(Received 27 July 1955)

Transcription

1 277 J. Physiol. (I956) I3I, THE REACTIONS OF THE BLOOD VESSELS OF THE HAND DURING INCREASES IN TRANSMURAL PRESSURE BY D. R. COLES AND A. D. M. GREENFIELD From the Department of Physiology, The Queen's University of Belfast (Received 27 July 1955) The work of Folkow (1949, 1953) on animals has re-directed interest to the suggestion of Bayliss (192) that peripheral vessels react by constriction to an increase in transmural pressure. Bayliss pointed out the importance of such a reaction in regulating the circulation, and Gaskell & Burton (1953) have emphasized its importance in adjusting the circulation to gravity. In the human subject it has been shown (Patterson & Shepherd, 1954) that the blood flow through the forearm is regularly decreased below the resting level after congestion of the veins for 5 min by inflation of a cuff on the upper arm to 8-11 mm Hg. This reaction was similar in normally innervated, sympathectomized and totally denervated arms. Greenfield & Patterson (1954) observed a local vasoconstriction in the forearm, following exposure of the arm to pressures 5 or 1 mm Hg below atmospheric. These reactions may represent a continuation of an increase in contractile force in the walls of the resistance vessels brought about by increased transmural pressure during venous congestion or exposure to subatmospheric pressure. Observations on the digital circulation made with the venous occlusion plethysmograph on moving a limb to the dependent position (Gaskell & Burton, 1953) and during local exposure to subatmospheric pressure (Yamada & Burton, 1954) have been considered to indicate a very considerable reduction in rate of flow with quite modest rises in transmural pressure. It is difficult to rely on this method for measuring flow in the digits when the veins are distended, and calorimetric observations in this laboratory have shown (Roddie, 1955) that when the arm is moved from the horizontal to the dependent position the heat elimination from the finger is significantly increased; from this it is deduced that the blood flow also is probably slightly increased. Observations of the oxygen saturation of antecubital venous blood (Rosensweig, 1955) support this conclusion. Roddie's and Rosensweig's observations suggest that modest increases in transmural pressure lead not to a sustained

2 278 D. R. COLES AND A. D. M. GREENFIELD constriction but probably to a slight dilatation of the resistance vessels in the human fingers and in the forearm and hand as a whole. Shanks's (1955) observations that when the venous pressure is raised the rate of heat elimination from the fingers is proportional to the arterio-venous pressure difference is additional evidence against sustained constriction. In all these cases it is possible that during the period of increased transmural pressure an increase in contractile force enables the resistance vessels more or less successfully to resist passive dilatation. On sudden reduction of the transmural pressure this could lead to the constriction observed by Patterson & Shepherd and by Greenfield & Patterson. In the experiments already reported observations during exposure have been confined to the effects of the relatively small increases in transmural pressure obtained by dependency or venous congestion. In the present experiments the effects of increases of transmural pressure up to 2 mm Hg have been observed. Some of these experiments have already been briefly described (Coles & Greenfield, 1955). METHODS The subjects were healthy young men. The main series of observations were made on two trained subjects, D.R.C. and A.D.M.G.; supplementary experiments were made on eight medical students. The laboratory temperature was between 2 and 22 C. The subject was comfortably seated for 3min before observations were begun. He wore normal indoor clothes with the sleeves down. Heat elimination was measured simultaneously from both fully dependent hands to calorimeters containing of water in the temperature range C. One hand, in a standard calorimeter (Greenfield & Scarborough, 1949) remained at atmospheric pressure throughout and served as a control; the other (experimental hand) was in a modified calorimeter in which the pressure could be reduced as desired (Fig. 1). This calorimeter was fitted with an airtightlid. The experimental hand entered through a hole in a sheet ofi in. rubber, cut to give a clearance of between 1 and 2 mm round the wrist. To the edge of this hole was attached a sleeve of rubbero7 mm thick; this was slightly loose on the arm, but formed an airtight seal with the arm when the pressure in the calorimeter was reduced below atmospheric. To prevent the sleeve herniating into the calorimeter or dragging on the wrist, and possibly restricting the circulation, a second layer of rubber around the lower part of the sleeve was attached by wires to a metal ring which surrounded the arm at a higher level. The hands were immersed to about the level of the distal skin crease on the wrists. Constancy of depth of immersion was checked in the earlier experiments by reference to a mark on the skin of the forearm, and maintained in the later experiments by holding the tip of the extended middle finger lightly against a shelf in the calorimeter. It was impossible entirely to prevent leakage of air into the calorimeter. The cooling effect of residual leaks on the water in the calorimeter was reduced by a baffle, and that on the wrist by a loose celluloid cuff. The pressure in the calorimeter was reduced and maintained below atmospheric by a pump (Edwards, type IV). A 151. air-reservoir prevented sudden changes of pressure. The pressure was adjusted by means of a variable leak, and measured by a mercury manometer. There was no difficulty in maintaining pressures steady to within ±2 mm Hg. The water in the calorimeter was constantly stirred, and its temperature was measured with a thermometer graduated to -1 C. Experimental procedure. Each experiment was divided into periods of 5 min each. Each thermometer was read at minute intervals. Heat elimination from both hands was first measured for two periods at atmospheric pressure. During the next minute the pressure in the experimental calorimeter was gradually reduced below atmospheric; the alteration in pressure on the bulb of the thermometer was found to affect the reading, and the apparent heat elimination in this

3 VASCULAR REACTIONS TO TRANSMURAL PRESSURE 279 minute was discarded. The heat elimination was then measured for two periods with the experimental hand at a steady subatmospheric pressure. During the following minute the pressure was returned to atmospheric and the apparent heat elimination again discarded. The heat elimination was often measured for two further periods with both hands at atmospheric pressure; in these cases the experimental hand could then be again exposed to subatmospheric pressure. The pressures used were 3, 6, 1, 15 and 2 mm Hg below atmospheric. Usually two or three different pressures were applied in succession, provided recovery from previous exposures appeared to be complete. The pressure differing least from atmospheric was applied first. To pump t.eak ~~~Ring Supporting wire Sleev'e Reservoir Celluloid cuff -Baffle Thermometer -- -= ~~~Shelf Calorimeter Fig. 1. Calorimeter for observations at subatmospheric pressure. Determination of the cooling rates of the calorimeters. At the end of most experiments cuffs on both arms were inflated to 26 mm Hg for 15 min to arrest the circulation as completely as possible. This allowed the core temperature of each hand to come into equilibrium with that of its calorimeter, and the cooling rates to be measured after equilibrium had been attained, usually about the 8th min. From the 1th min the experimental hand was exposed to subatmospheric pressure; this did not alter the cooling rate, showing that air leaks had a negligible cooling effect. The cooling rates were usually very small and rarely exceeded 5% of the rate ofrise of temperature when the circulation was free. Presentation of results. The aim of the investigation was to study the reactions of the vessels to local stress. Inevitably the local stress also resulted in some general alterations in the circulation, and even at rest there are continual small adjustments of the peripheral circulation, particularly in the hands. To deal with this situation the assumption was made (Greenfield & Patterson, 1954) that all general changes act symmetrically, and cause equal percentage (as opposed to absolute) effects on the two sides. Let Eb be the heat elimination from the experimental hand during the 5 min at atmospheric pressure immediately preceding the application of subatmospheric pressure. b be the corresponding heat elimination from the control hand. EO be the observed heat elimination from the experimental hand during the first (or second) 5 min of exposure to subatmospheric pressure. EX be the expected heat elimination from the experimental hand, had this been unaffected by purely local factors. co be the heat elimination from the control hand corresponding to Eo.

4 28 Then the assumption is that D. R. COLES AND A. D. M. GREENFIELD C =C-x or Ex = ceb The effect of local factors is to make the heat elimination Eo instead of Ex. The observed heat elimination may be expressed, as a percentage of the expected, by the formula Heat elimination %= Eo 1 Eo. Cb.1 x E,Eb. CO In the present experiments, in which the temperatures of the two calorimeters were usually within 1 C of each other throughout, the effect of making an allowance for the reduction in heat elimination from each volume of blood as the calorimeter temperature rises (Cooper, Cross, Greenfield, Hamilton & Scarborough, 1949) was to alter by less than 3 the value of 'heat elimination %'. The allowance was therefore omitted from the calculations. RESULTS Extracts from the protocol of a typical experiment are shown in Table 1. From to 1 min heat elimination was measured from both hands at atmospheric pressure. The period from 5 to 1 min may be regarded as a blank exposure of the experimental hand to zero subatmospheric pressure; the 'heat elimination %' for this period can then be calculated as shown in Table 1. Results from 1 to 49 min are omitted from the table; from 11 to 21 min the experimental hand was at -3 mm Hg, and from 33 to 43 min at -6 mm Hg. The table resumes at 49 min, with both hands at atmospheric pressure. From 55 to 65 min the experimental hand was at - 1 mm Hg. The calculations of 'heat elimination %' for the first and second 5 min of this exposure are shown. The cooling rates of both calorimeters were zero. In the formula for 'heat elimination %' the water equivalents of the calorimeters and contents cancel; the formula can therefore be entered directly with the temperature rise in C per min. If the correction of Cooper et al. (1949) for changing calorimeter temperature is applied to these figures, 'heat elimination %' becomes 98-6, 76-5 and 83-5 instead of 99, 78 and 86 respectively. The results of a number of such experiments on the two trained subjects are shown in Figs. 2 and 3. The experimental hand of each subject was exposed on seven occasions to - 3, -6 and - 1 mm Hg, and on four occasions to -15 and - 2 mm Hg. Results, calculated in exactly the same way, are also given for blank experiments in which the pressure on the experimental hand remained unchanged (mm Hg in the figures); the mean of these is, as expected, very close to 1 %. During the first 5 min of exposure (Fig. 2) there was at -3 mm Hg little alteration in 'heat elimination %', at -6 mm Hg a reduction, and at - 1 mm Hg a greater reduction. At - 15 mm Hg 'heat elimination %' was in both subjects increased on some occasions and decreased on others. At - 2 mm Hg it was invariably increased. During the second 5 min of exposure (Fig. 3), at -3, -6 and -1 mm Hg results

5 VASCULAR REACTIONS TO TRANSMURAL PRESSURE 281 were similar to those of the first 5 min. At - 15 and -2 mm Hg, the 'heat elimination %' in each experiment was somewhat higher than it had been during the first 5 min. TABLE 1. Extracts from protocol of a typical experiment Left (control) hand Right (experimental) hand Temp. rise Temp. rise, Time Thermometer 1O-3 C/ Thermometer 1-3 Cl (min) reading 5 min reading 5 min * * * Results omitted from 1 to 49 min * Suction on at -1 mm Hg 55 31* Suction off * Circulation arrested in both hands * Suction on at -6 mm Hg * Entering the formula; 'Heat elimination %'' Cb 1 Base-line period (5-1 min) = First 5 min at -1 mm Hg (55-6 min) = = Second 5 min at -1 mm Hg (6-65 min) = 1241 = 86. Exactly similar observations have been made on eight other subjects; the results of these, for the second 5 min of exposure, are shown in Fig. 4. The results were similar to thase on the two trained subjects, but were more scattered. In some subjects at - 1 mm Hg the 'heat elimination %' was increased, in others greatly reduced. No observations were made at - 2 mm Hg Ṡensations. A pressure of -3 mm Hg was hardly noticed. Pressures of -6 and -1 mm Hg caused a feeling of distension, and, for the first minute or so, a deep ache. Pressures of - 15 and - 2 mm Hg caused for the first minute or so a feeling of distension and a painful deep ache; the hand then became fairly comfortable, but progressively tense and stiff.

6 282 D. R. COLES AND A. D. M. GREENFIELD mm Hg below atmospheric pressure mm Hg below atmospheric pressure Fig. 2. Fig. 3. Fig. 2. 'Heat elimination %' from the whole hand during the first 5 min of exposure to subatmospheric pressure. *, A. D. M. G.; O, D. R. C. Numbers beside symbols indicate values off the scale of the figure. All observations were made at one or other of the pressures marked as abscissae, but overlapping symbols have been offset sideways. Fig. 3. 'Heat elimination %' from the whole hand during the second 5 min of exposure to subatmospheric pressure. Symbols as in Fig C 15 c 1 E -Z IIv I... en L Ju I t] y!v v a A I I I I I I mm Hg below atmospheric pressure 4 E 3 co -C r.2 M c IV1 C IV bo Ile ~~~~ H*--f-_1--- -_ I mm Hg below atmospheric pressure Fig. 4. Fig. 5. Fig. 4. 'Heat elimination %' from the7,whole hand during the second 5 min of exposure to sub atmospheric pressure. Observations on eight subjects, each of whom is represented by a different symbol. Fig. 5. Percentage increase in hand volume measured within 2 min after exposure for 1 min to subatmospheric pressure. *, A. D. M. G.; O, D. R. C. 6

7 VASCULAR REACTIONS TO TRANSMURAL PRESSURE 283 Appearances. In some calorimetric experiments the hands were removed from the calorimeter as soon as possible (about 1 min) after exposure to subatmospheric pressure. The control hand, having been dependent for 2 min, was a uniform reddish purple. The experimental hand, having been dependent for 2 min and subjected to subatmospheric pressure for the second 1 min, showed changes as follows: after -3 mm Hg, little difference from the control; after -6 mm Hg, more deeply coloured than the control; after -1 mm Hg, the hand and fingers were mottled with pale areas in a deep purple background, and the hand was somewhat swollen; after - 15 mm Hg, the dorsum of the hand was red and swollen, the fingers pale and mottled; after - 2 mm Hg, the whole hand except the fingers was grossly swollen and bright red, the fingers were somewhat swollen and rather pale. The colour reverted to normal in a few minutes after the exposures to -3, -6, - 1 or - 15 mm Hg, and in an hour or so after exposure to - 2 mm Hg. The oedema disappeared in a few hours. Petechial haemorrhages were rarely seen. Volume changes. In some experiments, illustrated in Fig. 5, the volume of the hands was measured before entering the calorimeters, and again as soon as possible (about 2 min) after exposure to subatmospheric pressure. The volumes were measured by water displacement in the narrowest practicable vessel, and the hand was immersed until 3 marks spaced round the circumference of the wrist simultaneously coincided with the water meniscus; the standard deviation from the mean of a series of such measurements on the same hand was 1-5 % of the hand volume. The measurements show that the dependent control hand increased in volume, and that the further increase brought about by exposure to -3 or -6 mm Hg was small. The increases in hand volume do not directly reflect the volume of oedema fluid, but the measurements make it clear that little more oedema fluid collected at -3 and -6 mm Hg than in the control hand. Did the seal at the wrist restrict the circulation? In some experiments an artificial circulation (Fig. 6 C) was used. This consisted of a tube which entered the calorimeter through the lid and left by passing between the wrist and the sleeve; the latter part, or artificial vein, was a thin-walled rubber tube made by sealing together the edges of two rubber ribbons. Water under a head of pressure of about 2 cm flowed freely through this system, whether the pressure in the calorimeter was atmospheric or subatmospheric in the range -3 to -2 mm Hg. The flow, however, was arrested by the inflation to 3 mm Hg of a pneumatic cuff applied over the sleeve. This seemed good evidence that although the artificial vein was readily compressed the artificial circulation was not restricted on application of subatmospheric pressure; the position of the artificial vein was at least as vulnerable as that of the real veins. In other experiments the wrist only was subjected to subatmospheric pressure, the wrist being sealed from the calorimeter by a second sleeve

8 284 D. R. COLES AND A. D. M. GREENFIELD (Fig. 6B). The upper sleeve had the same opportunity to restrict the circulation as in the normal experiments, but it was found that the application of the whole range of subatmospheric pressures was without appreciable effect on the 'heat elimination %' from the hand (Fig. 7). It was concluded that there was no appreciable restriction of the circulation at the wrist. A B C Fig. 6. A, Normal calorimeter system; B, arrangement for exposure of the wrist only to subatmospheric pressure; C, arrangement for testing for restriction of the circulation at the wrist. 2 fnni SVV co C.' C" & l -8- -o C 1 E 5 * DI DI mm Hg below atmospheric pressure mm Hg below atmospheric pressure Fig. 7. Fig. 8. Fig. 7. 'Heat elimination %' from the whole hand during the second 5 min of exposure of the wrist only to subatmospheric pressure. *, A.D.M.G.;, D.R.C. Fig. 8. 'Heat elimination %' from the distal parts of the fingers during the second 5 min of exposure of the whole hand to subatmospheric pressure. *, A.D. M.G.;, D. R. C. ~I

9 VASCULAR REACTIONS TO TRANSMURAL PRESSURE 285 Observations on the heat elimination from the fingers during exposure of the whole hand to subatmospheric pressure. These experiments differed from those already described in only two respects. The water-level in the calorimeters was reduced to 7 cm above the shelves on which the tips of the extended middle fingers rested. A second baffle, with suitable holes to admit the fingers, thermometer and stirrer, was fixed about 1 cm above the surface of the water. The results of experiments on the two trained subjects are shown in Fig. 8, and differ from the results on the hands (Fig. 3), mainly in the lower values of 'heat elimination %' during exposure to - 15 and -2 mm Hg. DISCUSSION The observed changes in heat elimination in these experiments could be caused in two main ways, alterations in heat clearance and alterations in blood flow. A. Alterations in heat clearance The amount of heat derived from each volume of blood may have been altered in three ways. (1) Precooling of blood arriving at the hand. As the subjects were sitting with the sleeves down in a comfortably warm room fluctuations in the temperature of the blood arriving at the wrists seem unlikely. Leakage of air past the wrist seal, and other events at this seal, may have cooled the blood on its way to the hand; such an effect is shown to be negligible by the experiments (Fig. 7) in which the wrist was exposed to suction without altering 'heat elimination %' from the hand. Draughts from leaks may have cooled the nonimmersed wrist, but such draughts were not felt subjectively, and the wrist was protected by a celluloid collar. Fluctuations in temperature of the arterial blood arriving at the immersed part of the hand may therefore be neglected. (2) Formation of oedema fluid. During the larger reductions in pressure much of the arriving blood appeared to remain in the hand as oedema fluid; this presumably had ample opportunity for heat exchange. (3) Insulation by oedema fluid. The oedema fluid may have insulated the circulating blood from the water in the calorimeter. On this point we have only indirect evidence. (a) 'Heat elimination %' was generally greater during the second than during the first 5 min at - 15 and -2 mm Hg, although the oedema was also greater. On the other hand, insulation by oedema fluid during the second 5 min may have masked an even larger rise in' heat elimination %'. (b) The quantity of oedema fluid (Fig. 5) was small after -6 and -1 mm Hg, the pressures at which the 'heat elimination %' was reduced. It seems unlikely that the oedema can have been responsible for the reduction.

10 286 D. R. COLES AND A. D. M. GREENFIELD These considerations make it probable that heat clearance was fairly constant and therefore that the 'heat elimination %' reflected reasonably accurately the rate of blood flow. B. Alterations in blood flow The immediate effect of local exposure to subatmospheric pressure is to increase the transmural pressure of all the blood vessels without altering the net perfusion pressure or the pressures within the vessels (Greenfield & Patterson, 1954). Subsequent adjustments may modify the transmural pressure, but make little difference to the net perfusion pressure. Alterations in blood flow in these experiments therefore indicate alterations in resistance to flow. Resistance to flow could be varied in three main ways. (1) Restriction at the wrist seal. Resistance might arise at the airtight seal between the wrist and the sleeve of the calorimeter. This has been excluded (Figs. 6, 7). (2) Compression by oedema fluid. Accumulation of oedema fluid may raise the tissue pressure, and so compress the vessels, and raise resistance. On theoretical grounds, the mean tissue pressure during exposure to subatmospheric pressure may be expected to approach but not to exceed the normal mean tissue pressure, and so to be incapable of causing compression of the blood vessels. On reverting to atmospheric pressure the mean tissue pressure rises, and may be sufficient to compress blood vessels. These theoretical considerations may be based on an over-simplification, and so be misleading. The following observations are therefore of value. (a) At -6 and -1 mm Hg, at which pressures blood flow is most reduced, there is little accumulation of oedema fluid. (b) After exposures to -15 and -2 mm Hg, 'heat elimination %' continues at a high level, well above 1. Had tissue pressure risen sufficiently to compress the vessels during exposure, it would presumably have sufficed to occlude them immediately afterwards. (3) Reactions of the resistance vessels. Resistance to flow may be altered by changes in the calibre of the resistance vessels due to active contraction or passive distension. It is suggested that such changes are primarily responsible for the alterations in 'heat elimination %' now reported. When the transmural pressure of the vessels of the dependent hand is increased by exposure to -6 or -1 mm Hg, there is a moderate constriction of the resistance vessels, and when it is increased by exposure to - 15 or - 2 mm Hg there is usually a large dilatation. It is uncertain at present whether the differences between the fingers and the whole hand (Figs. 3, 8) are due to local differences in the behaviour of the vessels, or to some interference in the hand with the vessels supplying the fingers.

11 VASCULAR REACTIONS TO TRANSMURAL PRESSURE 287 General discussion When the hand is lowered from the horizontal to the dependent position, the calculated increase in transmural pressure in the blood vessels in the fingers is about 56 mm Hg. When the pressure on the dependent hand is reduced below atmospheric the further increase in transmural pressure in the blood vessels is, approximately, equal to the pressure reduction. '-1 o cm below sternal angle *178 *373 I ~~~A 8 O O O a ^ ~~~~~~1od g 8o I * o -O E.N 5 'ZQ o 5 - E -6 II I mm Hg below atmo,spheric pressure Calculated increase in transmural pressure (mm Hg) Fig. 9. Average values of 'heat elimination %'., Roddie's (1955) observations on fingers supported at various distances below the sternal angle (top horizontal scale and left ordinate scale)., present observations on the dependent whole hand and A, on the dependent fingers during exposure to subatmospheric pressure (lower horizontal scale and right ordinate scale). Detached horizontal scale shows the total calculated increase in transmural pressure relative to the horizontal position for all observations, and takes account of both position and local subatmospheric pressure. Observations by Roddie (1955) on the effect of lowering the arm on the heat elimination from the fingers are shown in Fig. 9. This figure also shows the means of the results now reported on the heat elimination from the whole hand and from the fingers when the whole hand is exposed to subatmospheric pressure. The figure is so arranged that the abscissae represent calculated transmural pressure relative to the transmural pressure when the arm is held horizontally. The scales of 'heat elimination %' have been adjusted so that observations coincide at atmospheric pressure with the arm dependent. On increasing the transmural pressure by amounts up to about 9 mm Hg the 'heat elimination %' is increased. At increases of transmural pressure of 12 and 15 mm Hg, the 'heat elimination %' is perhaps slightly decreased. At 2 mm Hg or more, the 'heat elimination %' is greatly increased.

12 288 D. R. COLES AND A. D. M. GREENFIELD If the arguments already put forward for deducing changes in blood flow and in calibre of the resistance vessels are accepted, it may be concluded that there is no very considerable alteration in the rate of flow or vessel calibre until the transmural pressure is increased by more than 15 mm Hg. If finer differences are sought, there is some evidence that the smaller increases in pressure cause a small increase in flow, and that increases of 1 and 15 mm Hg cause the flow to revert to or even to fall a little below the basal value. From this it seems clear that there is a local reaction tending to stabilize resistance, and opposing, more or less successfully, passive distension of the resistance vessels within this range of pressures. The present observations throw no light on the mechanism of such a reaction. The increased circulation with very high transmural pressure may represent an inability of the resistance vessels to maintain size in spite of contraction, or may perhaps be a reaction to injury. SUMMARY 1. Heat elimination from the fully dependent hands has been measured during exposure of one hand to subatmospheric pressures of - 3, - 6, -1, -15 and -2 mm Hg for periods of 1 min. 2. The results have been adjusted to allow for general changes in the circulation revealed by the observations on the control hand. 3. During exposure to -3 mm Hg there was no significant change. 4. During exposure to -6 and - 1 mm Hg heat elimination was reduced. This is considered to indicate a reduction in the rate of blood flow brought about by a constriction of the vessels mainly responsible for resistance, in response to an increase in the transmural pressure in some or all of the vessels in the hand. 5. During the application of - 15 mm Hg the response was variable, heat elimination being sometimes increased and sometimes decreased. 6. During the application of -2 mm Hg, the heat elimination from the whole hand was always increased, and often greatly so. This indicates a dilatation of the resistance vessels. 7. It is concluded that there is a local response tending to stabilize the blood flow while the transmural pressure is increased by amounts up to 15 mm Hg. The present observations throw no light on the mechanism. We wish to thank the Trustees of the Sir Halley Stewart Trust for a grant to A. D. M. G. which defrayed part of the cost of this work. D. R. C. holds a Medical Research Council Fellowship in Clinical Research. We wish also to thank the subjects for their co-operation.

13 VASCULAR REACTIONS TO TRANSMURAL PRESSURE 289 REFERENCES BAYLISS, W. M. (192). On the local reactions of the arterial wall to changes of internal pressure. J. Physiol. 28, COLES, D. R. & GREENFIELD, A. D. M. (1955). Heat elimination from the hands during local exposure to subatmospheric pressure. J. Physiol. 128, 58P. COOPER, K. E., CROSS, K. W., GREENFIELD, A. D. M., HAMILTON, D. McK. & SCARBOROUGH, H. (1949). A comparison of methods for gauging the blood flow through the hand. Clin. Sci. 8, FoLow, B. (1949). Intravascular pressure as a factor regulating the tone of small vessels. Acta phy8iol. acand. 17, FOLKOw, B. (1953). A study of the factors influencing the tone of denervated blood vessels perfused at various pressures. Acta physiol. 8cand. 27, GASKELL, P. & BURTON, A. C. (1953). Local postural vasomotor reflexes arising from the limb veins. Circulation Res. 1, GREENFIELD, A. D. M. & PATTERSON, G. C. (1954). Reactions of the blood vessels of the human forearm to increases in transmural pressure. J. Physiol. 125, GREENFIELD, A. D. M. & SCARBOROuGH, H. (1949). An improved calorimeter for the hand. Clin. SCi. 8, PATTERSON, G. C. & SHEPHERD, J. T. (1954). The blood flow in the human forearm following venous congestion. J! Physiol. 125, RODDIE, R. A. (1955). The effect of arm position on the heat elimination from the fingers. J. appl. Physiol. 8, ROSENSWEIG, J. (1955). The effect of the position of the arm on the oxygen saturation of the effluent blood. J. Physiol. 129, SHANKS, R. G. (1955). The effect of venous congestion on the rate of heat elimination from the fingers. Clin. &i. 14, YAMADA, S. & BuiRTON, A. C. (1954). Effect of reduced tissue pressure on the blood flow of the fihgers; the veni-vasomotor reflex. J. appl. Physiol. 6, PHYSIO. CXXXI