[Oxyhemoglobin dissociation curve and P50 (author's transl)].
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Biomedical subjects
Publications and source records attributed to K Suwa.
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Hepatitis B surface antigen, in paraffin embedded sections, can be stained by victoria blue and recognized easily against the background, including the cytoplasm and nucleus, stained by nuclear fast red. This new staining method has many merits such as easy staining procedure, long stability of dye solution, negative stainability of ordinary bile pigment, etc., and seems to be quite useful for routine as well as research works in hepatology.
Changes in the pituitary-thyroid axis in patients with Hashimoto's thyroiditis following withdrawal of thyroid suppressive therapy were analyzed. The group of patients with thyroid adenoma served as control (group I). Patients with Hashimoto's thyroiditis were divided into 2 groups on the basis of serum TSH levels 8 weeks after discontinuing the exogenous thyroid hormone (group II, less than 10 microunits/ml; group III, more than 10 microunits/ml). During treatment with L-T4(200 micrograms/day) or L-T3(50 micrograms/day), there was no significant difference in serum T4-I and T3 levels among the three groups. Following L-T4 withdrawal, basal serum TSH levels were higher at 2 to 8 weeks in groups II and III than in group I. Serum TSH response to TRH was greater at 4 to 8 weeks in groups II and III than in group I. Following L-T3 withdrawal, basal serum TSH levels were higher at 1 and 2 weeks in group II than in group I, while those of group III were consistently higher during the study. Higher TSH responses to TRH were observed at 1 to 8 weeks in groups II and III. Neither basal nor TRH-induced prolactin (PRL) secretion differed significantly among the three groups. We have demonstrated that pituitary TSH secretion in patients with Hashimoto's thyroiditis is affected more by withdrawal of thyroid hormone therapy than in patients with thyroid adenoma. In addition, the present findings suggest a difference between the sensitivity of thyrotrophs and lactotrophs in Hashimoto's thyroiditis after prolonged thyroid therapy is discontinued.
A high-frequency ventilator was designed using a loudspeaker as a piston, driven by a power-amplifier. A sine-wave signal was introduced into the amplifier from an electronic oscillator. The mechanical and gas exchange characteristics of the ventilator were studied in vitro and in dogs. The volume output per stroke, when open to air, was between 100 and 200 ml up to 7 Hz, then gradually decreased as the frequency increased. A Wright respirometer appeared to measure the volume flow fairly accurately up to 14 Hz. The pressure output against a closed volume of 1.1 liters achieved a maximum of 29 mmHg at 7 Hz. It gradually decreased as the frequency was changed from 7 Hz. The loudspeaker worked in such a way that the volume output decreased considerably when it was forced to move against a closed space to generate pressure. Adequate ventilation was achieved in all dogs from 1.4 to 10 Hz. At 14 Hz, the results were variable, and at 20 Hz and above, gross hypoventilation always resulted. The PaO2 values were always over 440 mmHg when 0.8 liter/(kg . min) of oxygen was supplied into the respiratory circuit. A speaker ventilator has the advantage of easy assembly and the possibility of applying various flows by electrical control. Its disadvantages are a lack of power and the difficulty in establishing ventilatory volumes without actual measurement.
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From the data of the vasomotor waves (VMW) previously reported, we attempted to retrieve information of the gain and the dead-time of the feedback circuit involved. A mathematical analysis revealed a certain relationship between the gain and the dead-time for the VMW to occur in three models. Combining our result with the data of animal experiments obtained by other researchers, we could exclude one of three models, thereby setting the area of existence of gain-delay value. When we apply a value of 3.4 sec for dead-time, as extrapolated from the animal data, the static gain of the system is between 2.2 and 4.0. Contrary to those observed in animal experiments and to our own original speculation, the VMW in man during cardiopulmonary bypass is likely caused via baroreceptor (carotid sinus) reflex rather than through cerebral ischemic response.
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A hypothesis was established that, during emergence of inhalational anesthesia, hyperventilation and accompanying hypocapnia beyond a certain limit may actually disturb rather than enhance the washout of inhalational anesthetics from the brain because of a decreased cerebral blood flow. Two mathematical models were constructed and the washout of nitrous oxide, halothane and methoxyflurane were studied. In model I, the whole body consisted of a single compartment, and blood flow to this compartment was assumed to change proprotionally with the PaCO2. In model 2, the body was divided into two compartments, brain and the rest of the body. It was assumed that the blood flow to the brain compartment varies proportionally with the PaCO2, while that to the rest of the body remains constant. The analysis indicated that there indeed existed the PaCO2 values at which the washout of anesthetics from the brain can be maximally achieved. In model 1, they were 49.0, 22.1 and 9.7 mmHg for nitrous oxide, halothane, and methoxyflurane, respectively. In model 2, these PaCO2 values varied with time. While the hypothesis was proven to be valid, we conclude that it is of limited clinical significance. For halothane and methoxyflurane, these theoretically optimum PaCO2 values are sufficiently low. For nitrous oxide, the variation of PaCO2 makes little difference clinically, because its washout is fast enough regardless of PaCO2.
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