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Am J Physiol Regul Integr Comp Physiol 276: R731-R737, 1999;
0363-6119/99 $5.00
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Vol. 276, Issue 3, R731-R737, March 1999

Perfusion of the human finger during cold-induced vasodilatation

T. K. Bergersen1, J. Hisdal2, and L. Walløe1

1 Department of Physiology, University of Oslo, N-0317 Oslo; and 2 Sintef Unimed, Division of Extreme Work Environment, N-7034 Trondheim, Norway


    ABSTRACT
Top
Abstract
Introduction
METHODS
Results
Discussion
References

We have investigated the effect of severe local cooling on the vasomotor activity of the arteriovenous anastomoses (AVAs) and other finger vessels. The right third finger was subjected to local cooling (3°C) for 30-45 min in 21 healthy, thermoneutral subjects. Blood velocity in the third finger arteries of both hands was simultaneously recorded using ultrasound Doppler, and skin temperature and laser-Doppler flux from the pulp of the cooled finger were also recorded. The results demonstrate that the initial cold-induced vasoconstriction during severe local cooling involves constriction of the AVAs as well as the two main arteries supplying this finger. During cold-induced vasodilatation (CIVD), the maximum velocity values were not significantly different from those before cooling. Furthermore, the velocity fluctuations in the cooled finger were in most subjects found to be synchronous with the velocity fluctuations in the control finger. This indicates that the large blood flow to the finger and the high skin temperature during CIVD are caused by relaxation of the smooth muscle cells of the AVAs.

ultrasound Doppler; arteriovenous anastomoses


    INTRODUCTION
Top
Abstract
Introduction
METHODS
Results
Discussion
References

WHEN A HUMAN FINGER IS immersed in cold water, i.e., temperature below 15°C, the skin temperature falls and remains low for 5-10 min, but then increases abruptly (13, 14, 21). Lewis (21) first claimed that the high temperature is caused by local vasodilatation and applied the term "hunting reaction." The reaction was later known as cold-induced vasodilatation (CIVD).

Despite many studies, the mechanisms eliciting CIVD are not well understood (27). It has been suggested that CIVD is caused by the dilatation of arteriovenous anastomoses (AVAs) (10, 13, 16). However, because of the difficulties of measuring blood flow through the AVAs, the effect of local temperature on the vasomotor activity of the AVAs has not been much investigated. Bergersen et al. (3) found that the AVAs show an increasing inability to relax at skin temperatures below 35°C. Below ~21°C, sustained closure of the AVAs occurred.

In humans, AVAs are present in the skin of the hands, feet (15), ears (26), and nose (2, 24). In the hands, AVAs are located in the bed of the nails, at the fingertips, on the palm of the phalanxes, and in the thenar and hypothenar (13). The synchronous closing of the AVAs is most likely caused by bursts of efferent sympathetic impulses (5, 18, 25). The burst frequency is linked to the general heat balance of the body (6, 29). In situations where there is a need for heat conservation or heat elimination, the AVAs remain mainly closed or mainly open, respectively, resulting in almost nonfluctuating low or high blood velocity values in the afferent arteries. In a thermoneutral situation the AVAs constrict two or three times per minute, causing large, rapid blood velocity fluctuations in the afferent arteries. Vasomotion is believed to be synchronous in all skin AVAs, because blood flow variations in arteries supplying separate areas of skin, such as a hand and a foot, are found to be closely correlated (22, 29). Fluctuations in blood flow through AVAs also show a close connection with heart rate (HR) and arterial blood pressure variations (23). The fluctuations in blood flow are negatively correlated with fluctuations in mean arterial pressure (MAP), but the fluctuations in MAP precede the blood flow fluctuations by 2-3 s (3, 23).

The aim of the present study was to investigate the effect of severe local cooling on vasomotor activity in the AVAs and other finger vessels. Blood velocity measurements were made from the human finger using ultrasound Doppler and laser-Doppler methods. To relate these results to earlier investigations, skin temperature in the finger pulp was also recorded.


    METHODS
Top
Abstract
Introduction
METHODS
Results
Discussion
References

Subjects and Experimental Setup

Twenty-one healthy students aged 21-31 yr (10 females and 11 males) were investigated. The female subjects were studied during the estrogenic phase of their hormonal cycle (1). The subjects were nonsmokers and were not allowed to drink coffee or tea on the experimental day or to exercise or eat for at least 2 h before the start of the experiment. None of the subjects had any symptoms of cardiovascular disorders. Informed consent was obtained from all subjects and the experimental protocol was approved by the regional ethics committee. The experiments were carried out in a climatic chamber at an ambient temperature of 25-28°C and a relative humidity of 15%. The subjects were dressed in shorts and t-shirts and rested in a supine position on a bench. They were acclimatized for 30 min before the start of the experiment. The ambient temperature was adjusted to obtain large fluctuations in finger arterial velocity, indicating that the subjects were in the middle of their thermoneutral zone (29).

In all experiments, the right third finger was submerged to the metacarpophalangeal joint for 30-45 min after 10 min of control measurements. The thermostat-controlled water bath was held at 3°C. The control hand (always the left hand) rested in the air on the bench. Tympanic temperature was continuously recorded.

Protocols

Protocol 1. In 21 subjects, simultaneous continuous measurements were made of blood velocity in the radial third finger artery of both hands, together with measurements of MAP. In 14 of these subjects, the skin temperature in the pulp of the cooled finger was also recorded simultaneously.

Protocol 2. In 5 of the 21 subjects, laser-Doppler flux (LDF) and skin temperature in the pulp of the cooled finger were measured simultaneously, together with blood velocity in the radial finger artery of the same finger. The thermistor and laser-Doppler probes were placed close to each other on the fingertip.

Protocol 3. In three of these five subjects, simultaneous velocity measurements were made from both arteries supplying the cooled finger (ulnar finger artery and radial finger artery) together with LDF from the pulp of the same finger.

Instrumentation

Continuous blood velocity measurements were made using ultrasound Doppler systems (SD 100 and SD 50, Vingmed Sound). The operating frequencies were 6 MHz and 10 MHz to avoid interference between the instruments. The circular transducer had a fixed angle of 45° between the sound beam and the underlying skin surface. The transducers were fastened with adhesive plaster on the radial or the ulnar site of the proximal phalanxes of the third finger. Instantaneous cross-sectional mean velocities were calculated by the instruments and fed online to the computer for beat-by beat time averaging, gated by electrocardiogram R waves (23). LDF measurement were made using a laser-Doppler instrument (MBF3D; Moor Instruments, Devon, UK). The laser-Doppler probe was placed on the pulp of the right third finger. The noise-limiting filter of the instrument was set at its highest level (21 kHz), and the emitted wavelength was 820 nm. The flux output signal was filtered with a time constant of 0.1 s and sent to the computer for beat-by-beat averaging in the same manner as the ultrasound Doppler signal. Skin temperature was continuously recorded using thermistor probes with a time constant of 1.1 s (Yellow Springs Instruments 409). The thermistor probe was fastened to the pulp of the right third finger with surgical tape (3M-Blenderm). The tympanic temperature was measured continuously using an ear probe (Exacon, model 8940). Instantaneous arterial blood pressure was obtained from the left fourth finger using a photoplethysmographic device (Ohmeda 2300 Finapres, Madison, WI). The blood pressure data were fed to the computer, and MAP was calculated by numerical integration for each R-R interval.

Statistical Analysis

The correlation coefficients and time lags shown in Table 2 are calculated using 10-min recordings before cooling and the first 10 min of cooling during the first CIVD plateau. Cross-correlation was calculated between corresponding velocity values in the radial third finger artery of both hands and between corresponding MAP and velocity values in the artery of the cooled finger (Box-Jenkins time series analysis, BMDP-2T) (9). Before the calculations, the signals were converted to equidistant time samples by interpolation and high-pass filtered with a cutoff frequency of 0.01 Hz. Four subjects showing continuously low velocity values in the left (control) finger artery together with four subjects showing continuously low velocity values in the right (cooled) finger artery (CIVD onset time greater than immersion period?) were omitted from the analyses, so that n = 13. Blood velocity fluctuations were defined as permanently low when the maximum blood velocity value was always less than the 50th percentile of the blood velocity calculated from the 10-min control registration. The confidence intervals for the medians were calculated using nonparametric statistics (17).

The mean velocity and the range of short-term velocity variations, estimated as the 10th and 90th percentiles of the velocity measured, were calculated in a ±45-s sliding window. Before averaging between the subjects, all velocity recordings were scaled to convert the 10-min mean of the 90th percentile before cooling to unity (Table 1, Fig. 3A). This procedure was also followed for the recordings of MAP and HR (Fig. 3, B and C).

Onset Time of CIVD

The onset of a CIVD episode is characterized by large increases in arterial blood velocity, LDF, and skin temperature, usually from low plateau levels. Because the initial increase in these variables is gradual, it was considered necessary to implement some semiautomatic method to determine onset times. The following model was used: the variable y (velocity, flux, or temperature) was assumed to increase from a constant level according to a power function of time (t)
for <IT>t</IT> < par(3)
 <IT>y</IT> = par(1)
for <IT>t</IT> > par(3)
 <IT>y</IT> = par(1) + par(2) * [<IT>t</IT> − par(3)] ** par(4)
The four parameters, par(x), x = 1, 2, 3, or 4, of this equation were determined by nonlinear least-squares regression on a small segment of the data file around the onset time as roughly estimated by visual inspection of the graphs. The onset time is represented by par(3) in this equation. The estimated values of par(3) were generally insensitive to small changes in the delimitation of the data segment. The exponent par(4) was in all cases estimated to be between 1.0 and 4.0.


    RESULTS
Top
Abstract
Introduction
METHODS
Results
Discussion
References

Figure 1 shows simultaneous continuous recordings of skin temperature from the pulp of the cooled finger (Fig. 1A), arterial blood velocity in the cooled (Fig. 1B) and the control finger (Fig. 1C), and MAP (Fig. 1D) in one subject from protocol 1. The submersion period is illustrated by a solid line above Fig. 1A. Before cooling (0-10 min), the blood velocity in the two fingers shows the familiar large fluctuations seen in arteries supplying skin areas containing AVAs. When the right finger is submerged, the arterial blood velocity fluctuations in this finger cease abruptly and the velocity remains very low for 8 min before a rapid increase occurs, interpreted as CIVD. It can be seen that the CIVD in this subject lasts for ~21 min before a new strong vasoconstriction occurs. A similar CIVD cycle then starts ~10 min later. In the control finger, the blood velocity fluctuations are nearly unchanged throughout the session, indicating that the subject is in his thermoneutral zone throughout the experiment (Fig. 1C). There is no change in the short-term MAP variability during the experimental run (Fig. 1D).


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  		Fig. 1.   Simultaneous beat-by-beat averaged arterial blood velocity, skin temperature, and mean arterial pressure (MAP) from 1 subject during cooling of 1 finger in 3°C for 45 min (protocol 1, room temperature 28°C). Solid line at top indicates submersion period. A: skin temperature. B: blood velocity in radial third finger artery of cooled finger. C: blood velocity in radial third finger artery of control finger. D: MAP. Solid numbered lines, time intervals displayed in Fig. 2.

In the cooled finger, the maximum velocity values during CIVD, estimated as 90th percentiles, are not statistically significantly different from the values before cooling (P = 0.23, Table 1). However, a statistically significant increase can be seen in the 10th percentiles (P = 0.001, Table 1). Yet the blood velocity in the cooled finger still shows fluctuations during CIVD, although they are very small (Fig. 1B, 18-30 min).

                              
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  		Table 1.   Averaged relative velocities

To investigate whether the velocity fluctuations in the cooled finger during CIVD are caused by active vasomotor activity or are just passive reflections of MAP variations, cross-correlation was calculated between velocity fluctuations in the cooled and control finger and between fluctuations in the cooled finger and MAP, using the initial 10 min (before cooling) and the first 10 min of the first CIVD cycle in all subjects from protocol 1 (Table 2).

Before cooling, the blood velocity fluctuations in the two fingers show the familiar strong positive correlation (median r = 0.92, Table 2). The velocity fluctuations also show the familiar negative correlation with MAP fluctuations (median r = -0.5, Table 2), with a median time lag of 2.5 s. Table 2 shows that in most subjects, the blood velocity fluctuations in the cooled finger are also positively correlated with the fluctuations in the control finger during the CIVD response (n = 10). However, the blood velocity fluctuations in the artery of the cooled finger show a median delay of 3.9 s. In three subjects, the blood velocity fluctuations in the cooled finger are negatively correlated with fluctuations in the control finger.

                              
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  		Table 2.   Correlation coefficients and time lags

The correlation between the velocity fluctuations in the cooled finger and fluctuations in MAP varies between subjects. In the subjects with strong positive correlation between velocity fluctuations (n = 2), the correlation between velocity fluctuations in the cooled finger and MAP is negative, as in the control situation. However, the blood velocity fluctuations are delayed compared with the corresponding fluctuations in MAP. In the subjects with less-positive (n = 8) or negative correlation (n = 3) between velocity fluctuations, the correlation between velocity fluctuation and MAP is positive and there is no time lag (Table 2).

To see how velocity fluctuations change from the beginning to the end of the CIVD cycle, velocity samples from the recordings were carefully inspected at high time resolution. Figure 2 shows four sequential sections from the recording shown in Fig. 1, B and C (data samples are marked with horizontal lines in Fig. 1B), displayed at high time resolution. The line with symbols shows blood velocity in the control finger, and the line without symbols shows blood velocity in the cooled finger. Each symbol represents the average velocity during one heart cycle. Section 1 before cooling shows the familiar close correlation between blood velocity fluctuations in arteries supplying areas of skin containing AVAs (Table 2). Section 2 shows velocity fluctuations during CIVD. The vasoconstrictions in the cooled finger are weak and delayed compared with the corresponding vasoconstrictions in the control finger. Section 3 shows velocity fluctuations a few minutes later in the same CIVD cycle. It can be seen that the vasoconstrictions are now stronger and that one of them lasts for longer than the vasoconstrictions in the control finger. Section 4 shows velocity fluctuations at the end of the first CIVD cycle. Here, the velocity fluctuations on the cooled side are increasingly delayed, and most of the delay is caused by late onset of the relaxation phase. The late onset of relaxation appears to reduce the magnitude of the vasodilatation cycles substantially. Finally, vasodilatation fails to occur and the blood velocity remains continuously low, terminating the CIVD cycle.


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  		Fig. 2.   Four-minute periods of sequential sections of simultaneous spontaneous velocity fluctuations in cooled and control finger before cooling and during 1 cold-induced vasodilatation (CIVD) cycle, taken from recordings in Fig. 1 (4 sections are illustrated by numbered lines in Fig. 1). Lines with symbols show blood velocity in control finger, and lines without symbols show blood velocity in cooled finger. Each symbol represents average velocity during 1 heart cycle. A: before cooling. B and C: during CIVD. D: end of first CIVD cycle.

Figure 3 shows the mean of all 21 recordings from the velocity in the artery of the control finger (Fig. 3A), MAP (Fig. 3B), and HR (Fig. 3C) displayed as relative values. The 90th, 50th, and 10th percentiles of the normalized distribution are shown. It can be seen that the velocity values in the control finger are reduced (Fig. 3A, Table 1). Figure 3, B and C, shows that both MAP and HR increase steeply at 10 min, when the finger was submersed. However, whereas HR returns to the baseline after 4-5 min, MAP remains elevated throughout the session. This MAP pattern was typical of most of the subjects, but was not seen in the subject shown in Fig. 1 (Fig. 1D).


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  		Fig. 3.   A ±45-s sliding window average (middle traces) and range of short-term variations estimated as 90th (top traces) and 10th (bottom traces) percentiles of data samples in the window. Traces were normalized before averaging of all 21 recordings in protocol 1 from control finger artery (A), MAP (B), and heart rate (HR; C) during cooling of 1 finger in 3°C. Solid line at top indicates submersion period.

The tympanic temperature was stable throughout the session (Wilcoxon rank-sum test, 2-sided test, n = 21, P = 0.11).

In all experiments, the time period between submersion and the start of the first CIVD cycle was calculated. Surprisingly, in 5 of the 21 subjects in protocol 1, the skin temperature signal increased earlier than the blood velocity signal (Table 3). Both CIVD cycles shown in Fig. 1 illustrate this clearly. Furthermore, in four subjects, blood velocity in the cooled finger remained low throughout the entire immersion period whereas the onset of CIVD in the temperature signal occurred at the expected time.

                              
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  		Table 3.   Calculated onset time for CIVD in pulp temperature and velocity in radial finger artery of cooled finger

Protocol 2 and protocol 3 were run for those subjects in which the skin temperature increased earlier than the velocity signal. Figure 4 shows velocity in the radial finger artery (Fig. 4A), finger pulp temperature (Fig. 4B), and finger pulp LDF (Fig. 4C) recorded from the cooled finger in a subject in protocol 2 (same subject as illustrated in Fig. 1). The calculated onset of CIVD is illustrated by arrows. As usual, blood velocity and LDF show the characteristic large spontaneous fluctuations before cooling (0-10 min). After submersion, velocity, skin temperature, and LDF remain low before a rapid increase occurs in all three signals. In all subjects, the increase in the LDF signal precedes the increase in pulp temperature, indicating that the increase in temperature is always caused by increased skin perfusion (n = 5, median 1.38 min, Table 4).


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  		Fig. 4.   Complete data from cooled finger only from the same subject, displayed as in Fig. 1 (protocol 2, room temperature 28°C). Solid line at top indicates submersion period. Calculated onset of CIVD is indicated by arrows. A: blood velocity in radial third finger artery. B: pulp temperature. C: laser-Doppler flux (LDF) [in arbitrary units (au) × 103] from finger pulp.

                              
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  		Table 4.   Within-subject differences between onset time for CIVD in simultaneous recordings of pulp temperature and pulp LDF, velocity in radial finger artery and pulp temperature, and velocity in radial finger artery and velocity in ulnar finger artery

Figure 5 shows simultaneous recordings of blood velocity in both the radial (Fig. 5A) and the ulnar (Fig. 5B) finger artery of the cooled finger together with LDF (Fig. 5C) from the finger pulp (same subject as illustrated in Figs. 1 and 4, but using protocol 3). Figure 5 shows that the onset of CIVD is earlier in the ulnar finger artery (Fig. 5B) than in the radial finger artery (Fig. 5A). The onset of CIVD in the ulnar finger artery occurs at the same time as the increase in the laser-Doppler signal.


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  		Fig. 5.   Complete data from cooled finger from the same subject, displayed as in Figs. 1 and 4 (protocol 3, room temperature 28°C). Solid line at top indicates submersion period. Calculated onset of CIVD is indicated by arrows. A: blood velocity in radial third finger artery. B: blood velocity in ulnar third finger artery. C: LDF (au × 103) from finger pulp.

In four subjects, the velocity fluctuations in the control finger ceased and velocity was permanently very low throughout the experiment after submersion of the right finger. There was no significant difference in the onset time for CIVD in the velocity signal between subjects with persistent vasoconstriction in the control finger and those showing stable blood velocity fluctuations in the control finger throughout the immersion period (Wilcoxon rank-sum test, 2-sided test, n = 4, P = 0.47).


    DISCUSSION
Top
Abstract
Introduction
METHODS
Results
Discussion
References

The aim of the present study was to investigate the effect of severe local cooling of the finger on the vasomotor activity of the AVAs and other finger vessels. Before cooling, blood velocity in both fingers showed the familiar large, closely correlated fluctuations caused by synchronous opening and closing of the AVAs (22, 29). In nearly all subjects, these velocity fluctuations continued to be positively correlated with arterial blood velocity fluctuations in the control finger during CIVD, indicating that there was still vasomotor activity in the AVAs.

The maximum velocity values in the cooled finger, estimated as 90th percentiles, were not statistically significantly different from the maximum values before cooling. This indicates that the high velocity values during CIVD are caused by dilatation of the same vascular structures that are responsible for the high maximum velocity values before cooling, i.e., by dilatation of the AVAs.

Several investigators have suggested that CIVD is caused by opening of the AVAs. By using the 24Na clearance method, Edwards (10) showed that all total blood flow during CIVD in the rabbit ear took place through the AVAs. However, most investigators have only concluded indirectly that CIVD is caused by opening of AVAs because they have observed CIVD in skin areas containing AVAs (13, 16, 21). This is a rather inconclusive argument, because CIVD may also be observed in areas of skin that possibly do not contain AVAs, such as the forehead, forearm, dorsum of hand, thigh, and dorsum of foot (12, 30).

The results of the present study suggest that CIVD is a local mechanism. In nearly all subjects, the pattern of blood velocity fluctuations in the control finger was almost unchanged throughout the session. This means that the pattern of bursts of efferent sympathetic impulses to all skin AVAs was probably unchanged (7, 29) and that the subjects were in their thermoneutral zone. However, the maximum velocity values were somewhat reduced in the control finger. One possible explanation of this is an increase in vascular resistance in the ordinary arterioles in the skin. If this also happens in other areas of skin, it may explain the elevated MAP during the immersion period.

The mechanisms eliciting CIVD have been extensively discussed (19, 27, 28). It has been suggested that the high blood flow is caused by cold paralysis of the smooth muscle cells (19, 28). In this study, the pattern of fluctuations in blood velocity in the cooled finger during CIVD is best explained by such a mechanism. The blood velocity fluctuations in the cooled finger showed a delay compared with the corresponding fluctuations in the control finger and MAP. This may be explained by a reduction in the power of the smooth muscle cells to contract, which may also explain the increase in minimum velocity values. In some subjects, the fluctuations in the cooled finger were negatively correlated with fluctuations in the control finger and positively correlated with fluctuations in MAP, with no time lag. This fluctuation pattern indicates the presence of a passive vascular bed where velocity fluctuations merely reflect MAP variations. This could be caused by total paralysis of the AVAs in these subjects.

Termination of the CIVD cycle could be explained by an increase in the responsiveness of the vessels when the internal temperature of the finger rises (19, 28). The present study showed that the spontaneous vasomotor activity of the AVAs was stronger at the end of the CIVD cycle than at the start of the cycle (Fig. 2). This indicates that the spontaneous vasomotor activity of the AVAs returns if the influx of blood rewarms the AVAs sufficiently. The sustained vasoconstriction terminating the CIVD could thus be explained by cold-induced vasoconstriction.

The onset time for CIVD in the skin temperature signal (median 5.15 min, n = 14) is similar to that found in earlier reports (13, 14, 21). However, a new finding is that the increase in skin temperature is sometimes caused by increased blood flow in just one of the two arteries supplying the cooled finger. This indicates that the initial cold-induced vasoconstriction lasts for a little longer in one of the two supplying arteries than in the other. Bergersen et al. (3) found that the AVAs in the human finger show an increasing inability to relax during moderate local cooling and observed abrupt, sustained vasoconstriction below 21.5°C. Keatinge (19) further reports that if the tissue is cooled to not less than 15°C, the only effect normally seen is vasoconstriction. This means that the circulatory condition of the human finger at local temperatures between 21.5°C and 15°C is sustained vasoconstriction. If a local temperature of between 21.5 and 15°C results in constriction of the AVAs (and possibly the ordinary arterioles in the skin), as well as of the arteries supplying this finger, our results could be explained by earlier cold relaxation of the smooth muscle cells in one of the two supplying arteries. Cold relaxation of the arteries supplying the cooled finger would thus occur at two different skin temperatures.

In conclusion, CIVD in the human finger is a local vascular phenomenon caused by dilatation of the AVAs. The dilatation is caused by the effect of low temperature on the smooth muscle cells. Cold-induced vasoconstriction is caused by constriction of the AVAs as well as the arteries supplying the finger.

Perspectives

It is generally assumed that CIVD is an important mechanism in maintaining hand dexterity (20) and protecting the tissue against damage in the cold (21). Several authors have also found that the onset time for CIVD is longer or that CIVD is absent in hypothermic subjects with increased sympathetic tonus (8, 11, 31). An interesting question is thus whether the onset of CIVD is related to body temperature or to increased sympathetic tonus per se. In the present study, four subjects showed an abrupt sustained vasoconstriction in the control finger when the right finger was submersed, indicating increased sympathetic tonus. However, the onset time for CIVD was not significantly longer in these subjects. This may suggest that the onset of CIVD is independent of increased sympathetic tonus per se, which again supports the conclusion that CIVD is a local vascular phenomenon. However, the local response is in some way related to body core temperature.


    ACKNOWLEDGEMENTS

A preliminary report on some of the results has been presented to the Physiological Society (4).


    FOOTNOTES

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

Address for reprint requests: T. K. Bergersen, Dept. of Physiology, Univ. of Oslo, PO Box 1103 Blindern, N-0317 Oslo, Norway.

Received 2 July 1998; accepted in final form 23 November 1998.


    REFERENCES
Top
Abstract
Introduction
METHODS
Results
Discussion
References

1.   Bartelink, M. L., A. Wollersheim, A. Theeuwes, D. van Duren, and T. Thien. Changes in skin blood flow during the menstrual cycle: the influence of the menstrual cycle on the peripheral circulation in healthy female volunteers. Clin. Sci. (Colch.) 78: 527-532, 1990[Medline].

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9.   Dixon, W. J. BMDP Statistical Software Manual. Berkely, CA: University of California Press, 1990, vol. 1, p. 435-438.

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13.   Grant, R. T., and E. F. Bland. Observation on arteriovenous anastomoses in human skin and in the bird's foot with special reference to the reaction to cold. Heart 15: 385-411, 1931.

14.   Greenfield, A. D. M., and J. T. Shepherd. A quantitative study of the response to cold of the circulation through the fingers of normal subjects. Clin. Sci. (Colch.) 9: 323-347, 1950.

15.   Grosser, O. Ueber arterio-venøse anastomosen an den extremiteten beim menschen und den krallentragenden saugtieren. Arch. Mikr. Anat. 60: 191-216, 1902.

16.   Hertzman, A. B., and L. W. Roth. The absence of vasoconstrictor reflexes in the forehead circulation. Effects of cold. Am. J. Physiol. 136: 692-697, 1942.

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Am J Physiol Regul Integr Compar Physiol 276(3):R731-R737
0002-9513/99 $5.00 Copyright © 1999 the American Physiological Society


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