbide on casting of alloy for metal-ceramic restoration

Experimental gypsum-bonded investments containing 0.5-5.0 wt% NbC were prepared by mechanical mixing of each powder. Setting and thermal expansion measurement, compressive strength and casting accuracy for Ni-Cr alloy for metal-ceramic restoration were investigated. Analysis of NbC during heating was carried out by X-ray diffraction, TG-DTA and SEM. NbC was oxidized to Nb2O5 with a volume change between 300-600 degrees C, as in the following equation: 2NbC + 4 1/2O2----Nb2O5 + 2CO2 The theoretical volume of 1/2Nb2O5 calculated from the lattice constants according to JCPDS file was approximately 4 times larger than that of NbC. The experimental investments of 70 wt% cristobalite and 30 wt% gypsum containing 2.0, 3.0 and 5.0 wt% NbC showed large thermal expansion of 7.0, 10.0 and 13.0% respectively. The investment containing 2.0 wt% NbC showed nearly the same casting accuracy for Ni-Cr alloys for metal-ceramic restoration as the commercial phosphate-bonded investment.     

Synergism by sodium L-ascorbate but inhibition by L-ascorbic acid for sodium saccharin promotion of rat two-stage bladder carcinogenesis

Since both sodium L-ascorbate (Na-AsA) and sodium saccharin (Na-Sac) promote two-stage bladder carcinogenesis in rats, synergism of the two chemicals was investigated with special reference to the role of urinary pH and Na+ concentration. Male F344 rats were given 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine in the drinking water for 4 wk and then treated with basal diet containing 5% Na-Sac, 5% Na-AsA, 5% Na-Sac plus 5% Na-AsA, 5% L-ascorbic acid (AsA), 5% Na-Sac plus 5% AsA, or no added chemical for 32 wk. Treatment with Na-Sac or Na-AsA alone significantly increased the induction of neoplastic and preneoplastic lesions of the bladder. Na-Sac plus Na-AsA also induced these bladder lesions significantly when compared with the controls, and the number of lesions was greater than the sum of the lesions in the groups treated with Na-Sac alone or Na-AsA alone. In contrast, the induction of carcinomas and papillomas in rats treated with Na-Sac plus AsA was not significantly different from the controls. In addition Na-Sac plus Na-AsA produced an elevation of urinary pH and Na+ concentrations, although the increases were not different from those in rats fed Na-Sac or Na-AsA alone. Na-Sac plus AsA, however, did not cause elevation of urinary pH, although it increased urinary Na+ concentration. Thus, the bladder carcinogenesis promotion by Na-Sac was synergized by Na-AsA and inhibited by AsA. This modulation was associated with changes of urinary pH and Na+ concentration.     

Clinical evaluation of the sedative effect of HEMA solution on the hypersensitivity of dentin

The sedative effect of the dentin primer, 35% hydroxyethyl methacrylate (HEMA) solution, on dentin hypersensitivity was clinically evaluated. Exposed root surfaces of teeth were cleaned with neutralized 0.5 mol/L EDTA and treated with 35% HEMA solution followed by the application of a commercial dentin bonding agent. The extent of sedation was estimated by comparison of the responses before and after treatment to irritation by a cold water spray, compressed air blast and scratching with an explorer. The degree of the response to these irritations was decreased significantly upon the combined application of HEMA and commercially available dentin bonding agents though it was still ineffective in nearly 30% of the 48 cases tested.     

Various urinary properties in bladder tumor patients

Urinary electrolytes, pH, urea nitrogen, creatinine, uric acid and osmolarity were measured in patients with bladder tumors and compared with those of a control group. There were 41 bladder tumor patients ranging in age from 29 to 87 (average 64) years with a male:female ratio of 32:9. According to histopathological classification of the bladder tumors, there were 34 transitional cell carcinomas (TCC) (21 G1, 10 G2, 3 G3), four squamous cell carcinomas, two adenocarcinomas and one inverted papilloma. The control group comprised 29 patients ranging in age from 35 to 80 (average 63) years with a male:female ratio of 26:3. Four urine samples were collected from each patient: early morning on the day of admission, just after admission, early morning on the day of return to hospital after temporary discharge, immediately after return to hospital after temporary discharge. The results indicated that the urinary Ca2+ and uric acid values were significantly lower in the bladder tumor group than in the control group. The urinary pH tended to be somewhat higher than in the control group, and the pH values tended to be especially high in the TCC G3 patients. There were differences in the various urinary properties between the TCC G1 and G2 and the TCC G3 patients.