Use this URL to cite or link to this record in EThOS:
Title: Studies on some aspects of oxygen toxicity
Author: Macintyre, John
Awarding Body: University of Aberdeen
Current Institution: University of Aberdeen
Date of Award: 1973
Availability of Full Text:
Access from EThOS:
Full text unavailable from EThOS. Please try the link below.
Access from Institution:
The circulatory and metabolic effects of high oxygen pressures have fascinated research workers virtually since the time of Lavoisier. This interest has been more marked in the past decade or so with the application of hyparbaric oxygen to clinical practice (Boerema, 1965, Smith, 1964, 1966), In this respect, however, the major limiting factor to the therapeutic use of hyperbaric oxygen has been the phenomenon of oxygen toxicity. This thesis is concerned with the study of the setiological factors concerned in oxygen toxicity and the possible relationship between the metabolic affects of oxygen and oxygen toxicity. In order to achieve a meaningful assessment of the effects of high oxygen tensions, it was felt that the accuracy of the system of measurement of oxygen tension to be utilised in later experiments should first be validated. The accuracy of using 100 ul. samples of blood for P02 measurement on the Radiometer micro oxygen electrode over the range of oxygen tension 2-2400mm. Hg. was confirmed. It was shown that, if measurement of P02 could not be carried out Immediately after sampling, blood samples should be stored in glass capillary tubes or glass syringes at 4C in melting ice. A method of obtaining arterialised capillary blood samples from the ear lobe by means of massage with Thurfyl nicotinate was developed. Such samples give values of P02 which were in close agreement with values of arterial P02 in normal hyperoxic and hypoxic 'shocked' individuals, thus providing an alternative to the use of arterial blood senile. The addition of nitrogen as a supporting gas for the alveoli when high inspired oxygen tensions were administered to mice, postponed the onset of severe lung damage and death but could not prevent the manifestations of pulmonary oxygen poisoning. Abolition of systomic hyperoxia, whilst maintaining a high intra alveolar oxygen tension, did not prevent pulmonary oxygen poisoning. The more severe morphological and histological changes produced by oxygen poisoning to the lungs correlated with a diminution In surfactant activity of lung extracts and an unstable alveolar structure as diminution by volume/ pressure relationships of excised lungs. Oxygen at high tension appears to produce toxicity in the lungs by an intra pulmonary effect. Although there is no definitive proof of the mechanism whereby the pulmonary damage is produced, it appears that this may be due to a primary effect on the pulmonary vasculature. The renal blood flow In dogs was reduced by approximately one third when the animals breathed high oxygen tension. This diminution in renal perfusion was not abolished by selective pharmacological blockade of the renal sympathetic nerves. When the kidney was underperfused by inducing hypovolsemic hypotension in the animals the renal blood flow was still reduced hyporoxia. The reduction in perfusion did not occur until the renal tissue, as indicated by the renal venous oxygen tension, became super saturated with oxygen and the haemodynamic changes did not follow directly changes in arterial oxygen tension. There was no evidence to show that the conges in renal blood flow were secondary to changes in renal metabolism Induced hyperoxia. The changes in renal perfusion due to oxygen, however, appear to be due to a direct intra-renal effect of oxygen. Increased carbon dioxide tensions in the blood did not produce changes In renal blood flow or renal function until the carbon dioxide tension was above 70 MM. Hg. The changes in renal handling of electrolytes, which were studied, appeared only to reflect the reduction in total renal perfusion which occurred with gross hypercapnia. The effects of hypercapnia on the renal circulation could be abolished by renal nerve blockade and appeared to be mediated through the sympathetic Nervous system as part of an extra-renal effect. Infusion of mannitol prevented the changes in renal blood flow produced by hypercapnia. Carbon dioxide does not appear to play an important effect in the normal psychological control of renal blood flow. The responses produced in the renal circulation by changes in the blood tension of carbon dioxide and oxygen were different. The responses of the kidney following renal nerve blockade in the presence of high tensions of these gases were also dissimilar. Thus it must be concluded that their modes of action and importance in physiological control over renal blood flow are entirely dissimilar.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available