Use this URL to cite or link to this record in EThOS: https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.452527
Title: The effect of noradrenaline on the spinal cord circulation and its possible implications in the pathogenesis of acute spinal trauma
Author: Crawford, Robert Andrew
ISNI:       0000 0001 3395 9363
Awarding Body: University of Glasgow
Current Institution: University of Glasgow
Date of Award: 1978
Availability of Full Text:
Access from EThOS:
Access from Institution:
Abstract:
Acute blunt injury to the spinal cord is an important cause of disability in both man and the domestic animals. The reasons for the formation and spread of the haemorrhagic and necrotic lesion seen initially in the central grey matter of the cord following injury are poorly understood. Evidence has been presented implicating the neurotransmitter substance noradrenaline (NA) as a causative factor in the pathogenesis of the lesion. This thesis contains the results of investigations into the effects of NA on certain aspects of the spinal cord circulation and the histological appearance of the cord. The effect of intra-arterially administred NA on spinal cord blood flow (SCBF) before and after blood-cord barrier disruption was studied in dogs. Barrier disruption was accomplished with an intra-arterial bolus injection of 2.5K urea. Multiple ligations of branches of the posterior sorta and cannulae placement ensured that the urea was directed to the lumbar and sacral segments of the cord. SCBF was measured by the hydrogen clearance effect on SCBF. The intra-arterial infusion on NA (12 mug/min. & 30mug/min.) was without overall effect on SCBF. However, if the blood-cord barrier had previously been disrupted with hypertonic urea both concentrations of NA resulted in large reductions in SCBF, the larger dose causing the greater reduction. No such reductions in SCBF were seen with blood-cord barrier disruption and NA if the animals had been pretreated with the -adronergic blocker, phenoxybenzamine (1.5 mg/kg.). The evidence thus suggest that NA is capable of causing profound flow reductions in the normal spinal cord and that these reductions are mediated via alpha-adrenergic mechanisms. With the techniques utilised in these experiments it was not possible to determine whether the alpha-mediated reductions in SCBF were the result principally of a direct vascular action of NA or due to alpha-mediated changes in the metabolic demands of spinal cord tissue. The effect of NA upon the calibre of spinal cord pial vessels was also tested. Small volumes of various concentrations of NA, dissolved in mock cerebrospinal fluid (CSF) were injected via glass micropipettes into the subarachnoid space adjacent to the vessels under test. Spinal pial arteriolar diameter was measured by a television image-splitting techniques. The application of mock CSF alone resulted in a net vasodilatation of 8.4+/- 6.5% (X+/- -SD). After the effect of CSF had been subtracted from the overall response to NA and CSF, a dose-dependent constriction to NA was seen. A maximum constrictor response of 28.8+/-5.1% (X+/- -SD) occurred in response to an NA concentration of 5 X 10.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.452527  DOI: Not available
Share: