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Biomedical subjects

H Fukuda

Publications and source records attributed to H Fukuda.

At least 1,243 records · Page 69Linked to original sources
PubMed1976

Conduction of activity between muscles in the terminal region of the common bile duct and in the neighboring duodenum.

The relationship between muscle activity at the terminal region of the common bile duct and the duodenal muscle was examined in rabbits. The rhythmic muscle activity in the terminal region was synchronous with duodenal muscle activity. The activity of the latter muscle preceded the former. The activity at the terminal region synchronous with the rhythmic activity of the duodenal muscle sometimes disappeared spontaneously. The muscle activity of the ampulla and the spincter at the terminal region was sometimes independently lost. The conduction of excitation from the duodenal muscle to the terminal region appeared to be performed at several sites. The existence of a "conduction-shunt path" between the terminal region and the duodenum, as well as between the ampulla and the sphincter appeared probably. Some quantitative differences were found between the spincter, ampulla and duodenum in inhibitory effects to stimulation of splanchnic nerves and reflex effects and to excitatory effects of cholecystokinin-pancreoxymin and caerulein. These results seem to indicate that the sympathetic nerves and the intramural cholinergic neurones controlling these region carry out activities quantitatively different from each other.

Ampulla of Vater↗
PubMed1975

[Effects of transections and electrical coagulations in the medulla oblongata upon the activities in the respiratory muscles of the crucian carp (author's transl)].

The following conclusions may be drawn from the results in this work. The respiratory cycles are formed by the neuronal machinery in the reticular formation under the posterior part of the vagal motor nucleus. The motor neurones or the neuronal networks composing the motor nucleus of the respiratory muscles tonically discharge the action potentials, when the neurones or the networks are released from the inhibitory influences of the interneurones connecting the neuronal machinery to the motor neurones. Furthermore, the interneurones probably generate the tonic discharges after removing the inhibitory influences of the other interneurones or the neuronal machinery on them. A reflex mouth closing is elicited by a mechanical stimulus applying on the upper lip. The motor neurones of the m. adductor mandibulae are activated via only one synapse in the reflex. The reflex action potentials recorded from the motor nerve reduce in amplitude at the resting phase of the nerve in the respiratory cycles. These results suggest that the respiratory motor neurones are by nature spontaneous generators of the tonic action potentials and, in the time of the normal breathing, the tonic activity is interrupted by an inhibitory influence of the neuronal machinery generating the respiratory cycles.

Animals↗
PubMed1975

Stroboscopic microsurgery of the larynx.

An attempt was made to develop a new method of microsurgery of the larynx. A newly designed laryngostroboscope suitable for our purpose was employed in our new method. The vibratory pattern was stroboscopically examined through the operating microscope throughout the operative procedure while the patients who were able to phonate due to neuroleptanalgesia were asked to do so. Thus, the determination of the completion time of the operation was obtained mainly by the observation of stroboscopic vibratory patterns of the vocal cords. Since the beginning of 1972, this stroboscopic microsurgery of the larynx has been satisfactorily employed in more than 200 cases of various kinds of laryngeal lesions. As a result, a remarkable improvement of the postoperative voice was observed by phonatory examinations as well as by audible estimation.

Adult↗
PubMed1975

Changes in plasma thyroxine, triiodothyronine, and TSH during adaptation to iodine deficiency in the rat.

We have measured plasma thyroxine (T4), triiodothyronine (T3), and TSH with specific radioimmunoassays in rats during adaptation to severe iodine deficiency after they had previously received regimens supplying various quantities of iodine. Rats were maintained on a high-iodine diet (HID) containing 3 mg iodine/kg or a low-iodine diet (LID) containing 30 mug iodine/kg supplemented with 0.1, 0.2, or 0.4 mug iodine/ml of drinking water before swtiching to KID alone. Frequent serial blood samples were obtained up to 3 months, using 6 or more animals for each time interval. In animals originally fed HID, T4 remained at 4-6 mug/100 ml unitl the tenth day of LID, then rapidly decreased to a value of less than 0.4 mug/100 ml at 1 month. TSH was initially 50 muU/ml and increased linearly to 165 muU/ml on day 16. Thence there was a much more rapid rate of rise to 640 muU/ml at 38 days. The rats changed to LID alone after having been fed LID with iodine supplementation underwent similar qualitative hormonal changes. However, the decrease in plasma T4 and the increase in plasma TSH occurred sooner in the rats which had drunk water containing only 0.1 or 0.2 mug iodine/ml than in the previous experiment. Rats which had received 0.4 mug iodine/ml showed a pattern essentially identical to that of the animals which had been fed HID. plasma T3 did not change significantly in any of the experiments, remaining at 60-90 ng/100 ml, although there was a tendency for the values to be somewhat lower after several weeks of LID. There was a highly significant negative correlation of plasma T4 with plasma TSH. There was no significant correlation of plasma T3 with either plasma T4 or plasma TSH. It is concluded that the combined physiologic effect of plasma T4 and T3 concentration is more important in determining TSH secretion through negative feedback effects on the hypothalamus and/or pituitary than is the concentration of plasma T3.

Animals↗
PubMed1975

Acute effects of thyroxine, triiodothyronine, and iodide on thyrotropin secretion.

Rats fed a Purina or low-iodine diet (LID) for varying periods were serially sampled before and after a single iv injection of T4, T3, iodide or saline. Suboptimal replacement doses of T4 and T3 were given to rats fed LID for 2 months or 1 year (basal TSH, approximately 1000 and 2000 muU/ml, respectively). Both 1 mug T4 and 0.25 mug T3/100 g BW dropped plasma TSH to 70% of the initial level at 15 min and to 10--20% at 4 h. By 12 h TSH had begun to rise in 2-month LID rats, followed by a secondary decline 3--5 days after injection. Statistical comparison of the slopes of the initial TSH decline indicated there was no significant difference between the effect of T4 and T3. There effect of graded doses of T3 (0.01--0.3 mug/100 g) was also examined. There was a highly significant correlation of the magnitude of TSH suppression with the dose of T3 administered. Saline had no effect but 0.65 mug iodide/100 g BW (equal to that in 1 mug T4) had a delayed effect, depressing TSH to a minimum of 25% of the initial value at 48 h in 2-month LID rats. There was no difference in the effect of these doses of T4, T3, or saline in purina-fed rats (basal TSH, 170 muU/ml). T4 or T3 in physiologically equivalent doses thus produces an identical prompt rate of decrease in plasma TSH, indicating that both hormones possess intrinsic hormonal activity. The delayed effect of iodide is presumably because it must first be incorporated into T4 and T3 and secreted by the thyroid gland. The similarity of depression of plasma TSH by thyroid hormones or saline injection in Purina-fed rats is believed due to a nonspecific stress effect in these animals with a low basal rate of TSH secretion. The non-specific inhibition of TSH secretion is minimal in the iodine-deficient rats with a much higher basal rate of TSH secretion, presumably because of relative vectorial influences.

Animals↗
PubMed1975

Changes in plasma thyrotrophin, thyroxine, and triiodothyronine after acute or chronic administration of iodide to iodine-deficient rats.

The effect of chronic oral or acute iv administration of small graded doses of iodide was studied in severely iodine-deficient rats. Drinking water supplemented with 0.1, 0.2, or 0.4 mug 127I-/ml was given for up to 42 days. Plasma T3, which was initially in the normal range, increased 2--3-fold on days 1 and 2 after initiation of iodide supplementation, then dropped to approximately the intial concentration at day 3. Plasma T4, initially undetectable, was calculated to increase approximately 20-fold within one day after beginning iodide supplementation, but was still climbing into the normal range at day 3. In all groups, the initially high plasma TSH fell significantly by day 1 and was in approximately the normal range for iodine-sufficient rats by day 3. At 42 days, thyroid weight and 131I uptake were significantly elevated in all groups and inversely correlated with the dose of iodide, even though the thyroidal labeled T3/T4 ratio and plasma TSH, T4, and T3 were within the normal range. Intravenous injection of 0.1 or 0.5 mug 125I-/100 g caused an approximately 2-fold increase in plasma T3 within 24 h, which was not statistically different between the 2 groups. Plasma T4 rose to the normal range 24 h after 0.5 mug and was slightly, but significantly, elevated after 0.1 mug; it then declined in both groups. Twenty-four hours after injection of 2.5 mug 125I-/100 g, there was a significant fall in plasma T3, no change in plasma TSH, and no detectable plasma T4. Thereafter, there was a dramatic increase in plasma T4 and a fall in plasma TSH. The duration and degree of suppression of plasma TSH was related to the dose of iodide injected. We conclude that, under the conditions of our experiments, plasma T3 derives primarily from thyroidal secretion rather than from extra-thyroidal conversion of T4 to T3. Severely iodine-deficient rats secrete maximum quantities of TSH which are not increased by a further transient drop in plasma thyroid hormone concentration.

Administration, Oral↗
PubMed1975

Nyctohemeral and sex-related variations in plasma thyrotropin, thyroxine and triiodothyronine.

TSH, T4, and T3 were measured by radioimmunoassay in plasma samples obtained from 77 young adult male and 114 female rats fed a Purina high-iodine diet and maintained in an isolated room, 2-4/cage, at 24 +/- 1 C with light from 0600-1800 h. In one experiment, 7 male and 7 female rats were decapitated every 3 h for 30 consecutive h and trunk blood was collected. There was a clear nyctohemeral rhythm of plasma TSH in both sexes characterized by a zenith at 1200 h and a nadir between 1800 and 2100 h. The plasma TSH cycle was approximately 180 degrees out of phase and negatively correlated (P less than .05) with that of plasma corticosterone (B) in both sexes. Although glucocorticoids have been reported to suppress TSH secretion, there was no causal relationship between plasma B and TSH in our experiments since the TSH cycles were normal in chronically adrenalectomized rats. Normal TSH cyclicity was not observed in severely iodine-deficient rats with extremely high plasma TSH levels although the nyctohemeral B rhythm was normal. Plasma TSH was approximately twice as high in males as in females (overall mean +/- SE: M = 149 +/- 11, F = 81 +/- 7 muU/ml, p less than 0.001). There was no significant difference (P greater than 0.05) in plasma TSH at different stages of the estrous cycle. Plasma T4 was slightly, but significantly, higher in males than females (overall mean +/- SE: M = 6.4 +/- 0.1, F = 6.0 +/- 0.1 mug/100 ml; P less than 0.001), while T3 was higher in females than in males (overall mean +/- SE: M = 69.5 +/- 1.7, F = 80.3 +/- 2.1 ng/100 ml; P less than 0.001). No significant nyctohemeral rhythm was observed in plasma T4 or T3 in either sex. These observations indicate that: 1) There is a nyctohemeral rhythm of plasma TSH which is independent of plasma B fluctuations and not associated with proportional changes in plasma thyroid hormones. 2) A sustained high rate of TSH secretion abolishes the normal nyctohemeral plasma TSH rhythm. 3) There are significant differences in plasma concentrations of TSH, T4, and T3 between male and female rats.

Adrenal Glands↗
PubMed1975

The relative roles of iodination and iodothyronine content on thyroglobulin stability.

We have independently varied the degree of iodination and of iodothyronine formation over a wide range by acutely administering various doses of perchlorate and/or methimazole to severely iodine-deficient rats 30 min before giving 131-I- with graded quantities (1-100 mug of 127-I-). Thyroids were removed 4 h later and the soluble protein analyzed for labelled iodoamino acid composition and with sucrose density gradient ultracentrifugation. Since the total thyroid iodine content before administering 127I- was less than 1 mug, calculation of the degree of iodination and iodothyronine content of the labelled Tgb could be made from the known specificity of the injected labelled iodide. Newly organified iodine ranged from smaller than 0.1 to 1.4 mug/thyroid and labelled iodothyronines from smaller than 5 to 962 pmoles/thyroid. Both the degree of iodination and iodothyronine content varied directly with Tgb stability in the absence of inhibitors. But when Tgb iodination was kept constant, Tgb stability at pH 10.1 varied directly with iodothyronine content. When iodothyronine content was kept constant, Tgb stability was independent of the degree of iodination. Correlation of stability with iodothyronine content was highly significant (r=0.79, Psmaller than 0.001) but not of stability with iodine content (r=0.49, P larger than 0.05). We conclude that the primary determinant of Tgb stability in mild alkali is the iodothyronine content and not the degree of iodination of the protein. The increased Tgb stability may be induced by coupling between iodotyrosil residues of different 12 S subunits rather than between residues of the same 12 S subunit.

Animals↗