Journal of the Neurological Sciences, 27 (1976) 247-259 © Elsevier Scientific Publishing Coml~any, Amsterdam - Printed in The Netherlands

247

SPINAL CORD BLOOD FLOW AFTER ACUTE EXPERIMENTAL CORD INJURY IN DOGS

IAN R. GRIFFITHS

Department of Veterinary Surgery, University of Glasgow Veterinary Hospital, Bearsden, Glasgow, G61 1QH (Great Britain) (Received 11 July, 1975)

SUMMARY

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 PaOs 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 i 2.7; central white matter 14.4 ± 3.6 and peripheral white matter 15.1 4- 4.2 ml/100 g/min. Following a 300 G C F injury, a marked and progressive reduction in SCBF occurred in the grey and central white matter. This was present for the subsequent 4 hr o f the study. The flow was lower than pre-trauma values during the second hour in the grey matter (9.0 4- 1.4) and the third hour in the central white matter (10.8 4- 1.8). By the fifth hour after trauma the flow in the grey matter was 5.0 4- 3.5 and in the central white matter 9.7 4- 1.5. In the peripheral white matter the SCBF was 10 4- 3.7 during the third hour but subsequently the flow increased to 11.5 4- 3.9. Paired t-tests showed that this was 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 COs was lost after trauma and in some cases a steal phenomenon was present. The sensitivity to an increase in COs was 0.48 4- 0.23 ml/100 g/min Hg before injury and this decreased to 0.0075 40.137 during the second hour after injury. The vasodilatation to hypoxia (30--40 mm Hg) was also absent but the vasoconstrictor effect to low PaCOs 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 G C F injury. The results show that following injury the central areas o f the cord

This study was supported by the Wellcome Trust.

248 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.

INTRODUCTION

Acute concussive experimental injuries to the spinal cord are usually produced by the method of Allen (1911) as modified by Albin, White, Acosta-Rua and Yashon (1968). A given weight is dropped a known distance through a tube on to the exposed cord to produce an impact which is commonly expressed as the product of the weight and distance (g-cm force, GCF). The h~stopathological changes have been described by a number of authors (Assenmacher and Ducker 1971; Wagner, Dohrmann and Bucy 1971, Ducker, Kindt and Kempe 1971). Briefly, the findings, which vary in intensity and degree with the severity of the impact force, are as follows. There is an initial haemorrhage in the grey matter mainly in the perivascular space of small venules. The haemorrhages may coalesce and neutrophils may also be present in the parenchyma. Some of the vessels of the grey matter and central white matter are necrotic and demonstrate leakage of fibrin. The white matter is oedematous and contains many swollen axons and myelin sheaths. In 'severe injuries there is a progressive centrifugal involvement of the white matter with occasional sparing of the periphery. In less severe injuries the lesion is mainly confined to the central cord while the periphery tends to be much less involved. Microangiographic studies (Fried and Goodkin 1971; Fairholm and Turnbull 1971) demonstrated failure of vessels in the central areas of the cord to fill. Perfusion was present in peripheral areas although some vessels were abnormal in appearance. A vital study of spinal perfusion by Dohrmann, Wick and Bucy (1973) using the fluorescent dye, Thioflavine S, demonstrated similar findings. Perfusion in the grey matter and central white matter was severely reduced or absent, but was retained in the peripheral white matter. The spinal cord blood flow (SCBF) and tissue oxygen tensions following trauma have been investigated by a small number of workers whose results will be discussed later. The purpose of this study was to examine SCBF and vascular reactivity using the hydrogen clearance technique as previously described (Griffiths, Rowan and Crawford 1975). One advantage of this method is that the platinum recording electrodes can be placed in various areas of the grey or white matter, thus measuring micro-regional blood flow. It was hoped that with this approach the SCBF after trauma could be correlated with the previously described histological changes. L

MATERIALS AND METHODS

Twenty unselected mongrel dogs were used. They were anaesthetised with pentobarbitone and ventilated with a 50~ N20/02 mixture using a Palmer pump. Gallamine was used to produce muscle relaxation. Full details of the surgical preparation and recording systems for blood pressures, blood gases and blood flow

249 have been presented in a previous paper (Griffiths, Rowan and Crawford 1975). For reasons presented in this previous paper the flows from electrodes placed in the grey matter are calculated from the slow component of bi-exponential clearances. It should also be emphasised that the flow recorded from electrodes placed in grey matter represents the average SCBF and not the "true" grey matter flow. The term "grey matter flow" in the present experiments refers to the flow measured from electrodes placed in the grey matter. The L2 segment was used for this study. The platinum recording electrodes were placed in grey matter, central white matter or peripheral white matter. The majority of grey matter placements were in the intermediate grey matter. The central white matter was defined as extending from the grey matter to approximately 1/3 of the distance to the pia mater in the lateral funiculus. The peripheral white matter was the outer 2/3 of the lateral funiculus. Two electrodes were placed in each dog and the combination of electrodes in the grey and white matter varied from dog to dog. While the electrodes were polarising an impounder made of polytetrafluoroethylene (PTFE) was placed on the dural surface between the electrodes. It was supported inside a glass dropping tube and had an impact surface area of 12 mm 2 and a weight of 2 g. It remained in position throughout the experiment. At least 3 control measurements were made with normal PO2 and PCO2 together with low or high PCO2 or low PO2 value measurements. In many instances 6 control measurements were made. The cord was then injured by dropping a weight down the tube on to the impounder. The weight was either 15 g or 25 g and the disstance 20 cm. The impact force was therefore 300 or 500 g GCF. The weight was removed immediately after impact. The injury was followed by another period of electrode polarisation which prevented flow measurements being made for the 50-60 min after impact. Once polarisation was complete further measurements were made at normal PO2 and PCOz or varying blood gas tensions. Following the completion of the last measurement 1 ml/kg of 4 9/ooThioflavine S solution was injected intravenously. Thioflavine S is a fluorescent dye which stains vascular endothelium. Areas which retain a blood flow at the time of death can be demonstrated (Dohrmann et al. 1973). Cardiac arrest was induced about 10-15 sec after administration of Thioflavine S by injecting pentobarbitone. A heating current was then passed through the electrodes to mark their position, the cord was removed and fixed for 12 hr in 10 ~ formal saline. Blocks from the damaged area were frozen in liquid nitrogen and 100/~m cryostat sections mounted in 50 ~ glycerol and examined with a Zeiss IV F1 epifluorescence condensor for the demonstration of Thioflavine S fluorescence. Other blocks were embedded in paraffin wax and 8-/~m sections stained with haematoxylin and eosin for routine microscopy. RESULTS

300 GCF injury The pretrauma values of SCBF measured in the grey and white matter were similar to those reported previously (Griffiths et al. 1975). The flow in the grey matter

250

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Fig. 1. The absolute spinal cord blood flow in 3 areas of the spinal cord before and after a 300 G C F injury. The electrodes have been placed in the grey matter, central white matter or peripheral white matter and the key is shown. For details of significance, see text. The columns equal the mean plus I standard error.

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Fig. 2. The various parameters in a single experiment are demonstrated. The SCBF marked by a circle represents an electrode in the peripheral white matter and that marked by a square an electrode in the central white matter. The point of injury is denoted by the arrow. Before injury a normal response to a raised PaCOz and lowered PaO~ response are demonstrated. After trauma these responses are abolished and in the peripheral white matter a decrease in flow with a raised PaCO~ is demonstrated on two occasions (arrows). Although there is some fluctuation in blood pressure with the changes in blood gas the SCBF does not appear to follow passively the fluctuations in pressure.

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Fig. 3. The spinal cord blood flow has been plotted as a percentage of the mean pretrauma flow. The changes in the flow with time after a 300 GCF injury are shown in the three areas of the cord. Hyperaemic flows are encircled (hyperaemia has been taken as being 10 ~ more than the mean pretrauma flow). The hyperaemic flows in the grey and central white matter are from 1 dog and the hyperaemic flows in the peripheral white matter are from another case.

was 12.5 :k 2.7 ml/100 g/min, in the central white matter 14.4 ± 3.6 ml/100 g/min and in the peripheral white matter 15.1 i 4.2 ml/100 g/min. The results are presented in Fig. 1. The response of flow to changes in PaCO~ and PaO2 were also within the normal ranges. The mean absolute sensitivity to PaCO2 was 0.48 ~ 0.23 ml/100 g/ min/mm.Hg. An example of the pre-trauma response to hypoxia is shown in Fig. 2. Following injury with 300 GCF, marked changes in SCBF occurred. In Fig. 3 the results have been expressed as a percentage change of the mean normocarbic, normoxic pre-trauma flows. As shown in Figs. 1 and 3 the flow decreased in the grey matter in the majority of dogs and was significantly reduced (9.0 4- 1.4 ml/100 g/min, P < 0.001) between 1 and 2 hr after trauma. There was a further decrease between the second and third hours after trauma (7.2 ± 1.7 ml/100 g/min, P < 0.05). Although the flow remained at lowered values it did not further decrease significantly after the third hour. In the central white matter, the flow was reduced below pre-trauma values during the third hour (10.8 ± 1.9 ml/100 g/min, P < 0.05). In the peripheral white matter the flow was reduced during the third hour after trauma (10.5 :k 3.7 ml/ 100 g/min, P < 0.05) but then increased slightly to remain at 11.5 q- 3.9 ml/100 g/min. Analysis by paired t-tests showed that this value was still significantly below control values. The results as described above refer to the flows seen in the majority of cases. However, 2 dogs showed an increase in flow following trauma. In 1 dog the flow in the central white matter showed a persistent 30-37 ~ increase over the mean pretrauma flows and the grey matter flow was increased by 14 ~. These elevations were present for over 3 hr after trauma. In the other dog the increment in the peripheral white matter was much smaller (14~), and fell during the third hour to a level below that of the pre-trauma values.

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Fig. 4. The percentage change in flow or arterial COn is shown before and after a 300 G C F injury: Above the horizontal bar the effect of increasing PaCO2 is shown and below the .bar the effect of a decrease in PaCO~. The percentage change in either flow or CO~ has been calculated from the immediately preceding situation with normal PaCOu. Reactivity to low PaCOu is virtually abolished after injury. Note between 4 and 5 hr sufficient paradoxical reactions are present for the mean response to be a reduction in SCBF with an increase in CO2. Mean plus l SE are shown.

The response to CO2 was markedly altered after trauma. In the majority of instances an increase in PaCO~ caused either a fractional increase in flow or no response at all. The remainder of the electrodes (33 ~ ) registered a paradoxical response to CO2 with a decrease in flow. This steal phenomenon was seen in both grey and white matter. Fig. 4 illustrates the percentage change in flow and PaCO2 before and after trauma. The percentage change in each parameter was calculated from the difference between the immediately preceding normocarbic flow and the hypercarbic flow. Table 1 gives values for the absolute sensitivity to COg, All post-trauma sensitivities are markedly reduced but there is a progressive, though not significant, increase in sensitivity between the second and fifth hours. Fig. 2 illustrates the flow measurements in 1 dog in the central and peripheral white matter. Although the TABLE 1 CO2 SENSITIVITIES BEFORE A N D A F T E R 300 GCF T R A U M A A SCBF ml/lOOg/min/mm Hg) A Pa COu

Pre-trauma

N 11 M 0.48 i SD 0.23

Hours after trauma 2nd

3rd

4th

5th

8 0.0075 2_ 0.137

4 0.02 d0.06

10 0.046 ± 0.12

4 0.06 ± 0.12

253 post-trauma flows in the peripheral white matter were not markedly reduced the normal response to COz was totally lost and a steal phenomenon was present. Fig. 4 also demonstrates the pre- and post-trauma responses to low PaCO2 values. Insufficient observations were made for statistical assessment but the vasoconstrictive effect of low PaCO2 values appears better preserved after injury than does the response to high PaCOz values. The response to hypoxia was studied in only 3 dogs. The normal vasodilatory effect of PaOz 30-40 m m Hg was absent or reduced after trauma as illustrated in Fig. 2. In some dogs the responses to low PaO2 and high PaCO2 were not tested. The post-trauma flows behaved in a similar manner in dogs in which the response was tested. It seems unlikely therefore that high PaCO2 or low PaOz worsened the state of the damaged cord.

500 GCF injury Insufficient studies were made to allow statistical analysis of separate central and peripheral white matter flows. There appeared to be little difference between the responses in the 2 areas and the results have been pooled and are presented in Fig. 5. During the second hour after trauma the flow in the grey matter was decreased and remained low. In the white matter there was a progressive fall in flow which was not noted in the 300 G C F injury. The COz sensitivity, which was 0.43 ~ 0.24 ml/100 g/ min/mm Hg before injury, was virtually abolished after trauma (0.04 4- 0.178). Steal phenomena were again seen in several cords. There was a good correlation between the degree of Thioflavine S perfusion and the SCBF measured by the electrodes. When placed in areas of high fluorescence

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Fig. 5. The absolute blood flow before and after a 500 GCF injury. The horizontal bars represent electrodes in the grey matter and the hatched areas, electrodes in the white matter. Mean plus 1 SE is shown.

12.5 ± 2.7 14.4 4- 3.6 15.2 4- 4.3 13.2 4- 3.9 12.6 i 4.7

500 GCF grey white

Pre-trauma

300 GCF grey central white peripheral white

SCBF (ml/100 g/min) and location of electrode tip 0-1

7.5 ± 0.8 5.6 4- 2.1

9.0 4- 1.4 12.2 ± 2.3 12.2 4- 4.4

1-2

Time (hr) after impact

6.8 ± 1.9 5.0 q- 2.5

7.2 ± 1.7 10.9 4- 1.9 10.5 ± 3.8

2-3

6.2 ± 2.4 4.0 4- 2.1

8.0 -q- 1.4 9.8 -4- 2.1 11.9 ± 2.0

3-4

5.0 4- 3.5 9.8 ± 1.6 11.5 4- 3.9

4--5

SCBF BEFORE AND AT VARYING TIMES A F T E R I N J U R Y WITH EITHER 300 OR 500 GCF At 300 G C F electrodes have been placed in grey matter and central and peripheral white matter, and at 500 G C F the results from the central and peripheral white matter have been combined.

TABLE 2

4~

255 higher flows were recorded than from those electrodes in areas where fluorescence was decreased. When Thioflavine S was virtually absent the flow was in the 1-2 ml/ 100 g/min range. The routine histology demonstrated haemorrhages in the grey and central white matter together with degenerative changes in the neurones. The central white matter was disorganised in a pattern suggesting oedema. The appearance was similar to the pathology described in the introduction. DISCUSSION

The results of this study support the microangiographic findings of Fried and Goodkin (1971) and Fairholm and Turnbull (1971), and the perfusion study of Dohrmann et al. (1973); that is, the vasculature in the grey matter and central white matter is more severely affected than in the peripheral white matter. It is difficult to make exact correlations and comparisons between the different studies as various experimental species were involved and the exact specifications of the injury-producing device are not mentioned. Osterholm (1974) draws attention to the variation in impact force due to varying sizes ofimpounders. The dimensions of the present impounder have been quoted but the area of impact surface is far smaller than usual. This is to allow placement between the two recording electrodes. It was originally planned to use a smaller impact than 300 G C F but the rate of change of SCBF after trauma proved to be too slow for an initial study. Differences in the response of the circulation to 300 and 500 G C F injuries are however evident. Ducker and Perot (1971) have studied SCBF in dogs after 500 GCF injury. They used the la3Xe microinjection technique described by Smith, Pender and Alexander (1969). These latter authors attempted to place the a33Xe injection into the spinal grey matter by means of a micromanipulator. The mean SCBF was measured from the bi-exponential clearances which were usually recorded. It has never been demonstrated satisfactorily whether the recording is principally the flow in the grey matter, white matter or both. In an earlier paper (Griffiths 1973), the fast component was ascribed to grey matter and the slow to white matter. Recent experiences with hydrogen clearance (Griffiths et al. 1975) suggest that using highly diffusible indicators the average SCBF is measured and represents clearance from grey matter and immediately adjacent white matter. The average SCBF measured by Ducker and Perot (1971) can probably be regarded as analogous to the SCBF measured by the electrodes placed in grey matter in the present study. In these circumstances there is close agreement in results. In the majority of our dogs both 300 and 500 G C F injury produced a significant fall in flow which showed no tendency to return to normal over 5 hr. The percentage reduction in flow at 1 hr and 2 hr is similar in Ducker and Perot's (1971) study and our 500 G C F injury. The latter workers also showed a progressive fall in the tissue oxygen tension starting slightly later than the decrease in SCBF. Kelly, Lassiter, Calogero and Alexander (1970) also studied tissue oxygen tensions in the dorsal columns following 400 G C F injury and demonstrated a rapid and severe reduction in

256 oxygen tension. The results of Kobrine, Doyle and Martins (1975) of SCBF following trauma are also in agreement with the results presented. They demonstrated a progressive decrease in flow in the centre of the cord following a 600 GCF injury in monkeys. The flow in the central white matter of the lateral funiculi also showed a marked decrease after trauma. With both 300 and 500 GCF injuries a significant reduction in flow occurred later in time than in the grey matter. There was no tendency for the flow to return towards control values. In a previous study (Griffiths and Miller 1974) small veins and venules in the central white matter showed marked protein leaks and sometimes necrosis within 30 min of 500 GCF injury. This was particularly evident adjacent to the intermediolateral grey matter. The vasculature of the peripheral white matter appeared to react differently in the 300 and 500 G C F injuries. In the 300 G C F injury, an initial decrease in flow between 2 and 3 hr was followed by a slight though not significant increase. There was no progressive decrease in flow as in the grey and central white matter. Following a 500 G C F injury there was no return of blood flow towards control levels. The number of estimations in the peripheral white matter was limited in this latter investigation and will need to be confirmed in a later study. The return towards relatively normal flow in the peripheral white matter is supported by the angiographic study of Fairholm and Turnbull (1971) in rabbits and the fluorescent tracer study of Dohrmann et al. (1973) in cats. In our laboratory (unpublished results), we have observed on electron microscopy essentially normal vessels in the peripheral white matter. Kobrine et al. (1975) report that following 600 GCF injury in monkeys the flow in the lateral funiculus doubled, returning to control levels by 8 hr. Although we observed a small number with hyperaemia, they were exceptional and in this respect our results with both 300 G C F and 500 G C F injuries are in disagreement with those of Kobrine et al. (1975). The extent of the necrotic and degenerative lesions described by Kobrine et al. (1975) was apparently much smaller than in the present experiments. Their recording electrodes would therefore be placed further from the primary central cord lesion. It may be that this accounts for the discrepancy in the frequency of hyperaemic flows after trauma. Ducker and Kindt (1971) using a Peltier device to record bloodflow, demonstrated the loss of vasomotor reactivity to COz immediately after injury. No paradoxical reactions were reported in their study. The COz response was virtually abolished in the majority of dogs in the present experiments. In cords where a steal was present, the reduction in flow was small. There was a gradual but not significant improvement in the CO2 response after injury but whether it would recover completely with time, is not known. It is particularly interesting that the COz response was absent in the peripheral white matter following a 300 GCF injury although the resting SCBF was not markedly reduced. Similar paradoxical reactions to CO2 are known to occur in ischaemic brain after experimental middle cerebral artery (MCA) occlusion (Waltz 1970; Yamaguch/, Regli and Waltz 1971). A small but consistent steal phenomenon was seen in the peripheral white matter (Fig. 2), when the SCBF was not significantly

257 changed from pre-trauma levels. However, it has been shown (Griffiths and Miller 1974) that the walls of the vessels in the peripheral white matter are often abnormally permeable to protein even in the absence of increased protein in the neuropil. Steal phenomena have been demonstrated previously in the oedematous state following experimental cold injury to the spinal cord (Palleske 1969) and around spinal tumours in man (W/illenweber 1968). Palleske (1969) also demonstrated the inverse steal phenomenon in the oedematous cord. In the present study this was not found and the SCBF usually decreased with low PaCO2 levels. Sufficient results for statistical analysis were not available but it appeared that the response to low PaCOz was better preserved than the response to raised levels. The vasodilatatory effect of hypoxia was also absent in the injured cords, the vessels of which were therefore exhibiting typical vasoparalysis. Waltz (1970) noted that some time after ischaemia the cortex regained some of its reactivity to CO2. We have not studied the chronic changes in our dogs but it is likely that CO2 reactivity would return in the peripheral white matter. In contrast to the results of Kobrine et al. (1975), hyperaemia in the lateral funiculus was the exception rather than the rule. However, the pathogenesis of the hyperaemia is of interest. Focal hyperaemic areas are known to occur within and around ischaemic or infarcted areas of brain (Yamaguchi et al. 1971; Hoedt-Rasmussen, Skinhoj, Paulson, Ewald, Bjerrum, Fahrenkrug and Lassen 1967) or after head injury (Overgaard and Tweed 1974). In the present experiments hyperaemia was demonstrated in grey and white matter at both 300 and 500 GCF. It is certain that some hyperaemic flows were recorded from electrodes placed within the lesion and those recorded in the peripheral white matter were probably on the edge of the damaged area. Hyperaemia or "luxury perfusion" has been linked to tissue lactic acidosis (Lassen 1966). Cord lactate levels have been studied by Locke, Yashon, Feldman and Hunt (1971), who found a rise in tissue levels after trauma when compared to normal cord segments. The accumulation of acid metabolites and reduction of perivascular pH appears a reasonable explanation for both hyperaemia and paradox;cal reactions to CO2 (Brawley, Strandness and Kelly 1967). However, it is worth considering other possible causes of hyperaemia. Noradrenaline has been shown to increase cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRO2) and cerebral metabolic rate for glucose (CMR gluc.) (MacKenzie, McCulloch, O'Keane, Pickard and Harper 1976) following osmotic disruption of the blood-brain barrier. It is not known if this mechanism operates in the cord. Other amines such as histamine (Naftchi, Demeny, De Crescito, Tomasula, Flamm and Campbell 1974; Kobrine and Doyle 1975) may be implicated in the hyperaemia. It is possible that hyperaemia was present in our dogs during the first hour after trauma as a transient increase in flow during this period would not have been detected in the present experiments. These experiments together with certain other publications suggest that ischaemia is severe in the grey and central white matter after injury. The degree of ischaemia in the peripheral white matter probably depends to some degree on the magnitude of the impact. However, fibre degeneration can occur in this area in the presecne

258 of a relatively n o r m a l perfusion ( F a i r h o l m a n d T u r n b u l l 1971). In agreement with K o b r i n e et al. (1975) we feel that ischaemia is p r o b a b l y not the m a i n cause of damage in the peripheral white matter. It is not k n o w n with certainty whether the ischaemia is responsible for the central cord necrosis although we t h i n k that the ischaemia a n d some of the tissue damage are due to other factors. These other factors may be n o r a d r e n a l i n e or a n o t h e r vasoactive amine or some other agent. Whatever the initiating factor the central ischaemia will aggravate the lesion a n d reduce the possibility o f tissue recovery. ACKNOWLEDGEMENTS I a m grateful to Professor Sir William Weipers a n d Professor D. D. Lawson for their e n c o u r a g e m e n t , to Mr. I. M o w a t a n d Miss N. Burns for their technical assistance a n d to Mr. A. M a y for the photography.

REFERENCES Albin, M. S., R. J. White, G. Acosta-Rua and D. Yashon (1968) Study of functional recovery produced by delayed localised cooling after spinal cord injury in primates, J. Neurosurg., 29: 113-119. Allen, A. R. (1911) Surgery of experimental lesion of spinal cord equivalent to crush injury of fracture dislocation of spinal column - - A preliminary report, J. Amer. reed. Ass., 57: 878-880. Assenmacher, D. R. and T. B. Ducker (1971) Experimental traumatic paraplegia - - The vascular and pathological changes seen in reversible and irreversible spinal cord lesions, J. Bone Jt. Surg., 53A: 671-680. Brawley, B. W., D. E. Strandness and W. A. Kelly (1967) The physiologic response to therapy in experimental cerebral ischaemia, Arch. Neurol. (Chic.), 17: 180--187. Dohrmann, G. J., K. M. Wick and P. C. Bucy (1973) Spinal cord blood flow patterns in experimental traumatic paraplegia, J. Neurosurg., 38: 52-58. Ducker, T. B. and G. W. Kindt (1971) The effect of trauma on the vasomotor control of spinal cord blood flow, Current Top. surg. Res., 3 : 163-171. Ducker, T. B. and P. L. Perot (1971) Spinal cord oxygen and blood flow in trauma, Surg. Forum, 22: 413-415. Ducker, T. B., G. W. Kindt and L. G. Kempe (1971) Pathological findings in acute experimental spinal cord trauma, J. Neurosurg., 35: 700-708. Fairholm, D. J. and I. M. Turnbull (1971) Microangiographic study of experimental spinal cord injuries, J. Neurosurg., 35; 277-286. Fried, L. C. and R. Goodkin (1971) Microangiographic observations of the experimentally traumatised spinal cord, J. Neurosurg., 35: 709-714. Grifflths, I. R. (1973) Spinal cord blood flow in dogs, Part 1 (The normal flow), d. Neurol. Neurosurg. Psychiat., 36: 34--41. GriIfiths, I. R. and R. Miller (1974) Vascular permeability to protein and vasogenic oedema in experimental concussive injuries to the canine spinal cord, J. neurol. Sci., 22: 291-304. Grifliths, I. R., J. O. Rowan and R. A. Crawford (1975) Spinal cord blood flow measured by a hydrogen clearance technique, J. neuroL Sci., 26: 529-544. H~edt-Rasmussen, K., E. Skinhoj, O. Paulson, J. Ewald, J. K. Bjerrum, A. Fahrenkrug and N. A. Lassen (1967) Regional cerebral blood flow in acute apoplexy - - The luxury perfusion syndrome of brain tissue, Arch. NeuroL (Chic.), 17: 271-281. Kelly, D. L., A. R. Lassiter, J. A. Calogero and E. Alexander Jr. (1970) Effects of local hypothermia and tissue oxygen studies in experimental paraplegia, J. Neurosurg., 33 : 554-563.

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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 h...
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