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1 Institute of Health Science2 Graduate School of Human-Environment Studies, Kyushu University, Kasuga, Fukuoka 816-8580, Japan 3 Department of Exercise Science and Physiology, School of Health Sciences, Prefectural University of Hiroshima, Hiroshima 734-8558, Japan
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Abstract |
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(Received 15 August 2005;
accepted after revision 19 October 2005; first published online 20 October 2005)
Corresponding author N. Hayashi: Institute of Health Science, Kyushu University, Kasuga, Fukuoka 816-8580, Japan. Email: naohayashi{at}ihs.kyushu-u.ac.jp
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Introduction |
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With respect to the responses in visceral arteries, only one study has found that renal cortical blood flow decreases during mental tasks in human subjects (Middlekauff et al. 1997). Insufficient blood flow to splanchnic organs may be associated with tissue damage (Jakob, 2002), and hence a reduction in blood flow induced by chronic mental stress may lead to tissue damage. In addition, different arteries may respond differently even within the splanchnic organs, because vascular responses have been found to vary with the stimulus in animal studies (Gardiner et al. 1988; Broome et al. 2000; Di Giantomasso et al. 2002; Koba et al. in press). The absence of data on the time course of vascular and blood flow responses in visceral arteries to mental stress in humans prompted us to investigate blood flow in human visceral organs during mental stress.
We hypothesized that mental stress increases vascular resistance (VR) and consequently decreases blood flow to visceral organs, with the response magnitudes differing among visceral organs. To test this hypothesis, we observed blood pressure and blood flow response in renal (RA) and superior mesenteric (SMA) arteries during Stroop's colour word conflict test (CWT; Stroop, 1935) using Doppler ultrasound flowmetry.
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Methods |
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Sixteen young female subjects volunteered for the study. The subjects were normotensive, non-smokers, who were not taking any medication and had no history of autonomic dysfunction or cardiovascular disease. The Institutional Review Board of the Prefectural University of Hiroshima approved the experimental protocol and all subjects provided written informed consent prior to the study. All the protocols conformed to the Declaration of Helsinki. Each subject underwent a pilot examination prior to performing the main protocol. During these pilot experiments we found that high-quality B-mode images and Doppler recordings of either the RA or SMA could not be obtained in seven subjects, due mainly to the location and/or depth of the artery or to body movement by the respiratory cycle. Therefore, nine subjects (age, 22.7 ± 3.2 years; height, 157.1 ± 3.7 cm; weight, 47.1 ± 3.1 kg) were finally included in the experimental protocols.
Induction of mental stress
The subjects arrived in the laboratory after having abstained from caffeine and exercise for at least 1 day, and from food for at least 2 h. The experimental protocol was conducted in a semi recumbent position with the hip extended to approximately 130 deg with a thigh supporter in a quiet room. Mental stress was induced by a computerized version of the CWT (Stroop, 1935). This test was performed for 3 min to induce mental stress after 3 min of recording baseline data. A coloured word (yellow, blue, green, purple or red) written in an incongruent colour was displayed on a computer monitor. The subject was instructed to click the colour with which the word was written on the monitor. Prior to the test, each subject received instructions on how to perform the test, and practiced until she understood the test. The subject was also requested to make a score of criteria to complete a test that she had not been informed about. This was only for mental stress, so no subject was requested to perform the test twice. The test included 180 repetitions at 2-s intervals.
Measurements
Heart rate (HR), blood pressure (BP), and mean blood velocity (MBV) in the right RA and SMA were measured for 3 min at rest and for the following 3 min during the CWT. The BP was monitored every minute by an automatic sphygmomanometer (BP-306, Colin, Japan). In addition, the respiratory movement of the chest wall was monitored via mercury-in-silastic strain gauges to identify the respiratory phase for the detailed analysis of blood velocity in the visceral artery (see below). The CWT session was repeated twice in a random order because the RA and SMA cannot be measured simultaneously, with the repeated measurements separated by at least 30 min.
Recent advances in duplex ultrasonography enable the blood flow dynamics in intra-abdominal blood vessels such as the RA to be simultaneously visualized and measured (Carman et al. 2001; Lee & Grant, 2002). Accordingly, simultaneous pulsed and echo Doppler ultrasound flowmetry (EUB-525, Hitachi Medical, Japan) was used to measure the MBV in the RA and SMA while subjects performed the CWT. A curved-array Doppler-scan probe with a 2.5-MHz pulsed Doppler frequency was used. The use of this machine allows a real-time cross-sectional image (i.e. B-mode echo) to be displayed simultaneously with real-time Doppler spectral display and sound, enabling the experimenter to frequently visually realign the ultrasound beam with the artery so as to avoid failure in Doppler insonation due to blood vessel movement during the protocol.
The focal zone was at the depth of the RA or SMA, and the Doppler beam insonation angle was maintained at 50–60 deg. According to a previously described technique (Momen et al. 2003, 2004), to obtain the highest quality Doppler tracings were obtained by the experimenter determining the optimal positions of the Doppler probe (via an anterior abdominal approach) for each subject during the preliminary trial. After adjustment of the sample volume width to cover the target arterial diameter, the Doppler transducer should be normally maintained in a constant position on the subject's anterior abdominal wall. However, during our preliminary trials, we noted that the RA and SMA moved with respect to the abdominal wall during the inspiratory and expiratory phases of respiration, and thus we could not maintain high-quality velocity tracings during both phases of the respiratory cycle. Therefore, for each subject we obtained velocity data during the expiratory phase for all portions of the CWT protocol. Accordingly, for each subject, the data were obtained in the expiratory phase of the respiratory cycle. When the target artery was out of the observation range for about five adjacent beats, the experimenter readjusted the probe. No sudden changes in the measured blood flow resulted from such readjustment of the probe. No subjects performed the Valsalva manoeuvre during the protocols.
The audio-range signals for antegrade and retrograde velocities reflecting the moving blood cells and the ECG signal were digitally sampled at 20 kHz using an A/D convertor (PowerLab8/30, ADInstruments). The spectra of the audio-range signals were manipulated offline by our Doppler signal processing software (fast Fourier transform (FFT) analysis by 256-point Hamming window (i.e. every 12.8 ms)), and instantaneous MBV values were calculated. The velocity signals were recorded at 1 kHz on a computer system along with the ECG so that the data could be analysed on a beat-by-beat basis. The time-series data of HR, BP and MBV were averaged on a minute-by-minute basis. The VR was calculated as the quotient of MAF and the respective MBV value in accordance with previous studies (Momen et al. 2003, 2004), and is expressed here in arbitrary units (a.u).
Statistics
Data are expressed as means ± S.E.M. To test the time-series changes in each variable, the effect of time (at baseline, at the first, second and third minutes of CTW and recovery) on the absolute value was examined by repeated-measures ANOVA. When a significant F-value was detected over time, this was further examined by the Dunnett post hoc test against the control baseline condition (i.e. pre-CWT) for each artery. To test differences between the target arteries, the effects of time and the interaction on each percentage change from the baseline were examined by repeated-measures two-way ANOVA. In addition, to examine the consistency of responses between trials, linear regression was applied to the percentage change of HR and MAP at the third minute between the target arteries (i.e. RA and SMA). Statistical significance was accepted at P < 0.05. These statistical analyses were performed with SAS (ver.8.2., SAS Institute, NC, USA) at the Computing and Communications Center, Kyushu University, Japan.
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Results |
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The two-way ANOVA revealed that the relative changes in the MBV and VR from the baselines differed significantly between the RA and SMA, whereas they did not vary over time.
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Discussion |
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We observed that the blood flow to the kidney decreased within 1 min after starting the mental task. The kidneys receive a major fraction of the cardiac output at rest and the ratio of arterial flow to their mass is the largest of all organs. Sympathetic excitation during defence reactions, including mental stress, serves to prepare the animal by increasing blood flow to necessary organs (Hjemdahl et al. 1984). Thus a decreased blood flow to the kidney, as observed in the present study, is an effective part of the defence reaction to mental stress.
The vasoconstriction in visceral beds during mental stress may also be associated with vasodilation in skeletal muscles. For example, during mental stress there are large increases in blood flow to the forearm and calf (Halliwill et al. 1997; Carter et al. 2005). Thus, during mental stress there is a redistribution of cardiac output such that blood flow to skeletal muscles, but not visceral beds, increases.
Another type of mental stimulus – non-noxious alerting sound – to rabbits did not change renal flow, while it did decrease the mesenteric flow (Yu & Blessing, 1997). The present results contrast with this observation, which may reflect differences in the mental stimuli used (type and duration) or the use of different species. Reports of vascular responses to mental tasks in human visceral organs are limited and hence the reasons for this difference between the present and previous reports are unknown, and require further studies.
The increases in MAP and HR during the CWT in the present study are comparable to previous observations. The increase in MAP reportedly ranges from 13 to 22 mmHg, and the HR from 18 to 32 beats min–1 (Linde et al. 1989; Tidgren & Hjemdahl, 1989; Lindqvist et al. 1996; Halliwill et al. 1997; Middlekauff et al. 1997). The magnitude of perceived stress in the subjects in the present study may be similar to that in previous studies. The decrease of RA blood flow, however, was much smaller than the 35% decrease in renal cortical blood flow during the CWT reported by Middlekauff et al. (1997). This difference might be attributable to the use of different target sites.
The present study did not focus on the mechanism underlying the different vascular responses in organs. We can only speculate several candidate mechanisms. As for hormonal mechanisms, mental stress causes the secretion of catecholamine, renin and vasopressin (Tidgren & Hjemdahl, 1989; Lindqvist et al. 1996; 2004; Ito et al. 2003). In animal studies, the vascular responses induced by these hormones have been found to differ among visceral organs (Gardiner et al. 1988; Broome et al. 2000; Di Giantomasso et al. 2002). In humans, adrenaline (epinephrine)-induced vasodilatation is greater in the forearm than in the calf (Freyschuss et al. 1986). These observations indicate that humoral mechanisms may have induced the differing vascular responses observed in the present study. As for sympathetic nervous activity, it relates to blood flow in the kidney (Mueller et al. 1998). The sympathetic activity in an organ is not always related to the activity in other organs. Renal blood flow decreased with a concomitant increase in calf blood flow during electrical stimulation of a defence area, while at the same time the sympathetic nervous activity increased to a greater extent in the renal compared with the lumbar region (Koba et al. in press). Differential sympathetic activation to various physiological stimuli has been studied extensively (Morrison, 2001). Thus, a sympathetic neural mechanism is another reason why the vascular responses to mental stress differ between visceral organs. Nitric oxide (NO) may play a role in forearm vasodilatation during mental stress (Dietz et al. 1994; Cardillo et al. 1997). The NO synthase inhibitor and NO precursor affect blood flow in the SMA of dogs and during ovine endotoxaemia, but not in the RA, implying the differential effects of NO-mediated vasodilatation (Cobb et al. 1995; Allman et al. 1996). NO may be involved in the induction of differential vascular responses to mental stress.
The range of blood flow changes from resting to maximal vasodilatation normalized to the tissue mass is known to differ among various organs (Mellander & Johansson, 1968). In particular, in kidneys the degree of vasodilatation at rest is close to the maximal vasodilatation that can be evoked. Such differences in the resting vascular states between different organs could have influenced the different vascular responses in the RA and SMA observed in the present study.
In any case, while different vascular responses were observed in SMA and RA in the present study, the physiological significance of this difference is unclear. Further studies are needed to elucidate this issue.
Repetition of a mental task reportedly attenuates the response due to familiarization (Lindqvist et al. 2004), and the perceived stress affects the magnitude of the muscle sympathetic nerve activity (Callister et al. 1992). We found no differences in the pressor and cardioaccelerator responses between our two trials, measuring both the RA and SMA blood flow. In addition, the HR and BP responses in both trials showed a strong positive correlation, with the subjects showing similar responses. All subjects practised until they understood how to perform the test. Thus, familiarization seems to be sufficient to standardize the response. We randomized the order of the RA and SMA blood flow measurements, and the two trials did not affect the differences in the blood flow responses between the two arteries.
We did not record the precise diameters of the arteries due to technical difficulties. However, since the target vessels are not resistance vessels and there were no differences observed in the diameters on the B-mode echo images during trials, it is unlikely that changes in the diameters of arteries had a major effect on the present findings.
In summary, the present findings demonstrate that mental stress causes vasoconstriction in the renal and superior mesenteric arteries, which decreases blood flow in the renal artery but not in the superior mesenteric artery. The relative changes of blood flow and magnitude of vasoconstriction caused by mental stress from the baseline differed between the arteries. These results suggest that mental stress causes vasoconstriction in visceral arteries, and indicate that the magnitude of vasoconstriction differs among visceral organs.
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| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
) and renal artery (RA; •) measurement. The subjects performed the CWT from 180 to 360 s. Significant increases in MAP, HR and VR were observed throughout the CWT. Two-way ANOVA revealed that the relative changes in MBV and VR from the baseline values differed significantly between the RA and SMA. *Significantly different from baseline (P < 0.05)