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Biomedical subjects

J O Rowan

Publications and source records attributed to J O Rowan.

At least 37 records · Page 2Linked to original sources
PubMed1975

Spinal cord blood flow measured by a hydrogen clearance technique.

Spinal cord blood flow (SCBF) has been measured in segments of the thoracolumbar cord of dogs using the hydrogen clearance technique. Clearances were recorded and flows calculated from electrodes placed in grey and white matter. The position of the recording electrodes was marked by diathermy and confirmed in each experiment. The SCBF in the white matter for 82 clearances was 13.7+/-4.5 ml/100 g/min using pentobarbitone anaesthesia. In the grey matter both monoexponential and biexponential clearances were recorded from electrodes placed in grey matter. There was no difference in flows calculated from the monoexponentail and slow components. SCBF from the slow components or monoexponentials was 12.0+/-4.5 ml/100g/min. The flow from the fast component was 69+/-11 ml/100 g/min. with pentobarbitone anaesthesia and 97.5+/-32.9 ml/100g/min with alpha-chloralopse anaesthesia. The flow calculated from the fast component did not correlate to changes of PaCO2. The slow component of any biexponential clearances was used to calculate flows from electrodes placed in the grey matter. There was no significant difference between flows from the grey matter (calculated from the slow component) and the white matter. Simultaneously recorded cortical and sub-cortical -lows were higher than in spinal grey and white matter. There was considerable variation in flow from animal to animal. The area of spinal grey matter is small and surrounded by white matter and the flow recorded from electrodes placed in grey matter is probably the average SCBF representing a mixture of grey and white flow. This will arise because of the rapid diffusibility of hydrogen gas between the tissues. It is therefore difficult to ascribe the flow from a centrally placed cord electrode to a definite anatomical compartment.

Anesthesia, General↗
PubMed1975

Raised intracranial pressure and cerebral blood flow. 5. Effects of episodic intracranial pressure waves in primates.

The effects of episodic waves of intracranial pressure on cerebral blood flow were studied in primates. Six pressure waves each of 20 minutes' duration and ranging from 50 to 100 mmHg in magnitude were induced in baboons, at intervals of 30 minutes, in an attempt to simulate clinical plateau waves. With pressure waves up to 75 mmHg, cerebral blood flow remained at control levels despite falling cerebral perfusion pressures. Between the initial pressure waves a marked hyperaemia developed, with cerebral blood flow increasing by as much as 100%, and this appeared to be a means whereby adequate flow was maintained during pressure waves. Later pressure waves, up to 100 mmHg, eventually reduced blood flow below control levels, although moderately high flows were maintained during periods of very low perfusion pressure. Brain metabolism was affected by eht episodic pressure waves, although no consistent change was seen.

Acetoacetates↗
PubMed1974

Raised intracranial pressure and cerebral blood flow. 3. Venous outflow tract pressures and vascular resistances in experimental intracranial hypertension.

Pressure changes within the venous outflow tract from the brain were studied in anaesthetized baboons. Segmental vascular resistance changes were also calculated and the results correlated with the changes in cerebral blood flow, measured by the (133)Xenon clearance method. Three different methods were used to raise intracranial pressure: cisterna magna infusion, a supratentorial subdural balloon, and an infratentorial subdural balloon. A close correlation was found between the cortical vein pressure and intracranial pressure with all methods of raising intracranial pressure: the overall correlation coefficient was 0·98. In the majority of animals sagittal sinus pressure showed little change through a wide range of intracranial pressure. In three of the six animals in the cisterna magna infusion group, however, sagittal sinus pressure increased to levels approaching the intracranial pressure during the later stages of intracranial hypertension. Jugular venous pressure showed little change with increasing intracranial pressure. The relationship between cerebral prefusion pressure and cerebral blood flow differed according to the method of increasing intracranial pressure. This was due to differing patterns of change in prevenous vascular resistance as venous resistance increased progressively with increasing pressure in all three groups. The present results confirm, therefore, the validity of the current definition of cerebral perfusion pressure-that is, cerebral perfusion pressure is equal to mean arterial pressure minus mean intracranial pressure-by demonstrating that intracranial pressure does represent the effective cerebral venous outflow pressure.

Animals↗
PubMed1974

Raised intracranial pressure and cerebral blood flow. 4. Intracranial pressure gradients and regional cerebral blood flow.

Intracranial pressure was raised by expansion of a supratentorial subdural ballon in anaesthetized baboons. Pressures were measured at several sites, both supratentorial and infratentorial, and cerebral blood flow was measured in each cerebral hemisphere separately. Pressures recorded from the right and left lateral ventricles corresponded closely throughout. Highly significant correlations were also obtained between the pressures in the right and left subdural spaces and the mean intraventricular pressure. There was, thus, no evidence of intracompartmental pressure gradients within the supratentorial space. Pressure gradients did, however, develop between the supratentorial and infratentorial compartments in the majority of experiments, although the level of supratentorial pressure at which this occurred, varied. Despite the presence of a large mass lesion over the right cerebral hemisphere, no significant differences developed between levels of cerebral blood flow in the two hemispheres, although flow in the right hemisphere remained consistently slightly lower than that in the left after the ballon was inserted.

Animals↗
PubMed1973

Raised intracranial pressure and cerebral blood flow. 2. Supratentorial and infratentorial mass lesions in primates.

Changes in cerebral blood flow with increasing intracranial pressure were studied in anaesthetized baboons during expansion of a subdural balloon in one of two different sites. With an infratentorial balloon, cerebral blood flow bore no clear relation to intracranial pressure, but was linearly related to cerebral perfusion pressure. Apart from an initial change in some animals, cerebrovascular resistance remained constant with increasing intracranial pressure, and autoregulation appeared to be lost from the outset. With a supratentorial balloon, cerebral blood flow remained constant as intracranial pressure was increased to levels around 60 mm Hg, corresponding to a cerebral perfusion pressure range of approximately 100 to 40 mmHg. Cerebrovascular resistance fell progressively, and autoregulation appeared to be effective during this phase. At higher intracranial pressure levels (lower cerebral perfusion pressure levels), autoregulation was lost and cerebral blood flow became directly dependent on cerebral perfusion pressure. The importance of the cause of the increase in intracranial pressure on the response of the cerebral circulation and the relevance of these findings to the clinical situation are discussed.

Animals↗
PubMed1972

Raised intracranial pressure and cerebral blood flow. I. Cisterna magna infusion in primates.

Changes in cerebral blood flow during incremental increases of intracranial pressure produced by infusion of fluid into the cisterna magna were studied in anaesthetized baboons. Cerebral blood flow remained constant at intracranial pressure levels up to approximately 50 mm Hg. At intracranial pressure levels between 50-96 mm Hg a marked increase in cerebral blood flow occurred, associated with the development of systemic hypertension and changes in cerebrovascular resistance. Further increases of intracranial pressure led to a progressive fall in cerebral blood flow. Prior section of the cervical cord prevented both the increase in cerebral blood flow and the systemic hypertension. Alteration of cerebral perfusion pressure by bleeding during the hyperaemia in a further group of animals suggested that autoregulation was at least partially preserved during this phase. After maximum hyperaemia had occurred, however, autoregulation appeared to be lost. The clinical implications of these findings are discussed.

Animals↗
PubMed1970

Relationship between volume flow and velocity in the cerebral circulation.

The relationship between the velocity of the cerebral circulation and the cerebral blood flow was explored at varying levels of PaCO(2), systemic arterial pressure, intracranial pressure, and perfusion pressure, using radioisotope techniques in baboons. Only at low flow rates did velocity increase with flow, and then non-linearly; at high rates velocity increased progressively less. Changes in flow are reflected by changes in velocity in such restricted circumstances that mean circulation time is a very unreliable indication of cerebral blood flow.

Animals↗
PubMed1970

Limitations of circulation time in the diagnosis of intracranial disease.

The mode circulation time was measured using intravenously injected technetium 99(m) and a collimation system devised to discriminate between the right and left sides of the head. The results in 21 normal men were used as a basis of assessing the findings in 205 patients, made up of five diagnostic groups (ischaemia, haematoma, subarachnoid haemorrhage, intracranial tumour, and head injury). The average mode circulation time in the affected hemisphere for the three groups with vascular disease was increased, but even in these groups half the patients had a mode circulation time within 1 SD of normal mean; similar results were found for asymmetry between the hemispheres. In serial measurements in 45 patients no correlation was found between change in mode circulation time and the clinical state. That so many results are within the normal range limits the value of this method.

Blood Circulation Time↗