Captain Robert R. Stahl, MC, USAFR
Major Curtis P. Artz, MC, USA
Captain John M. Howard, MC, USAR
Fiorindo A. Simeone, M. D., F. A. C. S.

Methods

Table 1.
Observations on 23 Cases

Relationship Between Increase in Pulse Volume After Ulnar Nerve Block and Environmental Temperature

FIGURE1.
Relationship between absolute values of pulse volume before
and after ulnar nerve block and environmental temperature.

FIGURE2.
Relationship between percent increase in pulse volume after ulnar nerve
block and the various ranges of environmental temperature in which patients were studied.

Relationship Between Initial Absolute Values for Pulse Volume and Environmental Temperature

FIGURE3.
Relationship between the initial absolute values of pulse volume and
the various ranges of environmental temperature in which patients were studied.

Relationship Between the Administration of Morphine and the Initial Absolute Value for Pulse Volume

Relationship Between Blood Deficit and Pulse Volume

Relationship Between Type of Injury and Pulse Volume

Relationship Between Initial Absolute Pulse Volume,
Increase in Pulse Volume After Block, and Systolic Blood Pressure

Table 4. Relationship Between Pulse Volume and Systolic Blood Pressure

*Those patients who at some time before or during the study had some degree of systolic hypertension (140 or more mm. of mercury).
?Systolic blood pressure just 100 mm. of mercury at the time of the determination.

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strated in Figure 4. Again it is emphasized that the patients in whom systolic blood pressure was 140 or more millimeters of mercury reacted with relatively small increases in pulse volume after peripheral ulnar nerve block.

The group of patients in whom systolic blood pressure fell below 100mm. of mercury is so very small in comparison to the group in whom systolic pressure remained above 100 mm. that a correlation between pulse volume and systolic blood pressure is not justified.

Cases 12 and 16 both had moderate blood deficit; Case 20 had severe blood deficit. Cases 16 and 20 were both in the group in which systolic blood pressure was below 100 mm. of mercury. Case 12 had a systolic blood pressure of just 100 mm. of mercury at the time of the determination. Cases12 and 20 were both studied at relatively high ambient temperatures.

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Various types of blood pressure response were observed in this group of patients. The following categorizes the patients according to the type of systolic blood pressure* response:

1. Patients who were normotensive from the onset of injury until the completion of our studies without blood or fluid replacement-Cases2, 5, 8, 9, 14, 17, 19, 23.

2. Patients who were originally normotensive but became mildly hypertensive with fluid or blood replacement-Cases 1, 13.

3. Patients who were hypertensive from the onset of injury until completion of our studies without fluid or blood replacement-Cases4, 6, 7, 10, 18.

4. Patients who were at first hypotensive but became hypertensive with blood and fluid replacement; our studies were made during the hypertensive period-Cases 15, 21.

5. Patient who was at first hypotensive but became normotensive with fluid or blood replacement-Case 11.

6. Patients who were hypotensive from the onset of injury until completion of our studies-Cases 12, 16, 20, 22.

Two of the patients in the hypertensive group (Table 4) were studied in detail. Each of these patients is reported here in detail with case summaries and charts depicting the results of the study.

Case 4. A 21-year-old colored male was shot just outside his company area with an M1 rifle at 2400 hours on May 10, 1953.He arrived at the battalion aid station at 0030 hours on May 11, 1953,where his wounds were cleaned and dressed and he received penicillin, tetanus toxoid, and 15 mg. of morphine sulfate. He arrived at the clearing station at 0750 hours where he was again given 15 mg. of morphine sulfate. He was then evacuated to the 46th Army Surgical Hospital by helicopter, arriving there at 1020 on May 11, 1953.

On admission he was found to have an evulsive wound of the right lower thigh with associated fracture of the right femur. The patient was hypertensive on admission and remained so throughout the entire period preceding surgery. His skin was warm; nailbeds were pink; pulse was of good volume; he complained of slight intermittent pain in the right thigh at the site of injury. His total blood loss was estimated to be no more than 200 to 300 cc.

The interval of time elapsing between injury and the onset of our experimental procedure was approximately 10¹/2 hours. The duration of the study was approximately 5 hours.

Following a right ulnar nerve block the maximal percentage increase in pulse volume bilaterally was 93 per cent. However, during this period of time the room temperature increased from 73.4° to 75.2°F and the skin temperatures on both the blocked and unblocked sides increased to 15 degrees in the interval of time from the control tracings until the tracings were repeated after ulnar nerve block. It is obvious from these findings that the patient was in the process of stabilization in the presence of a somewhat changing environmental temperature. Consequently it is impossible to evaluate what 

*Patients who in the supine position had systolic blood pressures of 140 mm. of mercury and above were considered to be hypertensive.

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portion of the increase in pulse volume and skin temperature on the right side could be attributed to the right ulnar nerve block; the evaluation would be impossible because of the many variables involved.

At one point in the procedure 5 mg. of phentolamine was given intravenously. There was no appreciable change in the pulse volume on either the right or left sides after the administration of this drug. There was a slight transient drop in the diastolic blood pressure but little change in the systolic pressure.

At another point in the procedure 25 mg. of hexamethonium bromide was given intravenously at a rapid rate. The administration of this drug resulted in a maximal percentage increase in pulse volume in the left fifth finger of 24 per cent. There was an associated abrupt fall in both systolic and diastolic blood pressure (190/98 to 90/0) and an increase in pulse rate from 116 to 150 per minute. The patient complained of vertigo and it was necessary to tilt him head-down for a few minutes. The increase in digital pulse volume produced by this drug was very transient. The markedly hypotensive effects lasted for about 5 minutes, and then both systolic and diastolic pressures climbed gradually to the premedication level over a period of about 13 to 15 minutes.

During the experimental procedure the patient was covered with one wool blanket from the chest to his feet. After the administration of phentolamine and hexamethonium bromide blood pressures were taken at minute intervals by the cuff method on the right arm. The mechanics of the inflation of the blood pressure cuff tends to invalidate all plethysmographic determinations recorded from the right side because of the intermittent interruption of blood flow.

During anesthesia with pentothal the patient experienced another episode of hypotension. This tends to substantiate the thoughts of others who maintain that pentothal is a sympathetic ganglionic depressant agent. In this case there was similarity between the response to a known ganglionic blocking agent, hexamethonium, and the response to pentothal. The hypotensive phase occurring simultaneously with pentothal administration subsided only when the anesthetic agent was changed to gas, oxygen, and ether. The duration of anesthesia and surgery was approximately 1 hour,45 minutes.

The accompanying graph in Figure 5 depicts the results of the determinations.

Case 21. A 23-year-old colored male was injured by mortar fragments on July 18, 1953, at approximately 1330 hours. Blood pressure recorded at the battalion aid station was 50/40. He received 200cc. of serum albumin and 1,000 cc. of dextran in addition to 15 mg. of morphine sulfate at the aid station. The patient was evacuated by helicopter and arrived at the 46th Army Surgical Hospital at approximately 1600 hours on July 18, 1953.

Examination at the hospital revealed a traumatic amputation of the right lower leg and multiple large penetrating wounds of the left lower leg and small penetrating wounds of the right arm. Blood pressure was 70/30 and pulse 144 per minute. Preoperatively the patient received3,000 cc. of whole blood. At 1940 hours he was taken to surgery at which time both legs were amputated just below the knee joint. Surgery ended at 2140 hours; the patient received 2,500 cc. of whole blood during the surgical procedure.

Prior to surgery blood pressure ranged from 70 to 138systolic and from 30 to 80 diastolic. Following surgery the patient`s blood pressure began to rise gradually to reach hypertensive levels; at the eighth postoperative hour his blood pressure was 184/108. The studies were begun at approximately 11¹/2 hours following the completion of surgery at which time the blood pressure was 164/102. At the time of the study the patient was moderately apprehen-

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sive and emotional about the loss of his legs. His skin was warm to palpation; color was normal; he was perspiring profusely; and the pulse was rapid and full.

Pulse volumes and finger flows were recorded bilaterally from the tips of the fifth finger. Initial values on the right and left fingers for pulse volume were 3.20 and 3.75 cu. mm. per 5 cc. of finger, respectively. The values following right ulnar nerve block were 3.60 and3.75 cu. mm. per 5 cc. of finger, respectively. The slight increase on the right following right ulnar nerve block is insignificant. Following the nerve block there was complete anesthesia over the sensory distribution of the ulnar nerve in the hand. Finger flows actually decreased bilaterally after nerve block without any appreciable decrease in the blood pressure or pulse pressure.

Following this first part of the study the patient was given 225 mg. of sodium amytal intramuscularly. The patient became quite lethargic and began to sleep soundly. There was only slight decrease in systolic pressure (14 mm. of mercury) over the period of an hour following the administration of sodium amytal and then the pressure returned gradually to its original level. Pulse volumes at this time showed no appreciable consistent change as a result of sodium amytal sedation.

The environmental temperature during this study ranged from 84.4° to 90.3° F. These studies reveal that this man, even though hypertensive, did not show evidence of vasoconstriction in the skin and subcutaneous tissue as measured in the finger tip but, rather, was initially relatively vasodilated as one would expect a normal man to bein a very warm environment. Certainly if this patient had arteriolar constriction contributing to his hypertension it was not apparent in the skin and subcutaneous tissue of the finger tips.

The accompanying chart in Figure 6 depicts the results of the significant determinations during this study.

Fourteen of the twenty-three patients studied were considered to have skin temperature responses which were satisfactory for analysis. The initial skin temperatures at the base of the fifth finger on the side studied are plotted against the environmental temperature at the time in Figure 7.It will be observed that any point on the solid diagonal line represents a skin and an environmental temperature of the same magnitude. This line describes the behavior of the skin temperature under conditions of changing environmental temperature of a tissue which would theoretically be devoid of circulation, i. e., the skin temperature would be the same as that of the environment if sufficient time elapsed for equilibrium to be established. From this graph it will be seen that 11 of the 14 patients had initial skin temperatures which were above this line and indicating that the skin was warmer than the environment at the time of the determination. Three of the fourteen patients (Cases 14, 15, and 17) had skin temperatures slightly less than the environmental temperature. This could result

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only from perspiration and cooling due to evaporation from the skin surface or, possibly, from the fact that the patient was brought from a cool to a warm environment and had not reached equilibrium with the new environment. Cooling of the skin surface by evaporation or perspiration would tend to suggest that there was some degree of hyperactivity of the sympathetic nervous system. However, only 3 of the 14 patients demonstrated the phenomenon, all of which were considered to be in a state of slight blood deficit with systolic blood pressure above 100 mm. of mercury at the time of the skin temperature determination. One of these three patients became mildly hypertensive during the study.

The values depicted in Figure 7 are found in the data recorded in Table5.

FIGURE7.
Relationship between skin temperature before
ulnar nerve block and environmental temperature.

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Table 5. Relationship Between Skin Temperature and Environmental Temperature

All temperatures in degrees Fahrenheit.

The initial values for skin temperatures before ulnar block are plotted against the systolic blood pressure at the time of the temperature determination in Figure 8. Only 2 of the 14 patients had systolic blood pressures which were below 100 mm. of mercury at the time of the determination (Cases 12and 16). Both of these patients were considered to be in a state of moderate blood loss. The other 12 patients had slight blood deficit and all had systolic blood pressures over 100 mm. of mercury.

The graph in Figure 8 would indicate that there was a tendency for the patients with the highest systolic blood pressures to have the lower values for initial skin temperature before ulnar nerve block. Perhaps this indicates that there is some excessive degree of vasoconstriction in the vessels of the finger tip in this somewhat hypertensive group of patients.

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The values for skin temperature at the base of the fifth finger before and after ulnar nerve block are plotted against the environmental temperature in Figure 9. The vertical lines connect the determinations before and after block in a given patient and thus indicate the increase in temperature resulting from sympathetic paralysis. There is a tendency for those cases which were studied at higher environmental temperatures to show smaller increases in skin temperature after ulnar block. Three exceptions to this observation were Cases 1, 6, and 13 which were studied in a range of environmental temperature from 60° to 70° F. All three of these patients showed small increases after ulnar block and all had systolic blood pressures of 140 or more millimeters of mercury. These same three patients revealed relatively small increases in pulse volume after block. A possible explanation for the relatively small temperature and small pulse volume increases after sympathetic paralysis is that a circulating vasopressor substance could have maintained these peripheral vessels in a state

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of relative vasoconstriction following temporary denervation of the blood vessels.

In the normal human it has been shown by Morton and Scott⁵ that the normal maximal vasodilatation level for skin temperature after sympathectomy, procaine nerve block, or spinal anesthesia is approximately95° F. If it is assumed that the patients in this series had normal blood vessels and that satisfactory peripheral ulnar nerve blocks were obtained, the attainment of maximal vasodilatation would indicate that the patient had a normal blood volume and normal cardiac output. All of these patients had complete anesthesia in the skin of the hand innervated by the ulnar nerve following ulnar nerve block; thus, the belief was that the blocks were successful. Failure to obtain maximal vasodilatation in the vessels of the fifth finger after sympathetic paralysis indicates that there was a deficit of blood

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reaching the finger tip which could be due to oligemia and decreased cardiac output. Thus the degree to which these patients failed to reach the maximal vasodilatation level (95° F) after sympathetic paralysis should reflect the degree of oligemia and decreased cardiac output unless circulating vasopressor substances were responsible for vasoconstriction in these vessels. The degree to which the skin temperature at the base of the fifth finger failed to reach the maximal vasodilatation level is expressed by the ratio of experimental value for skin temperature after ulnar nerve block/theoretic maximal value (95° F) in Figures 10 and11. The solid black horizontal line represents a ratio of 0.95 or a skin temperature of approximately 90° F. Thus it is assumed, for purposes of discussion, that in the cases with ratios of 0.95 to 1.00 (skin temperatures of 90° to 95° F after ulnar nerve block) maximal vasodilatation had occurred. Thus all the ratios which were below this line represent patients in whom maximal vasodilatation was not present after ulnar nerve block. The relationship between this ratio and the environmental temperature is demonstrated in Figure 10. The relationship between this ratio and the systolic blood pressure is demonstrated in Figure 11. The data for these graphs are presented in Table 6.

Table 6. Relationship of Skin Temperature After Block to Theoretic Maximal

Case No.	Skin Temp. after Ulnar Block in Degrees F	Ratio-Experimental Skin Temp. after Ulnar Block/Theoretic Maximal (95°)	Systolic Blood Pressure in mm. of Mercury	Blood Deficit	Environmental Temp.
1	82.6	87	142*	Slight	60.1
2	85.5	90	134	Slight	77.9
3	93.7	98.6	128	Slight	71.0
5	100.2	105.4	120	Slight	72.9
6	81.8	86.1	140*	Slight	66.3
9	97.2	102	106	Slight	77.4
11	95.8	101	120	Slight	79.9
12	89.1	93.8	100	Moderate	75.8
13	84.6	89.0	140*	Slight	68.3
14	89.5	94.2	128	Slight	72.0
15	82.0	86.3	144*	Slight	75.2
16	93.6	98.5	98	Moderate	72.7
17	79.3	83.5	112	Slight	75.9
18	94.6	99.6	144*	Slight	71.2

*Indicates those patients who became hypertensive (systolic pressure 140 or more millimeters of mercury) prior to or during the determinations.

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FIGURE10.
Relationship between the ratio of experimental value of the skin temperature
after ulnar nerve block/theoretic maximal value and environmental temperature.

Of the 14 patients in whom skin temperature response was evaluated,8 or 57 per cent of the patients failed to reach the maximal vasodilatation level after ulnar block. Only one of these patients (Case 12) suffered moderate blood deficit; all of the remaining seven patients had only slight blood deficit at the time of the determination. Four of these eight patients had systolic blood pressures which were considered to be hypertensive at the time of the determination (Cases 1, 6, 13, and 15). In this hypertensive group, in which blood deficit was only slight, a circulating vasopressor substance could possibly be responsible for their failure to reach the maximal vasodilatation level following paralysis of the sympathetic supply to the vessels in the fifth finger tip; this, of course, is only speculation.

There were three other cases with slight blood loss which failed to reach the maximal vasodilatation level after sympathetic block (Cases 2,14, and 17). All of these three patients were normotensive on admission to the hospital and remained normotensive through the completion of the studies without fluid or blood replacement. There is no apparent explanation for their failure to reach the maximal vasodilatation level unless it bean expression of oligemia.

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FIGURE11.
Relationship between the ratio of experimental value of skin temperature
after ulnar nerve block/theoretic maximal value and the environmental temperature.

A correlation could not be established between the environmental temperature and whether or not patients reached the maximal vasodilatation level.

At present it is not possible to express definitely whether or not a given patient is vasoconstricted from observation of the absolute value of pulse volume. The range of pulse volume values at varying degrees of environmental temperature is unknown. It is conceivable that the range of values at any given temperature might be quite wide. Thus it is a decided disadvantage not to have baseline values with which to compare the patients in this series. Consequently there were limitations in the selection of a yardstick by which autonomic activity could be evaluated in these patients. Since the initial absolute value for pulse volume is somewhat of a variable, the degree of increase after sympathetic paralysis was chosen as a measure of autonomic activity. This is open to criticism because it must be assumed that a given degree of oligemia or a certain deficit of cardiac output will have the same relative effect on the rate of blood flow during vasoconstriction as during vasodilatation. There is no evidence at

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present upon which to base this assumption. Although the increase in pulse volume and skin temperature resulting from sympathetic paralysis is a measure of sympathetic activity in a given patient, one patient would not be comparable to another if there were great variability between patients in the degree of blood volume deficit. In this series of 23 patients, however, it was estimated clinically that 19 were in a state of slight blood deficit and I had no blood deficit; of the 3 remaining patients, 2 were in a state of moderate blood deficit and 1 in a state of severe blood deficit. It appears that difference in degree of oligemia was not a significant factor in most of these patients and the degree of increase in pulse volume and skin temperature after ulnar block should be a reasonably satisfactory approximation of vasomotor activity. The initial vasomotor activity as manifested by increase in pulse volume and skin temperature after sympathetic paralysis would also be a function of the initial environmental temperature.

The maximal vasodilatation level for pulse volume is not definitely established. An attempt was made to establish a theoretic maximal value from pulse volume studies, obtained by Simeone and associates,⁶ on 33 patients with normal circulation. These pulse volume studies had been made from the fifth finger on normal upper extremities after ulnar nerve block. It was found that the pulse volume values for these 33 patients, who were maximally vasodilated, were extremely variable. However, as suggested by one of us (F. A. S.), 10 cu. mm. per 5 cc. of finger have been used as the approximate theoretic maximal value for pulse volume after sympathetic paralysis.

The degree to which pulse volume failed to reach the maximal vasodilatation level is expressed by the ratio of experimental value for pulse volume after ulnar nerve block/theoretic maximal value (10 cu. mm./5 cc. of part)in Figures 12 and 13. The solid black line on these graphs represents a ratio of 1.00. The relationship between this ratio and the environmental temperature is demonstrated in Figure 12. The relationship between this ratio and the systolic blood pressure is demonstrated in Figure 13. Data from all 23 patients, relative to these graphs, are in Table 7.

All but three of the patients failed to reach the maximal vasodilatation level for pulse volume. The existence of a deficit by which patients failed to reach the maximal vasodilatation level even at high environmental temperatures indicates that the deficit is not due to unsatisfactory peripheral ulnar nerve blocks. Therefore, the deficit would indicate that these patients either had oligemia and decreased cardiac output or had a humoral vasopressor substance in their circulation. Unfortunately, the effects of oligemia per se could not be sepa-

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Table 7. Relationship of Pulse Volume After Block to Theoretic Maximal

Case No.	Pulse Volume after Block in cu. mm. per 5 cc. of Finger	Ratio-Pulse Volume after Block/Theoretic Maximal (10 cu. mm. per 5 cc. of Finger)	Systolic Blood Pressure	Blood Deficit	Environmental Temperature at Time of Pulse Volume Determination
1	4.55	0.46	142*	Slight	60.1
2	11.0	1.1	124	Slight	77.7
3	4.45	0.45	138	Slight	71.0
4	2.70	0.27	160*	Slight	75.2
5	8.85	0.89	120	Slight	72.9
6	4.30	0.43	144*	Slight	66.3
7	3.0	0.30	150*	Slight	85.5
8	14.75	1.48	116	Slight	82.6
9	6.55	0.66	106	Slight	77.4
10	5.75	0.58	140*	Slight	87.4
11	3.20	0.32	110	Slight	79.9
12	4.80	0.48	100	Moderate	75.8
13	2.35	0.24	140*	Slight	68.3
14	6.55	0.66	128	Slight	72.0
15	7.25	0.73	144*	Slight	75.2
16	6.0	0.60	96	Moderate	72.7
17	2.55	0.26	112	Slight	75.9
18	5.65	0.57	144*	Slight	71.2
19	5.70	0.57	124	Slight	86.0
20	3.40	0.34	70	Severe	90.3
21	3.60	0.36	160*	None	86.7
22	19.0	1.9	96	Slight	82.7
23	5.25	0.53	120	Slight	83.8

*Indicates patients who became hypertensive (systolic pressure 140 or more millimeters of mercury) at some time prior to or during the study.

rated from the possible effects of humoral agents. It seems most likely that a humoral vasopressor substance was operating to prevent large increases in pulse volume after ulnar block and to produce failure to reach the maximal vasodilatation level in the nine hypertensive patients. Since Regitine had very little effect when used in Case 4, it is suggestive, as Emlet² and Meier⁴ and their associates have pointed out, that if a humoral vasopressor agent was active, it was probably not adrenalin or noradrenalin.

The large degree by which most of these patients failed to reach the maximal vasodilatation level for both skin temperature and pulse volume after sympathetic paralysis would indicate that this deficit was not attributable to overactivity of the sympathetic nerves per se

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FIGURE12.
Relationship between the ratio of experimental value of pulse volume
after ulnar nerve block/theoretic maximal value and the environmental temperature.

FIGURE13.
Relationship between the ratio of experimental value of pulse volume
after ulnar nerve block/theoretic maximal value and the systolic blood pressure.

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but, rather, suggests that oligemia and decreased cardiac output or humoral vasoconstrictors were more important factors. The peripheral pallor seen in injured patients cannot be attributed entirely to exaggerated nervous activity. It has also been observed in Figure 9 that all but 3 of the 14 patients in whom skin temperatures were evaluated had an initial skin temperature greater than that of the environment. This finding would tend to indicate that there was no extraordinary overactivity of the sympathetic nerves.

From this study it can definitely be concluded that the sympathetic nervous system was functionally active in these patients and that sympathetic activity was not obliterated by the traumatic and circulatory insults experienced. However, the degree of activity in effect, i.e., normal activity, hypoactivity, or hyperactivity, could not be determined.

It must be realized that facilities did not exist in the field whereby environmental temperature and relative humidity could be controlled at a constant level during the period of study. However, should a constant temperature environment have been available, its proper utilization would have been impractical because of the short interval of time allowed for study on a wounded casualty prior to definitive surgery; a patient must be allowed to stabilize in a constant temperature environment for an hour or more before the constant temperature environment can be considered as a valuable control. When attempting to perform acute studies this is fraught with difficulties because of changes which could possibly occur in the individual as a result of the long period of stabilization.

Front a hemodynamic point of view it must be remembered that these plethysmographic studies reveal only changes in blood flow and pulse volume in the skin and subcutaneous tissue of the finger tip. These must not be misconstrued to be representative of flow or flow changes which might have been present in other vascular beds such as muscular, splanchnic, coronary, or pulmonary. The circulatory changes which occurred in these other vascular areas may have been quite different and independent from those occurring in skin and subcutaneous tissue of the finger tip.

Summary

1. Pulse volume and skin temperature determinations were made before and after ulnar nerve block from the fifth finger tip of 23 battle casualties admitted to a Mobile Army Surgical Hospital in Korea.

2. Patients who were studied in the higher ranges of environmental temperature revealed smaller increases in pulse volume after ulnar nerve block.

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3. Patients studied in the higher ranges of environmental temperature revealed larger initial absolute values for pulse volume.

4. A correlation could not be established between the initial absolute pulse volume value and the administration of morphine prior to the study.

5. Most of the patients studied, when evaluated clinically, were considered to be in a state of slight blood volume deficit. The patients who were more oligemic were too few to compare with this larger group. Consequently, a correlation could not be established between either the initial absolute pulse volume value or the degree of increase in pulse volume after nerve block and the degree of blood volume deficit. However, the patients whose systolic blood pressures were 140 or more millimeters of mercury, all of whom had slight or no blood loss, showed relatively small increases in pulse volume after nerve block.

6. A correlation could not be established between either the initial absolute pulse volume value or the degree of increase after ulnar nerve block and the type of injury, i.e., abdominal or extremity.

7. A correlation could not be established between either the initial absolute pulse volume or the increase in pulse volume after ulnar nerve block and the systolic blood pressure. Six types of blood pressure response were observed in these patients and these are recorded.

8. The case reports and studies on two patients with post-traumatic hypertension are presented in detail.

9. Fourteen patients had skin temperature responses which were satisfactory for evaluation. All but three of these patients had skin temperatures before ulnar nerve block which were greater than the environmental temperature.

10. There was a tendency for those patients with the highest systolic blood pressures to have lower values for initial absolute temperature before ulnar nerve block.

11. There was a tendency for smaller increases in skin temperature after ulnar nerve block to occur in those patients studied at higher environmental temperatures.

12. The large degree by which these patients failed to reach the theoretic maximal vasodilatation level after ulnar block, for both skin temperature and pulse volume, suggests that oligemia and decreased cardiac output were largely responsible for this deficit. However, in the nine hypertensive patients, all of whom had slight or no blood loss, the possibility of a hormonal vasoconstrictor substance being responsible for the major portion of the deficit is discussed. It was not possible to separate the components of the deficit into that attributable to oligemia and decreased cardiac output and that due to humoral vasoconstriction.

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13. From this study it can be definitely concluded that the sympathetic nervous system is functionally active in battle casualties. The traumatic and circulatory insults experienced by these patients did not obliterate the functional activity of the sympathetic nervous system. It was not possible to determine the degree of functional activity of the sympathetics which was operative, i. e., normal activity, hypoactivity, or hyperactivity.

References

1. Burton, A. C.: The Range and Variability of the Blood Flow in the Human Fingers and the Vasomotor Regulation of Body Temperature. Am. J. Physiol. 127: 437, 1939.

2. Emlet, J. R., Grimson, K. S., and Metcalf, B. H.: Comparison of Blocking Actions of Regitine and Benodaine Against Effects of Injected Levoepinephrine and Levoartenol. J. Pharm. 101: 10, 1951.

3. Goodman, L., and Gilman, A.: The Pharmacological Basis of Therapeutics, p. 201. The Macmillan Co., New York, 1941.

4. Meier, R., Yonkman, F. F., Craver, B. N., and Gross, F.: A New Imidazoline Derivative with Marked Adrenolytic Properties. Proc. Soc. Exper. Biol., N. Y. 71: 10, 1949.

5. Morton, J. J., and Scott, W. J. M.: A Study of the Measurement of Sympathetic Vasoconstrictor Activity Observed in the Lower Extremities. J. Clin. Invest. 9: 235, 1930.

6. Simeone, F. A.: Personal communication.

7. Simeone, F. A., Cranley, J. J., Grass, A. M., Linton, R. R., and Lynn, R. B.: An Oscillographic Plethysmograph Using a New Type of Transducer. Science 116: 355, 1952.