THE EFFECTS OF OXYGEN ON THE CIRCULATORY SYSTEM IN CONDITIONS OF ANOXIA AND ASPHYXIA

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Abstract
An analysis is presented of the blood pressure changes during anoxia, asphyxia, and oxygen administration, in 34 animal experiments. Similarly, in 30 human beings during decompression equivalent to altitudes ranging from 16,500 ft. to 29,000 ft., the blood pressure findings are correlated with the action of the heart and the state of the peripheral blood vessels, and the effect of subsequent administration of oxygen upon them is investigated.Sudden deprivation of oxygen leads to a vasoconstrictor response, which, in humans, manifests itself in facial pallor and elevation of the blood pressure. The administration of oxygen in the later stages of this response may produce a further transient elevation of the blood pressure, which is followed by a fall of blood pressure and slowing of the pulse. The rise of blood pressure caused by oxygen after a period of acute anoxia or asphyxia is due to an augmentation of the action of the heart and to an intensification of the vascular tone, the two phenomena contributing to the rise of blood pressure in a varying degree under different experimental conditions. In intact, anaesthetized cats the effect persists after adrenalectomy. In spinal preparations, previously kept on "minimal" respiration, the effect is greatly reduced by the removal of the suprarenal glands. The rise of blood pressure resulting from the administration of oxygen is abolished by the destruction of the spinal cord by pithing, and is therefore attributed to an excitation of the sympathetic centres. Evidence also is presented that suggests that the chemoreceptors participate in this response in intact anaesthetized animals.A protracted oxygen deficiency of a moderate degree leads to a vasodilator reaction. In human subjects it manifests itself in a gradual engorgement of the cutaneous blood vessels, often in a lowering of the blood pressure, and an increase of the pulse rate. Sudden administration of excessive quantities of oxygen under these conditions causes a further decline of blood pressure and a slowing of the pulse. An analysis of the fall of blood pressure caused by the administration of oxygen in conditions of prolonged hypo-oxygenation shows that it is not strictly related to changes in respiration or to acapnia, which occurs during breathing of air deficient in oxygen. Neither is it prevented by addition of carbon dioxide to the oxygen. However, under prevailing experimental conditions, this fall of blood pressure is almost invariably abolished by a bilateral vagotomy, is occasionally reduced by atropine, and is absent in spinal preparations, these observations indicating "that it is dependent on the functioning of the medullary reflex mechanisms.

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