The cerebral cortex of curarized, non-anesthetized dogs responded to a single stimulation of the thalamic somatosensory nucleus with an evoked potential consisting of a primary positive-negative diphasic complex (P-and N-waves) followed by a slow negative wave (SN-wave) of 100-150 msec in duration. The properties of the SN-wave were studied in comparison with those of the P-and the N-waves. 1, The localization of the SN-wave was limited within the somatoscnsory cortex, and its threshold was slightly lower than that of the primary complex. When the thalamic stimuli were applied at an appropriate frequency, the SN-wave responded in a waxing and waning fashion. 2. In light barbiturate anesthesia, the SN-wave became unstable more readily than did the primary complex. By high frequency stimulation of the midbrain reticular formation the P-wave was more or less suppressed, but the effects on the N-and the SN-waves were quite variable. 3. The SN-wave was more resistant to systemic asphyxia or topically applied KCl than was the N-wave. Strychnine augmented the primary complex, especially its N-wave, whereas the SN-wave was little affected. By topical treatment with GABA the N-wave was abolished and the SN-wave was extremely enhanced. 4. The intracortical recording revealed that the SN-wave originated from some deeper points of the cortex than those producing the primary complex.
Electrical properties of the spider muscle fiber were examined on M. flexor patellae longus and M. flexor patellae bilobatus of Atypus karschi DOENITZ. 1. The resting membrane potential ranged from -46 to -75 mV (mean -66 mV). 2. By stimulation of nerve strands, two kinds of responses, ‘fast’ and ‘slow’, were intracellularly recorded from a single muscle fiber. 3. ‘Fast’ responses consisted of initial slow and later abrupt rises of potential. The former is probably a junctional potential and the latter a spike having the all-or-none character. 4. ‘Slow’ responses are of graded and summative nature. 5. Most fibers produced only electrotonic and local potentials in response to direct catholdal polarization, but propagating action potentials were observed in a few cases. 6. The local potentials were oscillatory in most cases. The amplitudes of oscillations were, however, small compared to those in crustacean muscle fibers. 7. Electric constants of the fiber membrane were determined as follows: The effective resistance, Re, was 154.8 KΩ on the average; time constant, τm 7.9 msec.; specific membrane resistance, Rm, 131.7 Ωcm2; membrane capactiy, Cm, 60.6 F/cm2; and length constant, λ, 0.314mm in M. flexor patellae longus. The corresponding values obtained from M. flexor patellae bilobatus were as follows; Re 234.3 KΩ; τm, 14.3 msce.; Rm 504.4Ωcm2; Cm 28.9 μF/cm2; and λ 2.11mm. In these calculations the specific longitudinal resistance, Ri, was assumed to be 140 Ωcm. 8. The data were discussed from a comparative physiological point of view.
Hypertensive tendencies in the rural inhabitants of north-east Japan are discussed. in relation to data collected on the Pacific side of that area. Effects of environmental conditions on blood pressure level are considered under 3 headings; physical environment, diet and socioeconomic circumstances. It is reasonably certain that pressure is inversely related to temperature, but the effect of noise at place of work appears to be unimportant although it can cause a physiological rise. With regard to diet, the consumption of a large amount of polished rice with few vegetables but much salt seems to be a factor increasing the prevalence of hypertension and cerebral haemorrhage in these districts. The effects of socioeconomic circumstancesis less clear, perhaps because the extent of socioeconomic variation is limited in these rural districts. Further investigation of the factors influencing the hypertensive tendency in these areas is needed.
Electrocardiographic changes due to acute CO poisoning and those under the influences of the fluid infusion were observed in rabbits. 1) The progresses of CO-Hb level during and after the inhalation of CO gas were similar to those reported by previous investigators. The CO-Hb level never reached the saturation value. The drop of CO-Hb level for the first 30 minutes after the cessation of gas inhalation was more prompt in the animals poisoned with the gas inhalation for a shorter duration than in those for a longer duration. 2) The changes of E. C. G. during the gas inhalation were observed in twelve animals out of twenty. The changes were elevation or depression of the S-T segment and coronary, tent or flat T wave. There was no intimate correlation between the degree of E. C. G. changes and the CO-Hb level. The author infers that it may require a definite time duration, for which high concentration of CO-Hb level is maintained, to produce the changes in E. C. G. 3) Microscopic changes resemble those reported by many authors. Those changes were observed in the animals which did not show the changes in E. C. G. 4) Changes in E. C. G. during the gas inhalation disappeared soon after the cessation of gas inhalation and the E. C. G. returned back to normal after 24 hours. The acutely poisoned animals were infused Ringer-Locke solution added 12% bovine hemoglobin 24, 48 or 96 hours later. The disorders of E. C. G., namely, extrasystoles, remarkable displacement of the S-T segment or A-V block, appeared by the infusion. It is conceivable that the disturbances induced by CO poisoning remained as latent, although the changes of E. C. G. caused by gas inhalation returned to normal and that weakened hearts were unable to bear the burden of the infusion. Thus the cardiac damages must have become manifest.
Changes of the heart excitability were observed in dogs poisoned acutely with the inhalation of CO gas. 1) Due to the inhalation of 0.05 to 1% CO gas for 60 minutes, the remarkable prolongation of refractory periods was observed in all animals and the elevation of resting threshold was seen in a few animals. The lowering of heart excitability was shown not only during the gas inhalation but after its cessation. Then the strength-interval curve shifted to the right. 2) Due to the inhalation of 2.5% CO gas for 15 minutes, the heart excitability was decreased slightly during the gas inhalation and recovered soon by the inhalation of pure oxygen. Then the absolute refractory period was reduced. It requires a definite time duration for which the CO-Hb level is maintained at a certainly high level, to produce the lowering of the heart excitability. 3) Lowering of the heart excitability continued and became severe after the cessation of gas inhalation. The disturbances of heart muscles due to CO poisoning may be attributed to disturbances of myoglobin and/or cytochrome c. 4) The reduction of absolute refractory period was observed by the inhalation of 2.5% CO gas for 15 minutes and this may be attributed to the compensatory function in the early stage of hypoxemia.