A new method for difficult endotracheal intubation: the use of a jet stylet introducer and capnography.
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Biomedical subjects
Publications and source records attributed to R F Spencer.
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The effect of prenatal exposure to methadone via maternal osmotic minipumps on the expression of acetylcholinesterase (AChE) and choline acetyltransferase (ChAT) has been studied by light microscopy in the striatum of male and female rats. At postnatal day 10, rats of both sexes exhibit reduced intensity of ChAT-immunoreactive staining in striatal neurons in the methadone-treated group in comparison to either untreated or water-treated controls. Although the number and distribution of ChAT-immunoreactive neurons appear to be similar across all three groups, the size (cross-sectional area) of these neurons is significantly smaller in the methadone-treated animals. By postnatal day 22, there are no differences in the ChAT immunoreactivity of striatal neurons between the water-treated and methadone-treated animals. The size of these neurons in female animals of both treatment groups is significantly larger than those of male animals in the same groups at postnatal day 22. AChE histochemical staining is qualitatively similar between treatment groups in both age groups. Thus, prenatal exposure to methadone appears to produce a delay in the expression of ChAT in striatal neurons. It remains to be demonstrated whether these differences are a direct effect of methadone exposure or are a consequence of neonatal withdrawal.
The cat superior colliculus (SC) receives a dense cholinergic input from three brainstem nuclei, the pedunculopontine tegmental nucleus, the lateral dorsal tegmental nucleus, and the parabigeminal nucleus (PBG). The tegmental inputs project densely to the intermediate gray layer (IGL) and sparsely to the superficial layers. The PBG input probably projects only to the superficial layers. In the present study, the morphology of choline acetyltransferase (ChAT)-immunoreactive axons and synaptic endings in the superficial and deep layers of the SC was examined by light and electron microscopy to determine whether these cholinergic afferents form different types of synapses in the superficial and deep layers. Two types of fibers were found within the zonal (ZL) and upper superficial gray layers (SGL): small diameter fibers with few varicosities and larger diameter fibers with numerous varicosities. Quantitative analysis demonstrated a bimodal distribution of axon diameters, with one peak at approximately 0.3-0.5 micron and the other at 0.9-1.0 micron. On the other hand, ChAT-immunoreactive fibers in the IGL were almost all small and formed discrete patches within the IGL. Two types of ChAT-immunoreactive synaptic profiles were observed within the ZL and upper SGL using the electron microscope. The first type consisted of small terminals containing predominantly round synaptic vesicles and forming asymmetric synaptic contacts, mostly on dendrites. The second type was comprised of varicose profiles that also contained round synaptic vesicles. Their synaptic contacts were always symmetric in profile. ChAT-immunoreactive terminals in the IGL patches contained round or pleomorphic synaptic vesicles, and the postsynaptic densities varied from symmetric to asymmetric, including intermediate forms. However, no large varicose profiles were observed. This study suggests that cholinergic fibers include at least two different synaptic morphologies: small terminals with asymmetric thickenings and large varicose profiles with symmetric terminals. The large varicose profile in the superficial layers is absent in the IGL. This result suggests that the cholinergic inputs that innervate the superficial layers and the patches in the IGL of the cat SC differ in their synaptic organization and possibly also in their physiological actions.
The distribution and synaptic organization of GABAergic elements in the mammillary nuclei of rats have been examined by the immunocytochemical localization of GABA at the light and electron microscope levels. The distribution of GABA-immunoreactive fibres and terminals in the mammillary body is non-homogeneous. By light microscopy, small scattered immunoreactive terminals are observed in the pars medianus, pars posterior and ventral region of the pars medialis of the medial mammillary nucleus. Larger labelled terminals are found in the pars lateralis, the dorsal region of the pars medialis of the medial mammillary nucleus and the lateral mammillary nucleus. At the ultrastructural level, GABA-immunoreactive synaptic endings in the different subdivisions of the medial mammillary nucleus exhibit a widespread somadendritic distribution. By contrast, GABA-immunoreactive terminals within the lateral mammillary nucleus are located predominantly in the neuropil and less frequently on neuronal somata. GABA-immunoreactive synaptic endings contain pleiomorphic synaptic vesicles and have symmetrical synaptic contact zones with the somata and dendrites in the lateral and medial mammillary nuclei. After in vivo inhibition of GABA metabolism with amino-oxyacetic acid, light microscopic examination of the mammillary nuclei reveals numerous small GABA-immunoreactive cells in various subdivisions of the medial mammillary nucleus. No immunoreactive cells are observed, however, in the lateral mammillary nucleus. Electron microscopic examination demonstrates that the GABA-immunoreactive cells are astrocytes. In the labelled astrocytes, immunohistochemical reaction product is localized throughout the nucleus and cytoplasm of the cells, in thin sheet-like processes surrounding neuronal elements and in end-feet lining the basal lamina of capillaries. The results indicate that the mammillary nuclei in the rat receive a strong GABAergic innervation. Most if not all, of the GABA-immunoreactive synaptic endings in the mammillary nuclei probably arise from extrinsic inhibitory sources. The possible sources of the GABA-immunoreactive input to the mammillary complex are discussed.
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Hair cells of the avian inner ear have been shown to regenerate following acoustic or ototoxic insult. The consequences of this regeneration on the acoustic nerve have yet to be defined. The purpose of the present study was to use TEM analysis following cochlear damage and hair cell regeneration to describe afferent and efferent neural terminals on hair cells in the newly repopulated sensory epithelium. Following acoustic overstimulation (12 h, 115 dB SPL, 1500 Hz) adult quail were sacrificed immediately (0 day), or at 2, 12, or 24 weeks. Serial thin sections were taken from the embedded papilla in a plane tangential to the basilar membrane in the area consistent with regenerative activity. Immediately following noise exposure very few hair cells could be seen within the epithelia; afferent terminals on remaining cells appeared normal. Two weeks later afferent terminals showed signs of degeneration; efferent terminals were rarely seen on tall hair cells but remained relatively normal on short hair cells. Three to six months later afferent terminals had regained a more normal appearance but were less numerous on tall hair cells; some return of efferent-like terminals was seen often contacting two tall hair cells. Large normal appearing, efferent terminals remained on short hair cells. These results suggest that regenerated hair cells are likely to receive neural innervation. It would appear that some degeneration of afferent terminals takes place prior to final innervation of new hair cells.
We describe a case of combined volar dislocation of the lunate and dorsal dislocation of the remainder of the carpus. Such a combination is probably very rare and the possible mechanism of injury is discussed.
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1. The biochemical basis for the human renal Fanconi syndrome, including glucosuria, phosphaturia and aminoaciduria, remains enigmatic. This is due, in part, to the lack of an appropriate animal model. Since there is an association between the human genetic disease hereditary tyrosinaemia, for which urinary excretion of the compound succinylacetone constitutes a biochemical marker, and a renal Fanconi syndrome, we have examined the relationship between succinylacetone and renal tubular function in the rat. 2. Intraperitoneal injection of succinylacetone for 3 consecutive days into adult male Sprague-Dawley rats resulted in succinylacetone plasma concentration of 3 mmol/l. This concentration was associated with glucosuria, aminoaciduria, polyuria, reduced renal phosphate reabsorption and normal creatinine clearance. In addition, urinary porphobilinogen and total porphyrin excretions were markedly reduced. In animals permitted to recover for 7 days after succinylacetone administration, these renal functional changes remitted partially or completely. Ultrastructural examination of the kidneys after the 3 days of treatment showed no fine structural changes. 3. We conclude that the physiological alterations produced in normal rat renal tubules by succinylacetone provide the basis for the study of the biochemical changes underlying the human renal Fanconi syndrome.
The postnatal development of cholinergic afferents to the superior colliculus in neonatal cats was studied by using acetylcholinesterase (AChE) histochemistry, choline acetyltransferase (ChAT) immunohistochemistry, and retrograde transport of horseradish peroxidase (HRP). In the adult cat, the pattern of AChE staining was laminar specific. AChE was distributed continuously in the stratum griseum superficiale (SGS) but was organized as patches in the stratum griseum intermediate (SGI). Diffuse AChE staining also was present in the stratum griseum profundum (SGP) and the dorsolateral periaqueductal gray (PAG). At birth, however, AChE staining was barely detectable in the SGS and, aside from a few isolated labeled neurons, was absent from the SGI, SGP, and PAG. By 7 days postnatal (dpn), staining in the SGS was more apparent but did not change appreciably in the deeper laminae. A substantial increase in AChE staining occurred in the SGS at 14 dpn (several days after eye opening), at which time patches in the SGI first became apparent. By 28 dpn, the complete laminar-specific adult AChE staining pattern was present, though the staining intensity did not reach the adult level until 56 dpn. A protracted maturation of both AChE staining and ChAT immunoreactivity also was observed in the sources of cholinergic afferents to the superior colliculus, which include the parabigeminal nucleus, and the pedunculopontine (PPN) and lateral dorsal tegmental (LDTN) nuclei. AChE and ChAT-immunoreactive staining in each nucleus was weak at birth but increased during the ensuing 2 weeks. At 21 dpn, however, ChAT immunoreactivity virtually disappeared in the parabigeminal nucleus and significantly decreased in PPN and LDTN. The ChAT immunoreactivity in these nuclei then gradually increased reaching maximum levels by 28 dpn. At 35 dpn, AChE staining showed a significant, though temporary (4 weeks), decrease in the parabigeminal nucleus, but not in the PPN and LDTN, that subsequently increased to the adult level of staining at 70 dpn. The absence of AChE in the SGI in neonatal animals was correlated, at least in part, with a paucity of neurons in the brainstem cholinergic cell groups labeled by retrograde transport of HRP from the superior colliculus. Injections of HRP into the superior colliculus retrogradely labeled many neurons in the parabigeminal nucleus, but few, if any, neurons in the PPN or LDTN at 1 dpn. Retrogradely labeled neurons also were observed in the substantia nigra pars reticulata, albeit fewer in neonates than in adults.(ABSTRACT TRUNCATED AT 400 WORDS)
A total of 39 fractures of the diaphyses of long bones in 31 children were subjected to operative fixation. Indications for surgery included concomitant severe head injury, multiple injuries, patients nearing skeletal maturity, inability to obtain a satisfactory reduction by conservative means, severe soft-tissue injury with or without vascular trauma, long-standing neurological disorder with incapacity and contractures, malunion, and delayed union. Although long-bone diaphyseal fractures in children are generally managed non-operatively, the use of fixation may be indicated in certain cases.
A case of successful four-level anterior decompression for paraplegia due to metastatic breast carcinoma is reported. Posterior instrumentation carried out shortly afterwards provided sufficient additional stability for the patient to stand and walk. It is suggested that this form of aggressive management may provide excellent palliation in certain cases of extensive metastatic neoplastic disease.
We report three cases of progressive ulnar nerve palsy following fractures of the distal radius. One was an open injury and one involved dorsal displacement of the nerve through a dislocated distal radio-ulnar joint. All were associated with dense scar tissue formation around the nerve. Early surgical decompression was successful in all cases. An anatomical study indicated that the relative immunity of the nerve to injury in this region may be due to its greater excursion and mobility compared with the median nerve.
A case of digital periarticular heterotopic ossification is described. Such cases are extremely rare and diagnosis may be delayed. Spasticity, possibly in association with minor trauma, may contribute to the development of the process. Little experience exists of the management of such problems and a mobile joint may be difficult to achieve.
The inhibitory neurotransmitter gamma-aminobutyric acid (GABA) is found in the superior colliculus (SC) of many mammalian species. In cat, several distinct classes of putative GABAergic neuron have been identified using antibodies directed against the neurotransmitter. It is not known whether these classes are found in other species. To study this, we examined the distribution, morphology, ultrastructure, and synaptic organization of GABA immunoreactive neurons in the SC of the Rhesus monkey (Macaca mulatta). Antibody-labeled neurons were distributed throughout the monkey SC, but were most densely concentrated within the zonal and superficial gray layers (32.5% of the total). These neurons were all small cells ranging from 6.6-16.3 microns in average diameter, and had granule, pyriform, and horizontal morphologies. Four types of labeled profile were identified in single ultrathin sections with the electron microscope. Presynaptic dendrites (PSDs) contained pleomorphic vesicles, received synaptic input from unlabeled axon terminals, and sometimes formed symmetric synaptic contacts with postsynaptic profiles. Two subtypes were found. One type contained loose accumulations of synaptic vesicles throughout the profile and had a distinctive varicose shape. The other type contained small discrete clusters of synaptic vesicles near the site of synaptic apposition. The former were much more common. Profiles with typical axon terminal morphology were also found. These profiles usually contained numerous flattened vesicles and formed symmetric synapses with postsynaptic profiles, both dendrites and cell bodies. Some conventional dendrites and myelinated axons were also labeled. Serial ultrathin section reconstructions revealed that PSDs formed complex synaptic relationships with other elements. Retinal terminals, identified by their characteristic pale mitochondria, established synaptic contacts with both types of PSD. These PSDs also established contact with each other, providing a possible anatomical substrate for disinhibition. We conclude that the monkey SC has multiple GABAergic cell types, similar to those found in cat, and may represent an organization common to both mammals and some other vertebrate species. The circuitry established by these cell types may provide a mechanism for disinhibition as well as inhibition in the mammalian SC.
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