The effects of tonic and rhythmic contraction of the gut on venous blood flow and oxygen saturation in venous blood through an intestinal segment were investigated in anesthetized dogs.
Intestinal contraction caused periodicity not only in venous outflow but also in oxygen saturation in venous blood.
(1) It was observed in tonic contraction that augmentation of venous outflow synchronized with reduction of oxygen saturation in venous blood and that diminution of venous outflow produced an increase of oxygen saturation in venous blood.
(2) In rhythmic contraction, the correlation between venous outflow and oxygen saturation in venous blood could be classified into two patterns. In the first pattern fluctuations of venous outflow corresponded reciprocally to fluctuations of oxygen saturation, and in the second pattern both curves fluctuated parallel to each other.
The mechanism of the correlation between venous outflow and oxygen saturation in venous blood in each type is discussed.

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1. The relationship between intra-aortic pressure and rate of efferent discharge in the hepatic branch of the splanchnic nerve, and release of glucose from the liver was studied in toad in vivo.
2. The inverse relationship between intra-aortic pressure and efferent discharge rate in the hepatic nerve as well as amount of glucose release from the liver was observed.
3. The existence of a blood sugar control mechanism due to the baroreceptor reflex through sympathetic innervation of the liver was suggested.

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Effect of LATS or TSH on the G-6-PDH activity in mice thyroid was studied. By a single injection of TSH or LATS the increase of enzyme activity did not occur promptly. By the 10 days' injection of LATS or TSH, the enzyme activity increased significantly, being accompanied with the increase of thyroid weight. The augmentation rate of the enzyme activity in mice thyroid and of the thyroid weight were accelerated when LATS or TSH was injected for 10 days. These results suggest that LATS increases G-6-PDH in the thyroid similar to TSH.

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Four groups of male New Zealand white rabbits, Oryctolagus cuniculus, were used. Besides the control (Group 1, reared at Ta=25°C) and cold-acclimated (Group 2, reared at Ta=0°°) groups, two others were intermittently exposed, one to 0°C for 3 hr daily (Group 3), and the other to a hypobaric stress of 308 mmHg for 3 hr daily (Group 4) for 3 months. Hematocrit and RBC in Group 4 were 54.0%±0.9 SE and 758×104/mm³±40SE, respectively, significantly higher than those observed in the control.
Rectai (T_re) and mean skin (T_s) temperature, metabolic rate (M) and heart rate (HR) were measured after thermal steady state was obtained at ambient temperature (T_a) of 25°C and5°C. When T_a was lowered to 5°C, T_re of Group 1 fell considerably, while that in Groups 2 and 4 remained unchanged. T_s fell in all animais in cold environment, but the rate of fall was more conspicuous in the control. When exposedto T_a=5°C, M was found to increase in all animals, particularly in Groups 2 and 4 (by 189-216%). However, the extent of shivering seemed to be less in Group 2.
In the curarizedrabbits, infusion of norepinephrine (NE, 3μg/kg·min for 30 min, at T_a=25°C) caused a marked bradycardia. The decrease in HR was more pronounced in the controls and Group 4. NE infusion caused an increase in M in Group 2, but not in the controls. The increase in M was very slight in Group 4. NE did not cause an increase in body temperatures in all groups, but only a small increase in T_s in Group 2. On the contrary, T_re increased after NE infusion in the noncurarized rabbits. These results suggest that the rabbits acclimated to hypoxia also increase their tolerance to cold. However, it seemed possible that the mechanisms involved may be different between the cold-and hypoxia-acclimated groups.
Calorigenic responses to cold and to infhsed NE in Group 3 were simiLar to those in Group 2. The inter mittent exposures to cold also resulted in acclimation to cold in rabbits.

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The effect of caffeine on the neuromuscular transmission was investigated by recording the end-plate potential (e. p. p.) of the frog sartorius muscle using an intracellular microelectrode.
2. Caffeine increased the e. p. p. amplitude. The threshold concentration was about 0.5-1×10^-4g/ml. The amplitude of e. p. p. was 158±16 of control size in the presence of 3×10^-4g/ml caffeine.
3. The quantum content was increased in the presence of 2×10^-4g/ml and 2.5×10^-4g/ml caffeine by factors of about 1.5 and 2, respectively.
4. The frequency of the miniature end-plate potential (m. e. p. p.) was in creased by about 3-fold with 3×10^-4g/ ml caffeine without an appreciable increase of m. e. p. p. size.
5. The potentiating effect of caffeine became more marked when calcium concentration of the external medium was lowered, but the effect was usually transient when the calcium concentration was below 1/10 of the normal value.
6. After a train of stimuli at 50 Hz for 30 sec post-tetanic potentiation occurred in the presence of caffeine with the same time course as in the control Ringer's solution.
7. It is suggested that caffeine acts on the presynaptic nerve terminal and facilitates the release of calcium from the stored site within the nerve terminal.

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1. Effbcts of coronary occlusion and subsequent reoxygenation by release of occlusion on ventricular contractility and electrical activity were investigated using the blood-perfused papillary muscle of the canine right ventricle paced at 120/min at a constant temperature of 38-39°C.
2. In the early phase of hypoxia, 60-90 sec after occlusion, the maximal rate of tension development (dT/dt) was accelerated significantly, while the developed tension was decreased as a consequence of the shortening of the contractile process.
3. The acceleration of dT/dt was related to the number of contractions at 120-180 beats after the occlusion and was not affected by propranolol or reserpine pretreatment.
4. During reoxygenation following the release of occlusion the developed tension increased rapidly above control values in 45 sec as a result of a prolongation of the contractile process. The overshoot of developed tension lasted for 900 sec after release of occlusion, and dT/dt was depressed significantly throughout the period of reoxygenation.
5. During reoxygenation following various periods of occlusion from 15 to 180 sec, graded depression of dT/dt and prolongation of contraction occurred. These changes were closely correlated with the magnitudeand duration of reactive hyperemia.
6. The overshoot of contraction was markedly reduced by propranolol or reserpine pretreatment. The maximal response of reactive hypermia was not affected by propranolol, but the responses 30 and 60 sec atter release of occlusion were significantly decreased by propranolol.
7. Electrograms of the muscle (EMG) changed little during hypoxia and subsequent reoxygenation in contrast to the marked and characteristic changes in contraction.

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Bradycardiac response to nonapneic facial immersion in man was examined at water temperatures of 10, 20, 30, 35, 40, and 47°C. The response was mainly dependent on the water temperature. In general, the colder the water, the greater the response. However, the least response was noted at 40°C; at 47°C the bradycardia was greater than at 40°C. The bradycardiac response was generally more marked in trained swimmers and divers than in subjects unaccustomed to swimming. The magnitude of changes in facial skin temperature appeared to have an additional influence on the cardiac slowing. Heart rate reached the minimum value in 20-30 sec, then tended to return toward the initial rate during immersion. Stimulation of cutaneous cold receptors is assumed to be most responsible for the development of bradycardia on nonapneic facial immersion, and the return of heart rate during immersion may be attributed to adaptation of these receptors.

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Cats were trained to press a bar for a food reward in response to a buzzer tone lasting 1 sec (CS). The animals were rewarded when they pressed the bar with a fixed delay after the onset of CS. Flashes were repeated at 1.0 Hz following CS and evoked potentials of the visual cortex to these flashes (FEPs) were recorded and analyzed. When repetitive flashes followed CS, occurrence of bar pressing was timed more accurately than when they did not. It was found in this case that while an initial deflection of FEPs was left unchanged through one trial, the following components were inhibited immediately before bar pressing and facilitated after it.

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In order to clarify the nature of the secretory process of water in dog's submaxillary glands, the following experiments were carried out:(1) measurement of the secretory pressure, (2) measurement of osmolarity of saliva secreted against a high intraluminal pressure, and (3) observation of the effect on the intraluminal pressure of retrograde injection of a hypertonic sucrose solution or an isotonic NaCl solution. It was found that when the secreted saliva was lead to a vertical polyethylene tube the secretion continued until the salivary column reached a height of more than 350 cm with continuous stimulation of the chorda tympani. The osmotic pressure of saliva was examined when it was secreted by stimulation of the chorda tympani into a closed luminal system with a pressure transducer. Under the influence of high luminal pressure (250 mmHg), the osmotic pressure was found to be 350 mOsm, the value being significantly hypertonic as compared with serum. By using the equation ΔP=δRTΔC, which is applicable to the gland system under zero flow conditions, the value of a of the system for salt (probably NaCl) was calculated to be about 0.23. From these findings, it is concluded that the osmosis across some parts of the gland, probably the acinus and the intercalated duct, is very important in water secretion of dog's submaxillary glands, as proposed in the osmotic flow model of Lundberg, Petersen, and Slegers and van't Hof-Grootenboer.

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Maximum cardiac output (Q_max) was determined for 233 males (aged 9 through 53 years) and 102 females (aged 9 through 20 years) by the carbon dioxide rebreathing technique during bicycle exercise. Maximum cardiac output of the males progressively increased from 12.5 to 22.0 liter/min until age 17 through 18 years and was maintained at this level until age 24 years. From age 25 years a decrease in Q_max to 16.7 liter/min by age 53 years was observed. Q_max of the females increased from a level of 10.5 liter/min at age 9 years to a Qmaximum of 15.5 liter/min at age 18 years, maintaining this level through age 20 years. Male Q_max for comparable ages above 18 years was 30 % higher than female Q_max. Using the average Q_max value of males of 23-24 years as an optimum value, the decrement in Q_max with each year was approximately 0.9%.

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The effects of baroceptor reflex on the sympathetic nerve activity to the intestine (INA) and kidney (RNA) were compared in anesthetized cats. Grouped discharges synchronous with the cardiac cycle was not the major pattern in INA and approximately 73 % of the total INA was composed of a continuous or fluctuating pattern. With increase in mean aortic pressure from 116 to 216mmHg after administration of norepinephrine, INA showed various response patterns: initial inhibition followed by an increase (Type A), increase without inhibition (Type B), slight inhibition (Type C) and no change (Type D), whereas RNA decreased to the noise level. Type A and B were the most common response patterns. In the open loop condition, initial inhibition in Type A disappeared, while the increase of INA in Types A and B remained unchanged. When RNA was completely inhibited by baroceptor inputs during occlusion of the descending thoracic aorta, INA was not inhibited but rather slightly increased. It is concluded that INA showed quantitatively and qualitatively different responses to baroceptor inputs as compared to RNA.

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