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To identify central sites of potential CO2/H+-chemoreceptive neurons, and the mechanism responsible for neuronal chemosensitivity, intracellular recordings were made in rat tissue slices in two cardiopulmonary-related regions (i.e., nucleus tractus solitarii, NTS; nucleus ambiguus, AMBc) during exposure to high CO2. When the NTS was explored slices were bisected and the ventral half discarded. Utilizing such "dorsal" medullary slices removed any impinging synaptic input from putative chemoreceptors in the ventrolateral medulla. In the NTS, CO2-induced changes in firing rate were associated with membrane depolarizations ranging from 2-25 mV (n = 15). In some cases increased e.p.s.p. activity was observed during CO2 exposure. The CO2-induced depolarization occurred concomitantly with an increased input resistance ranging from 19-23 M omega (n = 5). The lower membrane conductance during hypercapnia suggests that CO2-induced depolarization is due to a decreased outward potassium conductance. Unlike neurons in the NTS, AMBc neurons were not spontaneously active and were rarely depolarized by hypercapnia. Eleven of 12 cells tested were either hyperpolarized by or insensitive to CO2. Only 1 neuron in the AMBc was depolarized and it also showed an increased input resistance during CO2 exposure. Our findings suggest that CO2/H+-related stimuli decrease potassium conductance which depolarizes the cell and increases firing rate. Although our in vitro studies cannot guarantee the specific function of these cells, we believe they may be involved with brain pH homeostasis and cardiopulmonary regulation.

This study evaluates the MR appearance of the kidney in diffuse renal parenchymal diseases, using precontrast, and immediate and delayed postgadolinium chelate (Gd), spoiled gradient echo (SGE), and pre- and post-Gd, T1-weighted, fat-suppressed spin-echo MR images to determine if characteristic findings exist for various types of renal disease. One hundred twenty-one patients with renal disease underwent MRI. Underlying diagnoses included: (a) glomerular disease (GD), (b) tubulointerstitial disease (TID), (c) microvascular disease (MVD), (d) ischemic nephropathy (INP), (e) obstructive nephropathy (ON), (f) infectious renal disease (IRD), (g) sickle cell disease (SCD), (h) renal cortical necrosis (CN), and (i) renal insufficiency of unknown etiology (UE). MR examinations of 22 patients with normal kidneys (NK) were evaluated as a control group. The presence of corticomedullary differentiation (CMD) demonstrated strong inverse correlation with serum creatinine concentration (SCr) (r = -.568, P < .001). Mean thickness of the renal cortex was 8.4 and 7.8 mm in patients with NK and Gd, respectively. The mean cortical thickness in patients with MVD, TID/Chemo, INP, and ON was 5.2, 5.6, 5.5, and 4.3 mm, respectively, significantly thinner than the renal cortex in the NK and GD groups (P < .01). Irregularity of the renal cortex was more frequent in MVD (60.9%), IRD (62.5%), ON (55.6%), and TID/other (53.8%) than in GD (3.8%) and NK (0%) (P < .01). Diffuse high SI of the entire medulla on delayed postcontrast images was observed in 25 (20.7%) of the patients with renal disease and none of the NK group. Although no pathognomonic features were found, certain findings were observed that may correlate with the etiology of the kidney disease and, therefore, assist in the differential diagnosis of renal parenchymal disease.

SUMMARY1. Previous work from this laboratory has indicated that the mesencephalon is the anatomical substrate for a mechanism capable of inhibiting central respiratory drive in glomectomized cats for periods of up to 1 h or more following brief exposure to systemic hypoxia; phrenic nerve activity was used as an index of central respiratory drive.2. The present study was undertaken to further localize the region responsible for the observed post-hypoxic inhibition of respiratory drive. We studied the phrenic nerve response to stimulations of the mesencephalon in anaesthetized, paralysed peripherally chemo-denervated cats with end-expired Pco2 and body temperature servo-controlled.3. Stimulations of two types were employed. Electrical stimulation allowed rapid determination of sites from which phrenic inhibition could be elicited. Microinjections of excitatory amino acids were used subsequently in order to confine excitation to neuronal cell bodies and not axons of passage.4. Stimulation of discrete regions of the ventromedial aspect of the mesencephalon in the vicinity of the red nucleus produced substantial inhibition of phrenic activity which lasted up to 45 min. Stimulation of other areas of the mesencephalon either produced no phrenic inhibition or resulted in a slight stimulation of phrenic activity.5. The results are discussed in the context of the central respiratory response to hypoxia.

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