Projections of thin (type-II) and thick (type-I) auditory-nerve fibers into the cochlear nucleus of the mouse.

Injections of horseradish peroxidase into the mouse spiral ganglion were used to label type-I and type-II afferent fibers. Axons presumed to be from type-II spiral ganglion cells because of their small diameter (less than 0.7 microns) and lack of nodes of Ranvier were traced to their terminations in the cochlear nucleus. Thicker fibers presumed to be from type-I ganglion cells were also reconstructed. Type-I and type-II axons labeled by basal turn injections bifurcate together in the dorsal part of the auditory nerve root, forming a branch that ascends into the anteroventral cochlear nucleus and a branch that descends into the posteroventral cochlear nucleus. Type-I fibers formed many collaterals ending in terminal swellings whereas type-II fibers were almost unbranched. Swellings from type-I and type-II fibers were often formed alongside one another. Examples of this proximity include terminal swellings of root collaterals in the auditory nerve root, as well as type-II en passant swellings and type-I terminal swellings throughout the ventral cochlear nucleus. The projections are dissimilar, however, since every type-II fiber projects at least one collateral to the granule-cell lamina. These collaterals usually end in neuropil forming the border between the ventral cochlear nucleus and the granule-cell lamina. In this border region, the type-II terminals overlap with those of branches from thick axons of the olivocochlear (efferent) bundle. Type-II fibers also differ from type-I fibers by only rarely coursing into the dorsal cochlear nucleus and by forming very few terminal swellings. En passant swellings, however, are numerous on type-II fibers, with ellipsoidal-shaped swellings prominent in the nerve root, and angular and complex-shaped swellings common nearer the terminals. We suggest that the latter swellings are associated with type-II synapses whereas the ellipsoidal swellings represent non-synaptic structures.

Determinants of oxygenation during hemodialysis and related procedures. A report of data acquired under varying conditions and a review of the literature.

A decrease in arterial oxygen tension during hemodialysis has been attributed to a number of factors. In order to more completely define these factors, we studied respiratory gas exchange, arterial blood gases and pH, and dialyzer flux of CO2 during pure ultrafiltration, three types of acetate dialysis, and sorbent regenerated bicarbonate dialysis in which the dialysate concentration of bicarbonate varies. Changes due to position and extracorporeal circulation of a 300-ml volume of blood (sham dialysis) were studied for any effect contributing to the hypoxemia noted with circulation through the membrane and variation in dialysate. Alveolar oxygen tension (PAO2) is calculated by the equation PAO2 = PIO2-PaCO2 (FIO2 + 1-FIO2/RE). RE is the ratio of CO2 excretion by the lung (VCO2) to oxygen consumption (VO2). RE equals RQ (metabolic quotient) when no extrapulmonary CO2 losses occur. Normals in a lounge chair had no change in RE and PAO2. RE decreased to 0.75 during sham dialysis and PAO2 decreased. During pure ultrafiltration RE decreased due to a decrease in VO2 and VCO2 with proportionately greater decrease in VCO2. PAO2 decreased accordingly. Acetate dialysis produced an increase in oxygen consumption without a proportional increase in CO2 excretion and both RQ and RE decreased. When PAO2 decreased during any of these procedures, arterial oxygen tension (PaO2) decreased without a change in A-aO2 gradient. No changes in PaCO2 were noted. RQ did not change during bicarbonate dialysis. At high bicarbonate dialysate concentrations, however, PaCO2 increased and PAO2 decreased. The major reason for hypoxemia during acetate dialysis is a decrease in alveolar oxygen tension due to changes in metabolism and a decrease in pulmonary CO2 excretion when CO2 is lost from the dialyzer. The increasing pH may contribute to the metabolic change during acetate dialysis and the hypoventilation during bicarbonate dialysis. There is little evidence to support an effect of pulmonary capillary obstruction or changes in oxyhemoglobin association on the decrease in arterial oxygen tension observed.

Determining P50 in the presence of carboxyhemoglobin.

A method is proposed, using mathematical solutions to the Roughton-Darling analysis, that theoretically can correct the measurements used for P50 determinations, whenever HbCO is present in blood, either initially or after equilibration. The resulting P50 is calculated in a "CO-free" state, independent of the actual presence of HbCO. This can be converted to a term designated T50, which indicates the in vivo shift caused by the concentration of HbCO measured. The concept was tested by comparing the P50 measurements in subjects with normal hemoglobins who differed by smoking habits (smokers vs. nonsmokers). The results showed similar mean values for this definition of P50, despite an average 10-fold difference in initial concentrations of HbCO. The method is applicable both to the single point principle, wherein P50 is estimated directly from venous blood measurements, and to standard tonometry-mixing techniques, as long as instrumentation includes the measurement of CO saturation.