Edinburgh University and the M.R.C. Climatic Unit, Oxford (Received 16 February 1953)

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1 581 J. Physiol. (I953) I2I, 58I-592 CARDIOVASCULAR RESPONSES TO BLADDER DISTENSION IN PARAPLEGIC PATIENTS BY D. J. C. CUNNINGHAM, L. GUTTMANN, D. WHITTERIDGE AND C. H. WYNDHAM From University Laboratory of Physiology, Oxford, Spinal Injuries Centre, Stoke Mandeville Hospital, Ministry of Pensions, Physiology Department, Edinburgh University and the M.R.C. Climatic Unit, Oxford (Received 16 February 1953) Guttmann & Whitteridge (1947) previously reported that, in patients with complete transverse lesions of the spinal cord above the mid-thoracic region, distension of the bladder produced a large rise of systolic blood pressure. In patients with lesions at or below the mid-thoracic region, the systolic blood pressure rose mm Hg at the most. From observations of skin temperature and pulse volume in the toes they concluded that, in all patients whose lesion was above segmental level L 2 and whose cord was isolated but undamaged, there was a cutaneous vasoconstriction in the legs. In the patients with high lesions, this vasoconstriction spread to the hands. They believed that the essential difference between the two groups of patients was that the peripheral resistance was increased in the patients with high lesions, but that in the patients with low lesions, owing to a compensatory vasodilatation in the upper half of the body, the peripheral resistance was little altered. Their experimental findings in paraplegic patients have been confirmed by Thompson & Witham (1948), Robertson & Wolff (1950) and by Pollock, Boshes, Char, Finkelman, Arieff & Brown (1951). Recently, Adams-Ray & Norlen (1951) have provided evidence of constriction of the vessels of the skin induced by bladder contraction in some normal subjects, as has More (unpublished observations). The work of Milwidsky & de Vries (1948), Pugh & Wyndham (1950) and of Brigden, Howarth & Sharpey-Schafer (1950) emphasized the necessity of a knowledge of cardiac output and muscle blood flow in order to interpret the vascular disturbances in the allied condition of spinal anaesthesia. The relative importance of changes in heart output and peripheral vasoconstriction was also discussed by Neumann, Foster & Rovenstine (1945), in the light of measurements of blood flow in the skin only. Further information therefore seemed to be desirable on cardiac output, muscle blood flow and splanchnic blood flow. We have now measured the first two factors.

2 582 D. J. C. CUNNINGHAM AND OTHERS MATERIAL AND EXPERIMENTAL METHODS We have studied in some detail five patients with spinal transection. Two had high lesions, one below C7 and the second below T 1. The third patient had an oblique lesion with sensory loss at T 10 on the right and T6 on the left. The fourth patient had a lesion at T6 on the left and T 7 on the right, and the fifth a transverse lesion at T7. In all cases the lesion is described in terms of the lowest segmental level at which sensation was still present. In all patients the lesions were complete clinically with loss of power and sensation, and loss of vascular response below the level of the lesions to thermal and painful stimuli applied to the head or face. The existence of a complete transection of the cord was verified at operation in subject (5) with a lesion at T7. Records from subject (2) have been published previously (Gilliatt, Guttmann & Whitteridge, 1947). At operation the cord was found to be 'not completely severed', but the transverse spinal syndrome remained clinically complete. In all these patients the occurrence of deep reflexes, flexor withdrawal, detrusor contractions of the bladder and vascular changes in the lower half of the body were taken as evidence that the isolated cord was capable of independent reflex activity. Two more patients had to be excluded from this series since their absent or sluggish withdrawal reflexes, absent detrusor contractions and absence of skin temperature changes below the level of the lesion suggested that there was a considerable degree of damage to the isolated segment of the cord. In the investigation on patients (1), (2) and (3), two series of observations were made on each patient. This was necessary as peripheral venous pressure, blood flow in the forearm and finger, and blood pressure could not all be measured simultaneously. The methods used for studying bladder pressure and volume, blood flow in the finger and pulse volume in the toe were described by Guttmann & Whitteridge (1947). The rate of increase in volume in forearm and calf during venous occlusion was measured by means of plethysmographs of the type described by Grant & Pearson (1938). Both were filled with water at 340 C, with air transmission to a float volume recorder, calibrated by air displacement from a 10 ml. syringe. Cardiac output (c.o.) was determined by Grollman's acetylene rebreathing method (Douglas & Priestley, 1948). The rebreathing bag was filled with a volume just short of the patient's vital capacity, consisting of a mixture of 30% acetylene in air. With training, rebreathing was satisfactory both in time taken and in amount of emptying of the bag. In the two patients with high lesions, vital capacity was of the order of 1X5 1., due partly to intercostal paralysis and partly to measurement in the recumbent position. It is therefore doubtful whether mixing of the gases in the lung-bag system was complete. Errors from this source were probably not excessive since the rate of uptake of both oxygen and acetylene would be affected in a similar manner, and the calculation of the cardiac output is based on the ratio between these rates. We therefore consider that any major change in cardiac output would become apparent even if the absolute values obtained are open to doubt. Oxygen consumption was determined by the Douglas bag method, the samples being collected over at least 5 min. Respiratory gas samples were analysed in duplicate. Venous pressure was measured by means of a saline manometer connected to a wide bore transfusion needle inserted into the antecubital vein. The patients lay flat with the foot of the bed tilted up by 1 ft. blocks and the arm abducted at the shoulder. They were allowed to reach a steady state in the new posture before venous pressures were recorded. The measurements were made in relation to the sternal angle. Blood pressure (B.P) was measured by the auscultatory method with a 4 in. cuff. With each patient we made observations on pulse rate, B.P. and peripheral blood flow during a control period in the warm room. The first measurements of heat output were made after J-1 hr. Further measurements were made when the blood pressure became steady during bladder distension, and finally when the B.P. became steady at about its original level. In patients (4) and (5) only measurements of forearm and calf blood flow and skin temperature were made.

3 BLADDER DISTENSION' IN PARAPLEGICS 583 RESULTS Heart output. The results of measurement of heart output by the acetylene method are given in Table 1. In the second set of observations on patient (3) the initial high value for cardiac output was probably due to overbreathing when he was unfamiliar with the respiratory valves and apparatus. The R.Q. was correspondingly high. In patient (1) there was on each occasion a small increase in cardiac output, but in patient (2), who also had a high lesion, there was a small decrease. We do not consider any of these changes significant, since with low vital capacities even mixing almost certainly did not take place. TABLE 1. Changes in blood pressure, heart rate, cardiac output and venous pressure A before, B during and C after bladder distension B.P. H.R. C.O. V.P. Patient and lesion Expt. Procedure (mm Hg) (beats/mm) (1./mm) (cm H20) Patient (3). Lesion T 10 on right, 1 A 135/75 76, 78 T6 on left B 145/80 76 C 140/80 74, 76 2 A 140/ to +2-E B 152/ to +4 C 145/ Patient (1). Lesion C7 1 A 120/ B 180/ C 110/ A 116/ B 186/ C 122/86 76 Patient (2). Lesion T 1 1 A 105/60 84 B 180/ C 140/ A 100/70 +1 B 200/ C 134/ Figures for total peripheral resistance are therefore misleading and have been omitted. In patients (1) and (2) the work of the left ventricle was considerably increased. Blood pressure. The B.P. changes in these patients agreed entirely with the previous findings. The blood pressure rose sharply in the patients with lesions above T 6 (Figs. 2, 3), but rose much less or not at all in patients with lower lesions (Figs. 1, 4 and 5). Muscle bloodflow. The observations on the patients (4) and (5) with approximately transverse lesions below T 6 are illuminating. When records were taken at the height of a detrusor contraction of the bladder there was a rise in blood flow in the forearm, and a fall in that in the calf (Figs. 4, 5). In patient (4) the blood flow through both forearm and calf was found to fluctuate widely while the bladder was distended; the greater changes coincided exactly with the peaks of the detrusor contraction, with a rapid return towards normal as soon as the detrusor action was over. If observations

4 I140 E c E E D. J. C. CUNNINGHAM AND OTHERS I I B.*..P P \.R _ P.R..\ o 30' E 20 U Minutes Fig. 1. Bladder distension in patient (1). Lesion below C7. From above downwards, blood pressure systolic and diastolic, pulse rate, venous pressure, bladder pressure, bladder volume. ml w 160 E BLP/ VO I I I I I I I I I I I I I I I BL..VOL. ~.-.1 I I I _.. :.. -; \,._._ /-- / _, 50~~~~s I I I I Minutes Fig. 2. Bladder distension in patient (2). Lesion below T1. From above downwards, blood pressure systolic and diastolic, pulse rate, venous pressure, bladder pressure, bladder volume C - v I u

5 BLADDER DISTENSION IN PARAPLEGICS 585 were not made at the height of the detrusor action the changes were small, e.g. Fig. 4 at 56 mi. In patient (5), however, in whom fluctuations in bladder pressure were less violent, there was a maintained fall in calf flow and a maintained rise in forearm flow throughout a period of distension (Fig. 5). In patient (3), in whom the transection was at T 10 on the right and T 6 on the left side, there was a fall in calf flow in the left leg with a rise in flow in the right. The left leg 120 oo 110 -I E 100 E 90 c 80 2E 70, 60 o 6 X 4 u I 40 E E P.R. V.P. BL. VOL Minutes Fig. 3. Bladder distension in patient (3). Lesion below T 10 on the right, T6 on the left. From above downwards, blood pressure systolic and diastolic, pulse rate, venous pressure, bladder pressure, bladder volume. was presumably supplied entirely by sympathetic fibres arising from the cord below the level of the lesion and behaved in the same way as the legs of patients (4) and (5). Although the vascular bed supplied by sympathetic fibres from the isolated part of the cord was small in this patient, the few measurements we made indicated that the blood flow in the forearm was more than doubled during bladder distension. There was also a rise in his finger blood flow from 1 to 11 ml./min. In two patients with high lesions (patients (1) and (2)) the blood flow through the calf was reduced during bladder distension. This is shown in Table 2.

6 586 D. J. C. CUNNINGHAM AND OTHERS There was, however, a very large increase in forearm blood flow in patient (2) (Table 2) on each occasion. A smaller rise occurred in patient (1), whose forearm was severely wasted owing to his lesion at C 7. These increases in forearm blood flow were unexpected, but after making these observations we noted in confirmation that, although the skin of the fingers was cold, the skin over the forearm muscles was hot. In patient (1) the increase in blood flow was at least 400 %, although the mean increase in B.P. was only 70 %. These patients also showed marked vasodilatation of the skin of the neck similar to that reported earlier (Guttmann & Whitteridge, 1947). E 12-0 B.P '" E2100 C. P.R. 70 E 4 6eg0E E 80-r 80l E2 Forehead 90 ALT 85 LL; 80 - RF1I= 75_*~ Minutes Fig. 4. Bladder distension in patient (4). Lesion below T6 on left, T7 on right. From above downwards, at the beginning of observations, blood pressure systolic and diastolic, pulse rate, blood flow in calf, 0 0, blood flow in forearm, 0 *, bladder pressure, bladder volume, skin temperatures from forehead, left halluxr (LT 1) and right thumb (RF 1). Skin blood flow. In general, the skin blood flow changes, when measured, were similar to those previously reported. In patient (2), however, there was a sharp initial rise in blood flow from 4 to 7 ml./100 ml. finger/mmn. This was converted to a constriction after about 15 min Re-examination of previous records shows that in three observations out of twelve there was a brief initial increase in blood flow in the finger at a time when the pulse volume in the toe was falling. This was well seen in patients in whom the bladder was filled at rates of about 20 ml./min.

7 BLADDER DISTENSION IN PARAPLEGICS 587 c 80 E 70,< 60 c 100 Ē Minutes Fig. 5. Bladder distension in patient (5). Lesion below T7. From above downwards at the beginning of observations, blood pressure systolic and diastolic, pulse rate, blood flow in calf, 0 O, blood flow in forearm 0-*, bladder pressure, bladder volume, skin temperatures from left hallux (LT 1), right forefinger (RF2), room temperature. TABL 2. Changes in blood flow The figures for blood flow in muscle are expressed in ml./100 ml. tissue/min and represent maximum changes. The figures for finger flow are expressed in arbitrary units. A before, B during bladder distension. Procedure (mm Hg) flow flow left right Mean B.P. Finger Arm Calf flow Calf flow Patient and lesion Expt. Patient (3). Lesion at T 10 1 A 105 1* 3.7 3X6 on right, T6 on left 2 B * Patient (2). Lesion at T 1 Patient (1). Lesion at C7 Patient (4). Lesion at T 6 Patient (5). 2 A 116 B A B A B A B A B A B * Flow expressed in arbitrary units zero 6* * * 8.6* 4-5 1* * * 0.45*

8 588 D. J. C. CUNNINGHAM AND OTHERS As the apparatus was unsuitable for measurements of skin flow, as opposed to pulse volume in the toes, we measured skin temperatures in the face, hands and feet on patients (4) and (5) (Figs. 4, 5). There was a sharp drop in the temperature of the toes in each case, but rectal and face temperatures rose. These findings agree with those of Guttmann & Whitteridge (1947). The situation was a little confused by a tendency for the calf volume curves to flatten out very early during the collection period. As this did not happen before the bladder constriction, we suspect that this was due to the onset of venous constriction, for which there is other evidence. Venous pressure. For a number of reasons we had to be content with measurements of peripheral venous pressure in these patients. Table 1 and Figs. 1-3 show the venous pressure changes, which are much more striking in the patients with high lesions. An increase in filling of the veins of the neck was observed in these and in the previous experiments. DISCUSSION A decreased blood flow in the toes can reasonably be inferred from the present and previous observations on skin temperature, and from observations on pulse volume in the toes. The present work suggests that in all patients there is also a decrease in flow in the calf when its sympathetic innervation is derived from the isolated cord. Adams-Ray & Norlen (1951) bave shown that in some normal human beings there is a decreased skin blood flow below the umbilicus when the bladder is distended, and they believe that this reflex constriction is normally limited to the segments which give rise to the sympathetic bladder innervation. More (unpublished observations) has catheterized two normal subjects, and has found that when the pressure in the bladder rises above 50 mm Hg, wide-spread vasoconstriction of the skin occurs. Large volumes of fluid in the bladder may produce no cutaneous constriction, if the bladder pressure remains low. The function of the reflex is not obvious, but it may form part of a Loven reflex by which the flow to the distended viscus might be increased. Measurements of blood flow in the wall of the distended viscus before and after denervation would seem to be bighly desirable. We have already shown that the rise in blood pressure is more closely related to the pressure in the bladder, than to its volume (cf. Watkins, 1938). A pressure of mm Hg might seriously interfere with the blood flow to the bladder wall and mucosa. Recently, Mohamed & Bean (1951) have drawn attention to the decrease in blood flow which occurs in a loop of intestine during tonic contraction. As regards patients with lesions below T6, it is clear that increased blood flow in the fingers and in the forearm while the B.P. rises only slightly, can be regarded as compensatory vasodilatation initiated by the carotid sinus

9 BLADDER DISTENSION IN PARAPLEGICS 589 (cf. Neuman et al. 1945). The same explanation would account for the fall in pulse rate. The large changes in forearm flow also suggest that muscle blood flow is affected by blood-pressure regulating mechanisms in these patients, perhaps to a greater extent than it is in normal subjects (cf. McDowall, 1950). In the patients with high lesions we suggest that the sequence of events is as follows. The distension of the bladder initiates vasoconstriction of the vessels of the skin of the legs and of the muscles. This leads to an increase in both systolic and diastolic B.P., particularly the latter. The reflex constriction spreads to all the sympathetic outflow of the isolated cord. If this spread is slow, there is at first a passive increase in flow in the fingers. If it is fast, the constriction in the fingers reduces the blood flow in spite of an increase in blood pressure. Subsequently, the finger blood flow remains very low or absent as long as the bladder is distended. At the height of the rise in bladder pressure and therefore in blood pressure, there are further changes in the upper part of the body. The patchy vasodilatation in the neck and face has been described previously. One of us (L. G.) has observed similar patchy vasodilatation in the skin of the face and neck in patients in whom posterior cervical nerve roots were stimulated in the course of operations. The vasodilatation in paraplegics may be due to an axon reflex, but if so the afferent limb remains obscure. The very great rise in forearm blood flow in patients with lesions above the level of the whole sympathetic outflow remains puzzling. If it is passive, due to the raised blood pressure, it is not clear why there should be a decrease and not an increase in blood flow in the legs. The observations of Pickering & Hess (1932) that there is greater sympathetic tone in the legs are not really relevant here, since they describe the situation when the vasomotor centre is able to modify the whole sympathetic outflow. It is worth stressing that this remarkable increase in muscle blood flow is only seen in areas in which the somatic sensory nerve supply is intact, and occurs in spite of the fact that the autonomic supply arises from the isolated cord. The change in venous pressure is interesting. For various reasons we measured the venous pressure at the elbow and did not try to use a cardiac catheter. Although local increases in venous pressure may at times occur in veins of the arm with an increase in arm muscle flow, the increase in the pressure in the veins of the neck provides strong evidence that our observed rises of venous pressure of 14 cm and of 7 cm reflect increases in the central venous pressure. Of the possible causes, we may consider back pressure effects transmitted across the lungs from the left heart and similar effects due to increased coronary flow, a direct effect of the decreased heart rate, and an effect on the venomotor system. During the increase of venous pressure from 0 to 14 cm H20, the systolic

10 590 D. J. C. CUNNINGHAM AND OTHERS blood pressure rose only from 100 to 140 mm Hg and the heart rate remained steady (Fig. 2). At this stage back pressure effects seem somewhat unlikely. When the blood pressure reached 200 mm Hg the work of the left ventricle was increased by 25%, and at the same stage in this patient Guttmann & Jones (unpublished observations) have observed radiographically an increase in the diastolic volume estimated at 4-5 times the increase in stroke volume. At this stage back pressure effects may well play an important part. In view of the work of Patterson & Starling (1914) on the denervated heart, a decrease in heart rate might be expected to cause a rise in venous pressure. In our experiments, however, the heart rate fell slightly at the first sign of a rise in blood pressure and remained steady during the greater part of the rise in venous pressure. The possibility remains that there is a powerful active vasoconstriction of the veins, produced by centres in the isolated cord and activated by visceral distension. Donegan (1921) produced evidence for such venous constriction in animals, and Doupe, Krynauw & Snodgrass (1938) have evidence of an active constriction in man, in response to brisk cooling of the whole body. These results make it clear that the changes in heart output are not responsible for the blood pressure changes, but that changes in peripheral vascular resistance play a very important part. It is also clear that our observations on muscle blood flow throw no light on the differences between patients with lesions above and below T 6. All patients studied have shown a decrease in blood flow in the calf during bladder distension when the leg was supplied entirely by fibres from the isolated cord. In all patients there has been an increase in blood flow in the forearm, though probably for different reasons in the two groups. In the patients with low lesions this increase is most probably due to a depressor reflex initiated by pressure receptors and mediated by autonomic fibres. Whatever may be the cause of the increased forearm flow in patients with high lesions, it cannot be due to this mechanism. The only difference which we have so far demonstrated between the two classes of patients is that those with low lesions show an increase in finger blood flow, those with high lesions show a decrease. The total blood flow to both hands when warm and at rest is about 200 ml./min (Greenfield, Shepherd & Whelan, 1951) and this is of course only a small fraction of the cardiac output. This difference in finger blood flow cannot therefore be responsible for the differences in blood pressure. We have of course been able to measure blood flow neither in the skin and muscles of the trunk nor in the splanchnic region. It is, however, worth remembering that the sympathetic supply to the hand is from segments T3-T9 and that the splanchnic fibres leave the cord from T5-T11. It is therefore possible that though constriction in the finger is not quantitatively important, it gives an indication of vasoconstriction in the splanchnic area due to fibres which arise from the same spinal segments.

11 BLADDER DISTENSION IN PARAPLEGICS 591 This splanchnic vasoconstriction could be responsible for the rise in peripheral resistance and the resulting rise in blood pressure. This explanation would be in close agreement with that put forward by Neumann et al. (1945), who observed a dilatation of the vessels of the toes in all patients during spinal anaesthesia but observed vasoconstriction in the fingers in all patients in whom the blood pressure was maintained. This work has consisted of detailed study of a very small number of patients. However, the two patients with high lesions (1) and (2) and the two patients with transverse low lesions (4) and (5) have behaved in all respects studied in the same way as the larger series of patients described by Guttmann & Whitteridge (1947). The behaviour of patient (3) who had an oblique lesion agrees with that of patients (4) and (5) as far as the territory supplied by fibres from the isolated cord is concerned. As differences between patients with transections at the same spinal level seem to be small, we think that these results may be generally applicable to paraplegics. SUMMARY 1. The heart output of three paraplegic patients during distension of the bladder has been measured by the acetylene method and found not to change significantly. 2. The blood flow in the forearm and calf has been measured in five patients. In three patients with lesions below T 6, the blood flow in muscle supplied with sympathetic fibres by the isolated cord showed a considerable decrease, whereas the blood flow in muscles supplied by sympathetic fibres controlled by the vasomotor centre increased. These changes were in the same direction as those previously observed in skin. 3. In two patients with lesions at T 1 and C 7, the blood in the calf decreased. The blood flow in the forearm greatly increased, although the flow through the skin of the fingers almost stopped. 4. A steep rise in venous pressure was seen in the patients with lesions at TI and C7. 5. Possible mechanisms for this increase in flow have been discussed. We have to acknowledge with thanks the assistance of Mr I. G. Lennox in some of these experiments, as well as a grant from the Medical Research Council for his expenses. REFERENCES ADAMS-RAY, J. & NORLEN, G. (1951). Bladder distension reflex with vasoconstriction in cutaneous venous capillaries. Acta physiol. scand. 23, BRIGDEN, W., HOWARTH, S. & SHARPEY-ScHAFER, E. P. (1950). Postural changes in the peripheral blood flow of normal subjects with observations on vasovagal fainting reactions as a result of tilting, the lordotic posture, pregnancy and spinal anaesthesia. Clin. Sci. 9, DoNEGAN, J. F. (1921). The physiology of the veins. J. Physiol. 55, DouGlAs, C. G. & PRIESTLEY, J. G. (1948). Human Physiology. Oxford: Clarendon Press.

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