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We proposed a model of human cardiovascular system that describes the cardiac cycle, the autonomic regulation of heart and vessels, the baroreflex, and the formation of arterial pressure. The model also makes allowance for the influence of respiration on these processes. It was found that an allowance for nonlinearity and insertion of a loop for the autonomic control of mean arterial pressure (having the form of self oscillating time-delay system) enables to obtain model signals with statistical and spectral characteristics that are qualitatively and quantitatively similar to.those for experimental signals. The model reproduces the phenomenon of synchronization of the loop for mean arterial pressure regulation with a basic frequency of approximately 10 s by the signal of respiration.

We studied the features of functional interaction between the subsystems of autonomic control of heart rate (HR) and arterial pressure (AP) giving rise to 0.1 Hz oscillations in R-R intervals (RRI) and photoplethysmogram (PPG). The study included 25 healthy subjects (6 women and 19 men) aged between 18 and 32 years. The signals of RRI, PPG and respiration were simultaneously recorded under breathing with a frequency linearly increasing from 0.05 Hz to 0.25 Hz within 25 minutes in a sitting position of a subject. The possibility of phase and frequency locking of 0.1 Hz oscillations in RRI and PPG by respiration is shown. We revealed that theses oscillations have different width and location of the intervals of phase and frequency locking by respiration. This distinction points to the functional independence between the mechanisms of autonomic control of 0.1 Hz oscillations in RRI and PPG.

We studied biophysical features of interaction between 0.1 Hz oscillations in heart rate variability (HRV) and distal blood flow (DBF) variability in healthy subjects and patients after acute myocardial infarction (MI). 125 patients after acute MI (72 male and 53 female) aged between 30 and 83 years and 33 healthy subjects (23 male and 10 female) aged between 20 and 46 years were included in the study. The duration of prospective study of MI patients was one year. We estimated the delay in coupling between 0.1 Hz oscillations in H RV and DBF variability. It is found out that in healthy subjects the delay in coupling from heart rate to DBF is less than delay in coupling from DBF to heart rate. Acute MI results mainly in disruption of coupling from heart rate to DBF. This coupling is partially restored in one year after acute MI, but the delay in coupling remains significantly smaller than in healthy subjects. The features of coupling from DBF to heart rate are restored in MI patients within three weeks after infarction. After this period the delay in this coupling in MI patients is approximately the same as it is in healthy subjects.