[Ultrastructural study of the human pterygopalatine ganglion].
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Biomedical subjects
Publications and source records attributed to A Konno.
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Cisplatin (CDDP) was microencapsulated with ethylcellulose, and microcapsules (CDDP-mc) were infused into the maxillary arteries of patients with various head and neck carcinomas. We then found that the CDDP level in the circulating blood was significantly lower than that in patients administrated intravenous non-excapsulated CDDP. However, significantly high concentrations of CDDP were found in the tissues of patients treated with CDDP-mc. Our results suggest that selective arterial infusions of CDDP-mc can exert an intensive topical antitumor effect through microinfarction of malignant tissues. The prolonged release of drug from the microcapsules has also been associated with minimal systemic side effects.
To evaluate how far the long-term survival rate could be improved by maximum combination of chemotherapy, radiotherapy, and surgery, we have performed a trial combination therapy consisting of Linac X-ray irradiation (200 rads X 30) and intraarterial infusion chemotherapy (5-fluorouracil 250 mg X 15), followed by sufficiently extensive maxillectomy and primary reconstruction. The 5-year crude and relative survival rate of 70 patients were 64.2 and 72.1% respectively. The 5-year crude survival rate in cases with squamous cell carcinoma was 73.1%. Twelve out of 70 patients died of cancer. Local recurrence was seen in 6 cases and the most frequent cause of death was distant metastasis which was seen in 25% of T4N0 cases and in 57% of T2-3N1-3 cases. The elderly patients over 71 years occupied 29.1% of the total cases. The 3-year and 5-year crude survival rates in these elderly patients were 75 and 50% respectively. Death due to cancer was seen only in 3 patients and the most frequent cause of death was due to senility and other unrelated causes. As far as squamous cell carcinoma is concerned, the post-therapeutic courses of our combination therapy have been satisfactory. However further revision of the trial therapy was deemed necessary in T4 and N1-3 maxillary cancer. By covering the entire wound surface after total and extended total maxillectomy by a thick flap, the post-operative facial deformity and functional impairment due to scar contracture of the wound could be effectively prevented.(ABSTRACT TRUNCATED AT 250 WORDS)
To elucidate a limit to the efficiency of the upper airway mucosa as an air conditioner, the temperatures of the inspiratory air and mucosa were measured in the cervical trachea. Both of them were affected only minimally by change of atmospheric air temperature during resting nose breathing, but were affected greatly by change of mode of breathing. During hyperventilation through the mouth, when the atmospheric air temperature was 1 degree C, a temperature difference of 9 degrees C was noted between inspiratory air in the cervical trachea and body temperature, together with a mucosal temperature fall by 1.86 +/- 0.61 degree C. Wearing of a mask caused a rise of 3 degrees C in the inspiratory air temperature in the cervical trachea.
For better understanding the nasal defense mechanism against infection, an experiment on bacterial inhalation was performed using rats with and without artificial nasal obstructions. Local antibodies in the nasal cavity may exert a wide defensive influence on inhaled pathogens. Their production can be affected by nasal obstruction.
Using [3H]-quinuclidinyl benzilate (QNB) as a radioligand, receptor binding assay was performed to evaluate the changes of the muscarinic receptor in the nasal mucosa of guinea pigs sensitized with toluene diisocyanate (TDI), which showed hypersensitive airway symptoms both in the lower airway and in the nose. The same study was performed in guinea pigs sensitized with bacterial crystalline alpha-amylase (BCA) which showed typical symptoms of bronchial asthma but without hypersensitive nasal symptoms. In the nasal mucosa of guinea pigs sensitized with TDI, an increased density of the muscarinic receptor was confirmed with no change in affinity of the receptor. However, in the nasal mucosa of guinea pigs sensitized with BCA, no changes were observed either in the density of the muscarinic receptor of the nasal mucosa or in its affinity. The increased density of the muscarinic receptor observed in subjects with nasal allergy, which was reported earlier, is not specifically related to IgE-mediated nasal allergy and is not induced by systemic sensitization itself but is assumed to be induced by some pathophysiological changes in the nasal mucosa including antigen-antibody reaction with development of hypersensitive nasal symptoms.
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In subjects with nasal allergy, neither cold exposure nor exercise enhanced the nasal responses induced by nasal antigen challenge but they rather tended to suppress it. Cold exposure caused nasal mucosal swelling but its extent did not differ significantly between the subjects with nasal allergy and the normal controls.
A nasal provocation test was performed by consecutively placing allergen discs on the nasal mucosa of patients with pollinosis. This brought easily the systemic symptoms such as cough, periorbital oedema, and urticaria. Similarly, the nasal administration of large doses of the allergen induced a change in the respiratory response in sensitized guinea pigs. These results indicate that nasal mucosa absorbs a high molecular substance such as allergens.
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The purpose of this study has been to evaluate the degree of participation of the direct and indirect effects of histamine on nasal vasculature and nasal glands in causing clinical manifestations of nasal allergy. Vidian neurectomy, which cuts almost all of the parasympathetic nerve supply and the major portion of the sympathetic supply to the nasal mucosa, apparently almost completely abolished nasal hypersecretion induced by antigen and by topical application of 20 micrograms or 100 micrograms of histamine. However, a maximum dose of histamine (5 mg) induced 0.32 +/- 0.14 ml/10 min of nasal secretion from vidian neurectomized nasal mucosa. Albumin values of nasal secretion induced by topical histamine (2 mg) were significantly higher than those induced by acetylcholine (20 mg). This shows that histamine, depending upon the quantity present in the nasal mucosa, causes various degrees of transudation of plasma by its direct effect on nasal vasculature, in contrast to the fairly direct glandular effect of acetylcholine. However, the content of total histamine in allergic nasal mucosa was 7.1 +/- 3.5 micrograms/g which does not differ from normal controls. Judging from these data, nasal secretion which could be induced by the direct effect of chemical mediators on the effector cells without involvement of cholinergic reflex excitation was assumed to be minimal.
Changes in pulmonary resistance induced by various nasal stimuli were recorded in 16 subjects with nasal allergy and 16 laryngectomized subjects. To avoid human errors in sampling respiratory curves, computer analysis was performed breath by breath, automatically and continuously. In the subjects with nasal allergy the nasal mucosa was stimulated with pressure using a nasal balloon, and by a paper patch with 0.1 ml of 5% histamine hydrochloride. Laryngectomized subjects were stimulated with pressure and by pepper powder. Nasal pressure stimulation up to 50 cm H2O did not cause a statistically significant change in the pulmonary resistance of both groups of subjects. Pepper stimulation caused a statistically significant increase of the pulmonary resistance amounting to 40.4 +/- 28.2% of the prestimulatory level. Histamine stimulation caused a statistically significant change of the pulmonary resistance, but it was difficult to discern whether it caused an increase or a decrease of the resistance. Maximum efforts were used to control the respiratory pattern using the metronome and by visual monitoring of the peak flow rate on the cathode ray oscilloscope, but pepper and histamine stimulation caused a statistically significant increase, although slight, of tidal volume. The effect of slight changes of respiratory patterns induced by nasorespiratory reflex on the observed change of pulmonary resistance could not be ruled out in this human study.
Change of serum norepinephrine level and nasal patency were measured in 10 normal volunteers during exercise and effect of unilateral cervical sympathetic ganglion block on exercise-induced shrinkage of nasal mucosa was evaluated. Serum norepinephrine elevated markedly after 10-min exercise. Unilateral blocking of cervical ganglion completely inhibited mucosal shrinkage induced by exercise in 8 of 10 subjects. Mucosal shrinkage during exercise in these subjects was assumed to be mediated through cervical sympathetic ganglion, and not by increase in circulating cathecolamine. However, in 2 subjects, moderate shrinkage of the nasal mucosa was observed in 10-min after initiation of exercise. It was impossible to rule out some effect of circulating cathecolamine on the capacitance vessels of the nasal mucosa completely.
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We evaluated the histogenesis of so-called mixed tumors of the parotid gland by comparing the tumor cells with normal parotid gland cells. Using the indirect technique of the enzyme antibody method, the paraffin sections of human parotid glands, initially reacted with 0.1 mg/ml of parotin solution in PBS for 20 min at 37 degrees C, were treated for 20 min at 37 degrees C with anti-parotin subunit rabbit IgG (0.01 mg/ml) containing 5 mg/ml BSA, and then with HRPO-labeled anti-rabbit gamma globulin antibodies (swine IgG). After a staining for enzyme by Karnovsky's method, DAB reactions were observed on the duct cells of human parotid glands in 12 of 13 cases. We surveyed the parotin binding as a marker of duct cell on the so-called mixed tumors of 11 cases. DAB reactions were recognized on the cells of myxoid portion, along with the polygonal cells of solid sheet, board cord, and ductular formation, but the cells of chondroid portion and the spindle-shaped cells forming trabecular structure did not.
The purpose of the present paper is to examine whether hypersensitivity of nasal mucosa observed in nasal allergy is cause or result of allergic reaction using the subjects with pollinosis in which the exposure period can be clearly distinguished. Subjects are 30 cases of Japanese cedar pollinosis and orchard grass pollinosis and 25 normal controls. Inferior turbinate of unilateral nasal cavity was stimulated by a piece of filter paper soaked with 0.02 ml of 0.1% and 0.5% histamine hydrochloride. Frequency of sneezing and amount of nasal secretion were measured quantatively and were compared among the subjects with pollinosis in season, off season, and normal controls. In subjects with pollinosis when stimulated with extrinsic histamine, frequency of sneezing and amount of nasal secretion were markedly enhanced in season, but during off season no apparent difference was observed compared with normal subjects. Relationship between frequency of sneezing and amount of nasal secretion indicated positive correlation (alpha less than 0.01). Positive correlation was also observed in amount of nasal secretion in ipsilateral and contralateral nasal cavity when unilateral nasal cavity was stimulated with histamine (alpha less than 0.01). Hyperrhinorrhea was closely related with hypersensitivity of nasal mucosa. The present study showed that hypersensitivity of nasal mucosa characteristic of nasal allergy is nonspecific and that it is largely a result of antigen antibody reaction, which in turn works in causing exaggeration of the allergic symptoms and allergic reaction through vicious cycle.
Four healthy adults with normal nose were asked to pedal an ergometer for 3 min or more at a load of 25, 50, and 75 W/min, respectively. The same procedure was repeated on the same subjects whose nostrils were plugged. Air-flow and pressure difference between the mesopharynx and the nares, FO2 and FCO2, percutaneous-PO2 and ScO2 were recorded on a polygraph. At the start of the exercise, respiration deepened. Nasal resistance (Rn) decreased within 30 s and kept low while the exercise lasted. TcPO2 initially increased slightly for 1 min, then decreased. ScO2 also showed the same pattern, but of very slight range. At the end of the exercise Rn returned to pre-exercise level after slight rebound increase. Recovery of tcPO2 delayed for 30 s and its rebound increase lasted for more than 5 min. In case of nasal obstruction, such sequential changes of these parameters were of the same pattern as those in normal noses but were more evident. The results demonstrated that in case of moderate or severe nasal obstruction the exercise created hypoventilation despite a marked increase in the breathing activity if nasal breathing was continued.