The respiratory system is known to interact significantly with the cardiovascular system. Respiratory arrhythmia is one of the most typical examples of this interaction.
In order to investigate this interaction, especially the arrhythmia, the ventilator volume, cardiac output, arterial pressure and heart rate were measured simultaneously on several normal subjects while they were breathing in various manners. Every quantity was measured completely noninvasively.
Since the ventilator volume changes almost proportionately with the electrical impedance at the thorax, the ventilator volume was estimated after measuring the impedance. Secondly, the cardiac output was measured by an electrical admittance method. Since, undesirable intervention may occur between sets of distinct electrodes, if such were used in simultaneously measuring the thoracic impedance and admittance, the method to avoid this intervention is also discussed. Thirdly, the arterial pressure was measured by using arterial pulse wave. Finally, the heart rate was calculated from the interval between two R waves on ECG.
The results are summarized as follows:
(1) The inspiratory effort in itself brings about a remarkable increase in the heart rate, while the cardiac output and arterial pressure decrease.
(2) The expiration does not have any effects on the heart rate.
(3) It can be suggested that the respiratory arrhythmia cleverly compensates for the decrease in the cardiac output that is caused by inspiratory actions.

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A new hardware simulator system has been developed in order to contribute to the study of the controlling mechanisms of the neuro-muscular system on the peristaltic movement in the gastro-intestines.
This model (simulator) is composed of the following three subsystems: (1) An electronic circuit membrane model which showed similar V-I-t (voltage-current-time) characteristics of the smooth muscle in both the voltage clamp and the current clamp experiments. The smooth muscle membrane model had active cable characteristics with the conduction velocity of about 3.5cm/s. (2) Simplified neural networks of the Meissner's and Auerbach's plexus, which were composed of the voltage-controlled oscillators and had analog signal processing and pulse transmission capabilities. (3) Transportation models which simulated the transportation of the inner food by the controlled muscle tension/contraction, and simulated the detection of the feedback quantities, i. e., the tension difference between the neighboring units depending upon the mass of the objective food.
Macroscopic peristaltic movements were fundamentally well simulated by the proposed model in spatio-temporal patterns of the movement (especially the controlling function of the Auerbach's plexus), transportation velocity of the food (1.2-1.9cm/min), etc. Since overall system was developed to work in real-time, the simulator could be directly combined with the physiological experiments for the quantitative evaluation, e. g., the measured multichannel nerve impulse trains could be put to the simulator.

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Patients with suspected Adams-Stokes syndrome are examined by Holter Monitoring. During the monitoring, there is the danger of syncopes and there have even been reports of sudden cardiac deaths. We have developed the pacemaker for the prevention of Adams-Stokes syndrome and sudden cardiac death while monitoring asystoles. The pacemaker has the following functions; 1) the longest escape interval of the pacemaker which is not more than the value inducing syncope is determined by the mean heart rate including the asystole, 2) once the pacemaker escapes, it continues pacing for a while at a physiological rate to cancell ischemias in organ tissues, 3) to prevent the overdrive suppression to the heart, pacing rate gradually declines and stops pacing until the next asystole. This pacemaker is useful not only in the diagnosis of Adams-Stokes syndrome, but also in the pathophysiological study and to know the time to quit pacing.

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Recent advance in electrophysiological studies have shown that there exist mechanical nociceptors which respond only to mechanical nociceptive stimuli such as pin indentation. Such mechanical nociceptive stimulus generates some mechanical deformation of the skin, and the nociceptors may respond to this deformation. That is when we have the sensation of pain. However, it is difficult to identify the mechanical factor as the direct adequate stimulus for pain reception. Therefore, the mechanical factor for prick pain sensation has been investigated by computer simulation of the elastic model of the skin. Referring to free nerve endings in the epidermis, pain receptors in the model were assumed to be scattered pseudorandomly within the skin at a certain depth. When the skin was regarded as being a semi-infinite uniform elastic medium, mechanical factors such as stress and strain at the pain receptors could be computed by applying three dimensional elastic theory. For six kinds of stimulus needles, “indentation thresholds”, indentation amplitude of the needle from the skin surface to the depth where the mechanical factor of one of the receptors exceeds the threshold of the receptor, and pain intensity at the threshold, which is defined as logarithm of transition velocity of the mechanical factor, were predicted by computer simulation. In all, twenty five kinds of mechanical factors were examined as the candidates of adequate stimulus. The results of the simulation were compared with the results of psychophysical experiments on human subjects. Among the candidates, vertical differential of vertical compressive strain and vertical differential of averaged horizontal tensile strain showed the best agreement between simulation and experimental results of both indentation threshold and pain intensity. This suggests that the differential of circumferential strain have the possibility of being the adequate mechanical factor for the sensory reception of pain.

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There are two main directions of studies which treat the information obtained from recorded electrocardiograms. One is the study of the waveform of the ECG which contains information about the cardiac activities. The other is the treatment of the time series analysis regarding R-R interval variability.
This paper describes time series analysis on the basis of R-R intervals from the view point of the latter. The R-R intervals were recorded continuously during rest, running load and recovery. We deal with the modeling of the R-R interval variability using autoregressive model. The spectral density function can be calculated from the autoregressive model parameters. The spectra of the R-R interval variability showed significant peaks around 0.10, 0.25, and 0.33 (beat)^-1 for healthy subjects at rest. The spectrum has large amount of power at the low frequency band. On the contrary, the periodicities of spectra for patients with ASD and arrythmia, such as AF, VPB, have large amount of power at high frequency band. The spectra of the R-R interval variability in running load also showed significant peak at high frequency of 0.50 (beat)^-1 for healthy athletes. The method in this paper is very practicable for the analysis of R-R interval variability.

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The relationship between the intrathoracic dipole and the surface potential distribution has been examined using a human torso model. The results of experiments show that a single dipole can cause multiple peaks of potential in the case of specific direction of the dipole, especially, when the direction of the dipole vector crosses at right angle to inhomogeneity such as lungs, multiple peaks are caused on the posterior thoracic surface.

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