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An investigation of the mechanisms regulating the blood volume and concentration of sodium in the plasma, in man, is presented. The relevant facts from the extensive literature were collected and a formal model proposed. This was simulated on an electronic analogue computer. The parameters of the analogue were adjusted and its structure modified, in order that the analogue should give results similar to those obtained by physiological experimentation. The initial step in the development of a suitable model was to define mechanic, known as the Basic System, for the control of the distribution of Water end electrolyte throughout the body compartments. The structure and elements of this system were derived from presently available physiological data,. The model was then elaborated by introducing- a bi-hormonal regulatory section. This consists of the mechanisms controlling the secretion rates of antidiuretic hormone (ADH) and aldosterone, and the intrerenal effects of these hormones. The hypothesis was introduced, and supported, that the excretion rates of water and sodium are proportional to glomerular filtration rate (GFR). A method was developed for the determination of the relationship between the plasma concentration of ADH and the reabsorption rate of water. The subsequent analogue simulation of the combined basic and regulatory system have results in reasonable agreement with those obtained in a range of physiological experiments. Attention has been drawn to the importance of the form of the input disturbance on the system response. The vasoconstrictive effect, arising subsequent to haemorrhage, was demonstrated successfully and some measure of agreement achieved in an attempt to simulate the response in the case of an injured hospital patient. Although not simulated, a mechanism for the control of the plasma concentration of potassium was derived. The results obtained from the analogue appear to support the physio-logical hypotheses involved. Further, the results suggest that the secretion rate of ADH may be dependent on blood volumes and the secretion rate of aldosterone may be dependent on the error in extracellular sodium mass (or concentration).

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In this thesis death was considered to be caused by the failure of the animal to recover from a period where the normal aerobic mechanisms of metabolism could not take place (defined as a period of anergia by Myers, 1973) which, in this case, was by sudden blockage of the route, from whatever cause, by which oxygen reaches the tissues. In a small animal model (the Wistar Albino rat) the anergic period (of twenty minutes duration) was initiated by administering excess ether to arrest breathing movements and hence access of oxygen to the circulation. However the subsequent changes in the physiology of the animals appeared to be more rapid than for the larger animals previously reported. The resuscitative method used was to artificially restore a well oxygenated circulation by perfusion with a small heart/lung machine and the indicator of the first stages of resuscitation was a return of electrical activity to the heart. It was found possible to perfuse and oxygenate these small animals at normal flow rates (45 ml. min[-1] for a 230 gram animal) but the aortic pressure generated was rather low at about 50 to 60 mm Hg. Although the use of angiotensin had no effect, adrenaline was found to increase this pressure to more normal values of 130 mm Hg or more. Nevertheless despite this perfusion there was no sign of any electrical activity from the hearts of the animals, at any time, despite the addition of artificial ventilation and both mechanical and electrical stimulation to the resuscitative procedures. It was possible that this may have been due to the use of the small animal model which had caused other difficulties with the provision of a suitable perfusate (bovine haemoglobin solution being finally selected) and some experimental problems caused by the physical size reductions in the equipment and techniques used.