Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.641944
Title: The effects of hypoxia on intracellular ion activities in mammalian heart
Author: Bright, C. M.
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 1990
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Abstract:
This thesis examines the effects of hypoxia on cardiac muscle. Changes in intracellular pH (pHi) were used as a marker for the cellular changes which occur during hypoxia and anoxia (the latter was produced by chemical removal of oxygen by sodium dithionite). Measurements were made of pHi in sheep Purkinje fibres and developed tension in ferret papillary muscle during both hypoxia and anoxia. Anoxia caused a larger fall in pHi and developed tension than hypoxia. The effects of prolonged exposure to hypoxia were examined on pHi and the ultrastructure in sheep Purkinje fibres and on developed tension and contracture in ferret papillary. Sheep Purkinje fibres appeared to be more resistant to hypoxic damage than ferret papillary muscle. The intracellular acidification and change in developed tension produced by sodium cyanide (NaCN) was compared with anoxia/hypoxia. Anoxia caused the largest intracellular acidification and there was no significant difference between the size of acidification produced by NaCN and hypoxia. Intracellular potassium activity decreased and intracellular sodium activity increased in hypoxia, both changes were larger in anoxia. A decrease in temperature from 35oC to 22oC was found to cause an intracellular alkalinisation and resulted in a smaller decrease in pHi and developed tension during hypoxia. Replacing glucose pyruvate or acetate had no effect on the decrease in pHi during hypoxia. Lacetate caused a larger intracellular acidification during hypoxia. Cinnamate was used to inhibit lactate efflux from the cells. It increased the size of the acidification of pHi during hypoxia and slowed the rate of recovery on reoxygenation. Inhibition of Na/H exchange had no effect on the decrease of pHi, while inhibition of the Cl-/HCO3- exchanger produced an increased intracellular acidification during hypoxia. The effect of extracellular pH (pHo) on pHi changes seen in hypoxia were investigated. Alkaline pHo (pH 8.4) resulted in a smaller decrease of pHi during hypoxia. The fall in developed tension during hypoxia was larger at pH 8.4 than at pH 7.4. Acidifying pHo (pH 6.4) caused a larger decrease in pHi during hypoxia and a larger fall in developed tension during hypoxia compared to pH 7.4. Changing from HEPES-buffered Tyrode to CO2/HCO3- buffered Tyrode resulted in an intracellular acidification but a smaller change in pHi during hypoxia. Increasing extracellular buffering power (with 40mM HEPES) reduced the size of the acidification of pHi during hypoxia. Many of the results obtained during hypoxia can be explained in terms of the production of lactic acid by the tissues and an increase in the intracellular inorganic phosphate concentration.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.641944  DOI: Not available
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