Abstract
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.