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Biomedical subjects

I R Griffiths

Publications and source records attributed to I R Griffiths.

At least 109 records · Page 6Linked to original sources
PubMed1979

Spinal cord blood flow and conduction during experimental cord compression in normotensive and hypotensive dogs.

Spinal cord blood flow (SCBF) and dorsal column conduction, as assessed by the dorsal column evoked potential (DCEP), were measured during subacute cord compression in dogs. Ventral, midline balloons were used to produce compression and a dorsally situated strain gauge transducer measured the cord pressure. In normotensive animals there was autoregulation of SCBF to perfusion pressures (PP) of 65 to 70 mm Hg, and up to cord pressures of 55 to 60 mm Hg. The DCEP amplitude was significantly decreased even during this autoregulatory period. Conduction failure occurred at PP of 20 to 30 mm Hg. Chemically produced hypotension (74 mm Hg) did not affect either SCBF or DCEP. Minimal compression superimposed on hypotension decreased both flow and DCEP amplitude. The results indicate that ischemia is probably not the cause of the impaired conduction although, as the degree of compression increases, the cord will become ischemic once the autoregulatory limit is passed.

Animals↗
PubMed1978

Early vascular changes in the spinal grey matter following impact injury.

The ultrastructural changes of the microvasculature in the spinal grey matter were studied after impact injuries of varying severity in cats. Survival times ranged from 3 min to 6 h after injuries. The main vessels affected were capillaries and postcapillary venules. Perivascular haemorrhage and protein extravasation were present immediately after impact. Astrocytic foot processes could be swollen or shrunken and of increased electron density. The extra cellular space (ECS) was often distended with proteinaceous material. Some vessels showed an apparent increase in vesicles and small dense inclusions were seen in pericytes. By 20--30 min after impact, a number of vessels at greater impact energies showed degenerative changes in organelles and endothelial gaps. The lumina of these vessels often contained plasma, platelets, red cells and occasional neutrophils. Similar changes were seen between 3 and 6 h and at this stage neutrophils and some monocytes were present in the perivascular spaces and neuropil. Endothelial balloons and pericytic dense inclusions were also seen. It is suggested that initial events are mechanical, perhaps due to a rapid displacement of blood in venules followed by arterial hypertension (which commonly accompanies spinal cord impacts). Although initially many lumena are patent by 30 min there is a difference between the lesser and greater severities of impact.

Animals↗
PubMed1978

Spinal cord compression and blood flow. I. The effect of raised cerebrospinal fluid pressure on spinal cord blood flow.

The effect of cerebrospinal fluid pressure (CSFP) on spinal cord blood flow (SCBF), measured by the hydrogen clearance technique, was studied in dogs. CSFP was altered by the infusion of mock CSF into the lumbar subarachnoid space. Occluding snares at T-13 limited the effect of raised pressure on the brain. As the perfusion pressure was reduced when the CSFP was increased, flow remained constant up to a perfusion pressure of approximately 50 mm Hg. Below this value, flow decreased with decreasing perfusion pressure. Normal flow values could be reestablished even at a raised CSFP if the perfusion pressure was increased by raising the arterial blood pressure. Rapid reduction of CSFP was accompanied by reactive hyperemia. The autoregulation of flow down to a perfusion pressure of 50 mm Hg was due to progressive decrease in vascular resistance. Carbon dioxide-responsiveness of the vessels was decreased markedly as the perfusion pressure was reduced.

Animals↗
PubMed1977

Canine giant axonal neuropathy.

The clinical and pathological details of a case of canine giant axonal neuropathy are presented. An 18-month-old alsatian had hind leg ataxia, weakness, hypotonia and loss of patellar reflexes. Electrophysiological studies demonstrated denervation of the distal hind leg muscles and abnormal nerve conduction velocities. Biopsy and post mortem examination of the peripheral nervous system (PNS) demonstrated large anoxal swellings, up to 28mu in diameter. Electron microscopy showed these swellings to be composed almost entirely of neurofilaments. Similar giant axons were found in the central nervous system (CNS) and the distribution of the lesions in the CNS and PNS was suggestive of a 'Dying Back' disease. The possible aetiology of this new canine condition is discussed.

Animals↗
PubMed1977

A correlation of the endoscopic and pathological changes in subclinical pathology of the horse's larynx.

The larynges of 6 horses were examined endoscopically and the findings correlated with the gross and histological appearance of the intrinsic laryngeal muscles and their nerve supply. In all cases it appeared that the balance between abductor and adductor muscle groups had been lost due to preferential atrophy of individual muscles or groups of muscles. The laryngeal abnormalities recorded were asymmetry of the larynx with asynchronous left sided abduction and fluttering or trembling of the left vocal cord and arytenoid cartilage. It is suggested that these changes represent the early signs of a progressive lesion which may result in left sided laryngeal hemiplegia.

Animals↗
PubMed1977

The effect of norepinephrine on the spinal cord circulation and its possible implications in the pathogenesis of acute spinal trauma.

The effect of intra-arterially administered norepinephrine (NE) upon spinal cord blood flow (SCBF), before and after disruption of the blood-cord barrier was studied in dogs. Barrier disruption was accomplished with an intra-arterial bolus injection of 2.5 M urea. Multiple ligations of branches of the posterior aorta and cannula placements ensured that the urea was directed to the lumbar and sacral segments of the cord. The SCBF was measured by the hydrogen clearance method. Intra-arterial urea by itself had no significant effect on SCBF. The intra-arterial infusion of NE (12 microgram/min and 30 microgram/min) was without overall effect on SCBF. However, if the blood-cord barrier had been previously disrupted with hypertonic urea, both concentrations of NE resulted in large reductions in SCBF. No such reductions in SCBF were seen with blood-cord barrier disruption and NE if the animals had been pre-treated with the alpha-blocker, phenoxybenzamine (1.5 mg/kg). Some aspects of the possible involvement of NE in the pathophysiology of acute spinal injury are discussed.

Animals↗
PubMed1977

Age related changes in the motor nerve conduction velocity in dogs.

The motor nerve conduction velocity (NCV) was studied in the ulnar and sciatic-tibial nerves of dogs of various ages. The adult values are reached between six months and one year of age. The NCV remains on a plateau range of approximately 60 +/- 10 m/sec from one to seven years of age. After seven years there is a gradual decline in NCV so that by 10 years the velocity is reduced by 10-15 per cent. In addition to the reduction of velocity there is also an increased dispersion of the evoked muscle action potential.

Aging↗
PubMed1976

Spinal cord blood flow after acute experimental cord injury in dogs.

Spinal cord blood flow (SCBF) was measured in dogs before and following acute injury with 300 or 500 g-cm force (GCF). In addition, the responses to high and low PaCO2 and low PaO2 levels were studied. The hydrogen clearance technique was used and 0.3 mm platinum electrodes were placed in grey matter, central white matter or peripheral white matter of the L2 segment. The pre-trauma flows were: grey matter 12.5 +/- 2.7; central white matter 14.4 +/- 3.6 and peripheral white matter 15.1 +/- 4.2 ml/100g/min. Following a 300 GCF injury, a marked and progressive reduction in SCBF occurred in the grey and central white matter. This was present for the subsequent 4 hr of the study. The flow was lower than pre-trauma values during the second hour in the grey matter (9.0 +/- 1.4) and the third hour in the central white matter (10.8 +/- 1.8). By the fifth hour after trauma the flow in the grey matter was 5.0 +/- 3.5 and in the central white matter 9.7 +/- 1.5. In the peripheral white matter the SCBF was 10 +/-3.7 during the third hour but subsequently the flow increased to 11.5 +/- 3.9. Paired t-tests showed that this still significantly lower than pre-trauma levels. Two dogs showed a hyperaemic response which was persistent in one case but only temporary in the other dog. The vasodilatatory effect of CO2 was lost after trauma and in some cases a steal phenomenon was present. The sensitivity to an increase in CO2 was 0.48 +/- 0.23 ml/100g/min Hg before injury and this decreased to 0.0075 +/- 0.137 during the second hour after injury. The vasodilatation to hypoxia (30-40 mm Hg) was also absent but the vasoconstrictor effect to low PaCO2 appeared better preserved. These findings also applied to the peripheral white matter where the SCBF was not significantly reduced. The results were similar but more pronounced after 500 GCF injury. The results show that following injury the central areas of the cord become rapidly and progressively ischaemic. The peripheral white matter does retain a reasonably normal flow depending on the magnitude of the impact force. However, the vessels in all these areas lose their ability to respond to normal physiological stimuli.

Acute Disease↗