The ultrastructure of the cervical spinal ganglia in rat was studied by means of transmission electronmicroscope. In 100 ultrathin sections we found 4 axodendrite-like synapses. The authors believe that the presynaptic terminals might come from the sympathetic ganglia, the postsynaptic elements might be the peripheral or central processes of the spinal ganglia. From the viewpoint of functional significance, it seems to us that the axodendrite-like synapses may serve as the morphological basis of presynaptic control of sympathetic nerve over the peripheral primary afferent informations. Key words: spinal ganglia, axodendrite-like synapses, sympathetic nerve, presynaptic control

The present paper aims at investigation of the adrenergic innervation of spinal ganglia of rats (15 rats) by the fluorescence histochemical method. It is confirmed that the sympathetic adrenergic nerves exist in dorsal root sensory ganglion, and their CA-containing terminals with varicosities show specific and intensive fluorescence encircling the ganglion-satellite cell complexes, some of which are in close contact resembling synapses in shape. It is suggested that in the spinal ganglia of the rat there might be synaptic connections existing between the terminals of sympathetic nerve and the sensory neurons. The present paper provides some morphological basis for Santini’s theory of peripheral “Sympatheticsensory Loop”.

In this study, morphological observations were made on 216 cases of reactive hyperplasia (RH) in lymph nodes. For certain cases of the series, E-rosette formation test in cell suspension from lymph tissue, nonspecific acid esterase and double peroxidase-antiperoxidase marking (D PAP) on lymph tissue sections were also performed. According to the major architecture of lymph nodes and cytological features of hyperplastic cells as well as the modern immune function concept, RH was divided into six types, each of which was subdivided into several subtypes, providing respective histomorphological evidences for recognizing the characteristics of RH.

The aspect of Mg⁺⁺ metabolism was studied in 83 patients with congestive heart failure (CHF). The result indicated that CHF per se and treatment with digoxin were not the causes of Mg⁺⁺ depletion. Pronounced diuresis induced by diuretics increased markedly renal excretion of Mg⁺⁺ and, in consequence, lowered the plasma Mg⁺⁺ in 55% of the patients. The hypomagnesemia was not associated with decreased RBC Mg⁺⁺, and was usually transient and asymptomatic. When in addition to diuretics there were other factors known to promote extra Mg⁺⁺ loss, the hypomagnesemia became more severe, the RBC Mg⁺⁺ level might be decreased in association with it. A part of these patients might develop symptomatic Mg⁺⁺ deficiency, the chief clinical manifestations of which included changes in neuromuscular excitability, mental disturbances and cardiac arrhythmia, often accompanied by hypopotassemia, hypocalcemia and metabolic alkalosis. The important role played by the Mg⁺⁺ depletion in causing relevant symptoms and other electrolyte disturbances might be identified by careful analysis of the whole situation of the patient and the therapeutic test with Mg⁺⁺. The lowering of the plasma and RBC Mg⁺⁺ levels, the decrease in the 24 h urinary Mg⁺⁺ excretion could be used as routine laboratory diagnostic criteria of Mg⁺⁺ deficiency, and the application of the Mg⁺⁺ loading test as an important diagnostic procedure and at the same time a therapeutic test should be used more frequently in the future.

The experiments were performed on 97 albino rabbits. GABA administered through injection into the fourth ventricle caused inhibition on respiratory movement or decrease in phrenic nerve discharge activity. Diazepam produced similar effects as GABA. GABA receptor antagonists, bicuculline and picrotoxin, could reverse the respiratory depressant effect of GABA. Either bicuculline or picrotoxin given alone caused an increase in respiration. These results suggest that endogeneous GABA might be an inhibitory neurotransmitter involved in the central regulation of respiration.