معرفی خود و واکنش پذیری قلبی عروقی
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|39011||1999||14 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : International Journal of Psychophysiology, Volume 32, Issue 1, 1 April 1999, Pages 75–88
Abstract This research was concerned with two issues: first, whether cardiovascular response patterns to a social stressor (i.e. self-presentation under evaluative circumstances) differ as a function of one's ability to control the impression one makes on others; second, whether cognitive appraisals are necessary or sufficient for the cardiovascular components of emotional arousal. Forty-two male subjects (Ss), monitored for cardiac impedance and blood pressure, were shown a previously recorded videotape of themselves in which each S verbally described personal aspects about himself. Ss in an Active condition were allowed to mark segments of the tape they wanted to re-shoot before the tape was evaluated by reviewers. Ss in a Passive condition viewed their tape but could not indicate whether to revise it. Control conditions allowed assessment of the activity entailed in tape marking and of evaluation per se. Self-reports of stress, threat, and coping ability regarding the upcoming task were taken. Blood pressure elevations occurred equally in both experimental conditions, but apparently through different underlying mechanisms. The Active condition produced myocardial responses (increased ejection fraction), while the Passive condition produced a vascular response (increased total peripheral resistance). However, while cardiovascular reactivity patterns did differ as a function of the opportunity to control the impression one could make on evaluative others, they did not differ as a function of having appraised the task as a challenge or as a threat. Consideration also is given to the conditions necessary for cognitive appraisal to occur and to influence reactivity.
Introduction The present study is concerned primarily with cardiovascular activity during situations in which people can or cannot control their self-presentations under evaluative conditions. A second issue concerns whether cognitive appraisals are necessary or sufficient for such cardiovascular patterns. Cardiovascular reactivity to physical and social psychological demands has long been of interest in psychophysiological research, both for its potential pathogenic significance (Anderson et al., 1993, Saab and Schneiderman, 1993 and Uchino et al., 1995) and for the information it provides about autonomic functioning and autonomic space (Berntson et al., 1991 and Cacioppo, 1994). The study of reactivity to social stressors may be especially important, given their ubiquity in everyday life, especially since reactivity to less explicitly social stressors, such as mental arithmetic, is not necessarily predictive of reactivity to patently social stressors (Lassner et al., 1994Al'Absi et al., 1997). Self-presentation is a ubiquitous feature of daily life. Baumeister (1982)identifies two main self-presentational motives: (1) pleasing an audience; and (2) constructing one's public self congruent to one's ideal. According to Baumeister, the intention behind self-presentation does not need to be conscious, nor does the impression need to be accurate either objectively or in the self-presenter's own view. Self-presenters, in an effort to construct and protect a set of desired identity images, have been shown to modify their attitudes according to the probable reactions of audiences (Schlenker and Weigold, 1990). Moreover, when people want to make a favorable impression but doubt that they will succeed, social anxiety occurs (Schlenker and Leary, 1982). Leitenberg refers to social anxiety as ``ubiquitous'' and notes that it involves feelings of apprehension, self-consciousness, and emotional distress in anticipated or actual social-evaluative situations (Leitenberg, 1990). Spielberger (Spielberger, 1979) has described such anxiety as a dominant fact of modern life. Self-presentation, then, is ubiquitous and often stressful, particularly in evaluative circumstances. However, very little if any research has explored physiological reactivity in association with situations that impede the opportunity to create a desired self impression. Such stress should be reflected in patterns of cardiovascular reactivity, patterns which in turn might have serious health implications (Folkow, 1978). A related issue concerns a person's assessment of how threatening a situation is. The model of stress of Lazarus and Folkman (1987)posits that cognitive appraisal processes intervene between the initial perception and subsequent experience of a potentially stressful situation. These appraisals are thought to shape emotional, physiological, and behavioral responses to such events. Tomaka et al. (1993)tested Lazarus and Folkman's model and discovered that different patterns of cardiovascular reactivity were associated with one's perceived ability to cope with the situation. To Tomaka and associates, high perceived coping ability generally will lower or preclude stress, while low perceived coping ability generally will increase stress. Operationally, they dichotomized groups according to a ratio of participants' judgments of how threatening an upcoming task (e.g. mental arithmetic) was relative to how able the participant felt to cope with the task. A relatively high ratio represented threat, and a relatively low ratio represented challenge. Increased myocardial reactivity was associated with greater challenge and less perceived stress, and increased vascular responsivity was associated with greater threat and more perceived stress. However, cardiovascular reactivity patterns also have been found to vary with the type of stressful situation — specifically, with whether the situation allows action by the person or imposes passivity (Baumeister, 1982, Lovallo et al., 1985 and Sherwood et al., 1990a). Therefore, the action opportunities afforded by a stressful situation might be an important modulator of cardiovascular reactivity, whether the action affordances are imposed by the situation or construed by the person's own appraisal. How a person reacts physiologically to stressful social situations has important health implications, since reactivity patterns have been linked with immunosuppression (Cacioppo, 1994) and potentially with coronary heart disease (Blascovich and Katkin, 1993). However, the nature of the relationship is not well understood, either physiologically or psychologically. In addition, the ecological validity of common laboratory stressors is often questionable. Tasks performed in the laboratory typically involve cognitive (e.g. mental arithmetic) or physical (e.g. cold pressor) challenges. However, cardiovascular responses to these tasks might not be closely correlated with cardiovascular responses to interpersonal stressors (Matthews et al., 1986, Smith and O'Keeffe, 1988 and Lassner et al., 1994), yet interpersonal events are central to the experience of daily stress (Bolger et al., 1989). Therefore, it would be useful to develop psychophysiological laboratory procedures that explicitly reflect the self-presentation and impression management research in social psychology (Baumeister, 1982 and Schlenker and Weigold, 1990) — that is, procedures which manipulate the subject's opportunity to manage the information presented to others about himself or herself. Because cognitive appraisals might be involved, it also would be useful to assess the subject's judgment of the task as a threat or a challenge. This focus on the social psychophysiological correlates of the situation would complement the more common focus on individual differences (see also Burns, 1995 and Marwitz and Stemmler, 1998). The experiment reported here was designed in accord with the preceding considerations. It incorporated an evaluative self-presentation task, an active coping opportunity or a passive coping demand, and an assessment of the subject's appraisal of the task as a challenge or a threat. We were particularly interested in identifying physiological mechanisms that underlay any obtained cardiovascular reactivity differences between subjects. Furthermore, we wanted to look at the physiological mechanisms in subjects who were free from the gross motor movements associated with actively speaking, such as activation of the vocal apparatus, hand and head gesticulations, and clearing of the throat. One purpose of this paper is to examine whether, under evaluative circumstances, cardiovascular responses are modified by people's perceived ability to manage the impressions others are likely to get of them. A second concern is whether a cognitive appraisal of the self-presentational situation as a threat or a challenge is necessary or sufficient to generate differential cardiovascular reactivities. Based on existing literature and the above considerations, cardiovascular reactivity patterns were hypothesized to vary as a function of: 1. Presence (vs. absence) of opportunity to control the impression given of oneself. This hypothesis compares an Active condition in which the S has the opportunity to modify a video of his behavior before others evaluate it with a Passive condition in which the S views the video but does not have the opportunity to modify it. Support for the hypothesis also will require that any reactivity differences are not due to a difference in attentional and motoric demands. 2. Appraisal of the task as a threat (vs. as a challenge). This hypothesis compares those subjects in the Active Experimental condition who assessed the task as a threat (high threat/low coping ability) with those who assessed it as a challenge (low threat/high coping ability). 3. Degree of threat posed by the task, as judged by those subjects who had no opportunity to control the impression given to others. Looking only at subjects in the Passive Experimental condition, where there was no experimentally provided opportunity to cope, this hypothesis compares subjects who assessed the degree of threat posed by the task as high with those who assessed it as low.
نتیجه گیری انگلیسی
Results 3.1. Baseline differences A MANOVA with task condition as the between-subjects factor and the physiological data from the final minute of baseline period (CO, SV, EF, HR, SBP, DBP, and TPR) as the dependent variable set revealed no baseline differences between groups. Additionally, subject ages were evenly distributed across groups. Therefore, reactivity scores (differences from baseline) were used in subsequent analyses (Llabre et al., 1991, Kamarck et al., 1992 and Tomaka et al., 1993). A summary of reactivity means and standard deviations, along with confidence intervals and selected a priori t-tests, is given in Table 1. Table 1. Mean reactivities and contrasts Variable Condition Mean S.D.(N−1) CI(0.95) CI(0.99) P-values (t-tests, two-tail) SBP Active Experimental 6.52 8.27 3.54 4.65 AE vs. PE 0.67 Passive Experimental 5.56 6.20 2.65 3.49 AE vs. AC 0.15 Passive Control 5.02 5.57 2.51 3.29 PE vs. PC 0.76 Active Control 3.30 5.13 2.31 3.03 DBP Active Experimental 5.81 5.10 2.18 2.87 AE vs. PE 0.90 Passive Experimental 5.98 3.82 1.64 2.15 AE vs. AC 0.01 Passive Control 3.42 3.95 1.78 2.34 PE vs. PC 0.04 Active Control 1.67 4.61 2.07 2.72 EF Active Experimental 2.14 2.21 0.94 1.24 AE vs. PE 0.04 Passive Experimental 0.59 2.53 1.08 1.42 AE vs. AC 0.01 Passive Control 0.39 2.48 1.12 1.47 PE vs. PC 0.90 Active Control 0.30 1.90 0.85 1.12 AE vs. PC 0.02 SV Active Experimental 4.47 9.61 4.11 5.40 AE vs. PE 0.10 Passive Experimental 0.36 7.12 3.04 4.00 AE vs. AC 0.53 Passive Control 1.48 8.14 3.66 4.81 PE vs. PC 0.64 Active Control 2.96 8.03 3.61 4.75 TPR Active Experimental 33.03 109.95 47.03 61.80 AE vs. PE 0.00 Passive Experimental 139.18 94.68 40.49 53.21 AE vs. AC 0.65 Passive Control 58.75 82.55 37.12 48.78 PE vs. PC 0.00 Active Control 19.53 73.50 33.05 43.43 AE vs. PC 0.21 HR Active Experimental −0.31 7.70 3.29 4.33 AE vs. PE 0.20 Passive Experimental −2.72 3.58 1.53 2.01 AE vs. AC 0.54 Passive Control −1.83 4.31 1.94 2.54 PE vs. PC 0.57 Active Control −1.49 3.56 1.60 2.10 CO Active Experimental 0.38 1.20 0.52 0.67 AE vs. PE 0.02 Passive Experimental −0.29 0.40 0.17 0.23 AE vs. AC 0.24 Passive Control −0.14 0.39 0.17 0.23 PE vs. PC 0.23 Active Control 0.03 0.41 0.19 0.24 Notes. CO, cardiac output (l/min.); SV, stroke volume (average ml/beat); EF, ejection fraction (average % ejected per beat, calculated as given in footnote 1); HR, heart rate (b.p.m.); SBP, systolic blood pressure (mmHg); DBP, diastolic blood pressure (mmHg); TPR, total peripheral resistance (dyne-s*cm−5). See text for details. CI, confidence interval, at 0.95 and 0.99. Entries in bold identify reactivities that differ significantly from zero. The last two columns summarize the t-test results, two-tailed, of differences between the two experimental groups (AE vs. PE) and between each experimental group and its control condition (AE vs. AC, and PE vs. PC), and for EF and TPR, between AE and PC. Table options 3.2. Hypotheses Hypothesis 1 (importance of opportunity to control impression created) was first tested by comparing the AE and PE conditions in a 2×3 MANOVA (Active vs. Passive vs. task minutes), with all seven physiological measures as dependent variables. The two groups differed significantly in cardiovascular reactivity (F6,246=12.19, P<0.001). Examination of Table 1 reveals that dependable reactivity differences between the Active and Passive Experimental conditions occurred for EF, CO and TRP, with SV showing a trend at P<0.10. Specifically, the rise in EF was much greater in the AE condition than in the PE condition, which did not differ from zero rise. SV showed the same pattern, but not significantly. CO rose in AE but not dependably, while it fell significantly in PE (P<0.01), producing a dependable difference between the two conditions (AE>PE). In contrast, TPR reactivity was much greater in PE than in AE (and was not dependably different from zero in the latter condition). None of the other physiological variables showed differential reactivities between the AE and PE conditions, although reactivities of all were significantly different from zero in at least one of the two experimental conditions. The strong rise of SBP and DBP in both AE and PE conditions is noteworthy, since secondary analyses revealed that the conditions differed in the underlying mechanism by which the BP increases were produced (see below). The AE-by-PE comparisons, then, support Hypothesis 1 for at least two myocardial variables (EF, CO and perhaps SV: AE>PE) and one vascular variable (TPR:PE>AE). A priori examination of the Control conditions in Table 1 addresses whether those reactivity differences were due to experimentally extraneous factors, such as motor and attentional demands (AE vs. AC for EF and CO), or simply watching oneself in the absence of evaluative potential (PE vs. PC for TPR). It can be seen that TPR rise in PE was much greater than in PC (although TPR did rise modestly in PC); and EF reactivity in AE was much greater than in AC, in which it did not differ dependably from zero. The picture for CO is more complex. The AE and AC reactivities did not differ, but neither was the AE reactivity dependably greater than zero. The significant AE>PE contrast was due to the significant fall in CO reactivity in the PE condition; neither of the two Active conditions produced a significant rise in CO. Furthermore, the fall in CO in the PE condition reflects the fall in HR in that same condition. Finally, SV rose significantly in AE and modestly but not dependably in AC. The difference between AE and AC was not significant, albeit in the right direction.3 In sum, the clearest support for Hypothesis 1 is given by EF and TPR, with most modest support from SV. Hypotheses 2 and 3, dealing with threat and coping appraisals, were not confirmed. Specifically, neither the threatened vs. challenged subjects in the AE condition nor the high vs. low threat subjects in the PE condition differed in CV reactivity. However, among AE subjects the threatened (high threat/low cope) subgroup reported greater retrospective stress than the challenged (low threat/high cope) subgroup. Thus, their self-reports were consistent, but they did not covary with the physiological measures. Closer examination, though, reveals that the parsing task, which was the object of the rating scale, generated a relatively low ratio with little variation in the AE group. The mean ratio in AE was 0.364, variance 0.058, range 0.143–0.857, and a median of 0.286. The median split might not have contained enough variation to correlate reliably with the cardiovascular measures. 3.3. Secondary analyses: multiple regressions of SBP and DBP Secondary analyses were conducted to explore further the differential cardiovascular impact of the two experimental conditions (AE and PE). Blood pressure (both SBP and DBP) rose similarly in AE and PE, and the other results suggested that those phenotypically similar changes were generated by different cardiovascular processes. This was examined through a series of multiple regressions, following a hierarchical strategy (Cohen and Cohen, 1983). Specifically, SBP and DBP reactivities were regressed, separately, on EF and SV reactivities jointly, on TPR reactivities, and on EF, SV and TPR reactivities jointly. Each of the analyses was done separately for the Active and Passive Experimental conditions. The hierarchical procedure allowed a comparison of the relative contributions of myocardial (EF and SV) and vascular (TPR) mechanisms to the reactivities of the two blood pressure measurements. The results of the regression analyses are shown in Table 2, and the increments in Table 3. The latter table is most relevant to this report. Changes in blood pressure were explained differently in the two experimental conditions and for the two blood pressure measures. Changes in SBP were explained better by myocardial variation (SV and EF) than by vascular (TPR) variation. This is particularly so in the Active Experimental condition, relative to the Passive Experimental. Changes in DBP were explained better by vascular variation than by myocardial variation in the Passive Experimental condition, while neither myocardial nor vascular change is independently useful in the Active Experimental condition. Table 2. Regression coefficients Regression equation Active Experimental Passive Experimental R2 BTPR BSV BEF R2 BTPR BSV BEF SBP=f(SV+EF) 0.24 Inap 0.48 −0.38 0.20 Inap 0.09 0.92 SBP=f(SV+EF+TPR) 0.32 0.03 0.79 −1.13 0.24 0.02 0.22 0.87 SBP=f(TRP) 0.00 0.00 Inap Inap 0.00 0.00 Inap Inap DBP=f(SV+EF) 0.11 Inap −0.11 1.08 0.00 Inap −0.03 0.09 DBP=f(SV+EF+TPR) 0.22 0.02 0.11 0.54 0.23 0.02 0.16 0.02 DBP=f(TPR) 0.08 0.01 Inap Inap 0.16 0.02 Inap Inap Notes. The B coefficients are the raw partial regression coefficients for the variables entered in the equation for a given row of the table. Italicized R2 values are significant at P<0.10; none was significant at P<0.05. `Inap' indicates inapplicable. Table options Table 3. Incremental contributions to blood pressure reactivities Increments in R2 (P) Active Experimental condition Step 1 SBP=f(SV+EF) DBP=f(SV+EF) Step 2 SBP=f(SV+EF+TPR) DBP=f(SV+EF+TPR) R2 Increment 0.08 (ns) 0.11 (ns) Step 3 SBP=f(TPR) DBP=f(TPR) Step 4 SBP=f(TPR+SV+EF) DBP=f(TPR+SV+EF) R2 Increment 0.32 (0.04) 0.14 (ns) Passive Experimental condition Step 1 SBP=f(SV+EF) DBP=f(SV+EF) Step 2 SBP=f(SV+EF+TPR) DBP=f(SV+EF+TPR) R2 Increment 0.04 (ns) 0.23 (0.04) Step 3 SBP=f(TPR) DBP=f(TPR) Step 4 SBP=f(TPR+SV+EF) DBP=f(TPR+SV+EF) R2 Increment 0.24 (0.10) 0.07 (ns) Notes. The table reflects the contributions of myocardial and vascular factors to blood pressure changes, based on the R2 values shown in Table 2. A significant increment of Step 2 over Step 1 indicates that TPR produced a significant increment in the explained proportion of variance of SBP (or DBP) over that explained by SV and EF. A significant increment in Step 4 over Step 3 indicates that SV and EF jointly produced a significant increment in the explained proportion of variance of SBP (or DBP) over that explained by TPR. Calculation of the significance levels of the increments followed Cohen and Cohen (1983, p. 146).