دانلود مقاله ISI انگلیسی شماره 39050
عنوان فارسی مقاله

تنفس، شرطی سازی ترس و ارتباط آن با واکنش پذیری قلبی

کد مقاله سال انتشار مقاله انگلیسی ترجمه فارسی تعداد کلمات
39050 2009 6 صفحه PDF سفارش دهید محاسبه نشده
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عنوان انگلیسی
Fear-conditioned respiration and its association to cardiac reactivity
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Biological Psychology, Volume 80, Issue 2, February 2009, Pages 212–217

کلمات کلیدی
تهویه ترس - تنفس - ضربان قلب - تنفس
پیش نمایش مقاله
پیش نمایش مقاله تنفس، شرطی سازی ترس و ارتباط آن با واکنش پذیری قلبی

چکیده انگلیسی

Abstract This study aimed to investigate ventilatory correlates of conditioned fear responses. Respiratory, end-tidal carbon dioxide pressure (PetCO2) and heart rate changes were studied in a differential fear-conditioning paradigm. Forty-two participants viewed pictures of faces. One picture (CS+) was followed by a human scream (US) during the acquisition phase, but not in a subsequent extinction phase. Conditioning of PetCO2 (decrease), respiratory cycle time (decrease) and inspiratory duty time (increase) was established and subsequently extinguished. When participants were clustered according to their conditioned PetCO2 responses during acquisition, only a group showing a conditioned decrease in PetCO2 showed also a differential cardiac acceleration, a decrease in expiratory duration and an increase in inspiratory duty time in response to the CS+. These results suggest that preparation for defensive action is characterized by a tendency towards hyperventilation and cardiac acceleration.

مقدمه انگلیسی

Introduction Both clinical phenomenology and theory highlight the centrality of respiratory behavior and respiratory distress in states of fear (e.g., Ley, 1985, Gorman et al., 2000, Sinha et al., 2000 and Wilhelm et al., 2001). Despite this, ventilatory correlates of conditioned fear responses in humans are not well documented, perhaps because, compared to other psychophysiological measures of learning (e.g., heart rate), changes in the mechanics of respiration are slower and more variable. A more tractable respiratory parameter, however, may be carbon dioxide pressure, since, in many circumstances, healthy subjects are able to regulate arterial carbon dioxide pressure, maintaining it within relatively narrow limits. As a consequence, normal breathing is characterized by little variability in carbon dioxide pressure (Shea, 1997), compared to the variability in respiratory timing and volume parameters (Bruce and Daubenspeck, 1995). In the current study, we assessed end-tidal carbon dioxide pressure (PetCO2, a valid approximation of arterial CO2 pressure; Gardner, 1996 and Pahn et al., 1987) during affective conditioning. PetCO2 is thought to be less variable than timing and volume parameters of breathing. Moreover, it is the only relevant outcome measure in the context of hyperventilation, which reflects a breathing pattern in excess of metabolic needs that occurs during emotional arousal, particularly fear (Van Diest et al., 2001a, Van Diest et al., 2001b and Van Diest et al., 2005). The control of breathing is a complex interplay that relies on many factors, including the bulbopontine respiratory network, central and peripheral chemoreceptor control, modulation of respiratory muscles by mechanoreceptors, and numerous suprapontine networks located in the limbic, cerebellar, and cortical areas (Gallego et al., 2001 and Shea, 1996). It is not currently known how these different networks interact during an emotional event and in which measures they are reflected. Addressing this concern, Boiten, 1993 and Boiten, 1998 suggested that, in addition to assessing traditional respiratory parameters of depth (tidal volume) and rate (total cycle time, inspiratory time, expiratory time and post-expiratory pause) of breathing, compound measures should also be pursued. One such parameter is the ratio of inspiratory time to the total breathing cycle time (inspiratory duty cycle), which reflects the cyclical on/off switching of the central inspiratory drive mechanism (Gautier, 1980). Several authors suggest that, in contrast to volume parameters, this timing parameter is weakly controlled by the chemical drive to breathe, allowing for its modulation by non-metabolic factors (Gallego et al., 1996 and Rafferty and Gardner, 1996). Thus, to the extent that respiratory changes in anticipation of an aversive event are not driven by changes in metabolism, one would expect to see effects of affective learning on timing, compared to volume parameters. This is exactly what has been observed in studies of humans using a standard aversive conditioning paradigm (e.g., tone CS and shock US; Ley, 1999). Obrist (1968) described important interindividual differences in the direction of the conditioned breathing responses: whereas most participants showed a slightly increased breathing frequency following conditioning, a subgroup of participants showed a marked decrease in respiratory activity in response to the CS. The latter also showed a more sustained conditioned cardiac deceleration. Similar to respiration, fear-conditioned heart rate responses also show different patterns among individuals (Hamm and Vaitl, 1996, Hodes et al., 1985 and Moratti and Keil, 2005). Heart rate decreases or increases have been interpreted as distinguishing between defensive attention and fear in the context of the defense cascade model (Lang et al., 1997). This model describes an aversive motivational circuit that, with increasing arousal, triggers reactions ranging from orienting to fight/flight. The associated autonomic and somatic responses can be functionally organized into two broad output classes of defensive immobility and attention (i.e., freezing and hypervigilance in which the organism is passive, but primed to respond) and defensive action (contextual variations in fight/flight that are more or less direct responses to nociception or imminent attack). Whereas defensive attention is associated with cardiac deceleration, cardiac acceleration prepares the organism to actively escape from an imminent threat, and previous studies have found that different individuals show different cardiac reactions following aversive conditioning (Hamm and Vaitl, 1996 and Hodes et al., 1985). For instance, when a picture was paired with a loud noise, participants could be clustered based on their conditioned heart rate responses, which consisted of acceleration or deceleration (Hodes et al., 1985). Compared to individuals showing cardiac deceleration, individuals showing a conditioned cardiac acceleration to the CS+, also reported greater fear to the CS+ than the CS− (Hodes et al., 1985), showed more resistance to extinction in electrodermal responses (Hodes et al., 1985) and displayed potentiated startle responses to the CS+ (Hamm and Vaitl, 1996). This pattern of results is interpreted as indicating that, whereas all participants learned an anticipatory orienting response (late interval heart rate deceleration), only accelerators showed a conditioned preparation for defensive action. Several findings from other studies suggest that respiration also distinguishes between defensive attention and action. Decreases in breathing frequency and/or a tendency towards expiration (i.e., decreased inspiratory duty cycle time) have been reported as part of the orienting response and during sustained attention in humans (Barry, 1982, Boiten et al., 1994, Denot-Ledunois et al., 1998, Obrist et al., 1969 and Stekelenburg and Van Boxtel, 2001). This may either be a direct consequence of a decreased somatic activity during defensive immobility (Obrist et al., 1969), or, it may be functional to inhibit breathing under threat for two reasons: (1) prompting an increase in blood flow to the brain, due to the cerebrovascular dilating effect of CO2 (Giardino et al., 2007 and Kastrup et al., 1998), or (2) suppressing the noise associated with breathing in the presence of a predator (Fokkema, 1999). Defensive action, on the other hand, seems to prompt an increased cardio-respiratory activation, as well as a tendency towards hyperventilation (decreased PetCO2; Van Diest et al., 2001a and Van Diest et al., 2001b). The present study aimed to investigate fear conditioning of breathing behavior. To this end, respiratory and PetCO2, as well as heart rate responses, were studied during a prototypical affective learning paradigm. Pictures of human faces served as the conditioned stimulus (CS), a loud human scream as the unconditioned stimulus (US). We expected that differential conditioning of respiratory timing parameters, PetCO2 and heart rate would be established during acquisition and dissipate during a subsequent extinction phase. In addition, we expected that heart rate responses would closely follow respiratory timing and PetCO2 responses.

نتیجه گیری انگلیسی

. Results 3.1. Respiration During acquisition, participants breathed faster (had a shorter total respiratory cycle time) in response to the CS+ compared to the CS−, F(1, 36) = 6.66, p < .01, View the MathML sourceηp2=.16; see Table 1. Table 1. Mean (S.D.) respiratory responses during each block of acquisition and extinction. Acquisition Extinction Block 1 Block 2 Block 3 Block 1 Block 2 CS+ CS− CS+ CS− CS+ CS− CS+ CS− CS+ CS− Ttot −0.1 (0.6) 0.1 (0.6) −0.1 (0.7) −0.0 (0.6) −0.2 (0.9) 0.2 (0.5) −0.2 (0.9) −0.0 (0.8) −0.1 (1.0) −0.0 (0.6) Ti −0.0 (0.3) 0.0 (0.3) 0.1 (0.3) 0.0 (0.2) 0.1 (0.2) 0.1 (0.3) 0.1 (0.3) 0.1 (0.4) 0.1 (0.4) 0.0 (0.6) Te 0.0 (0.5) 0.1 (0.4) 0.1 (0.4) 0.1 (0.3) 0.1 (0.4) 0.1 (0.3) −0.1 (0.5) 0.0 (0.6) 0.1 (0.5) −0.1 (0.4) Pexpin 0.0 (0.7) 0.1 (0.7) −0.2 (0.5) −0.1 (0.4) −0.2) (0.5) −0.1 (0.3) −0.2 (0.6) −0.0 (0.7) −0.1 (0.7) 0.1 (0.8) Ti/Ttot 0.01 (0.06) 0.00 (0.05) 0.03 (0.07) 0.00 (0.05) 0.03 (0.09) 0.02 (0.05) 0.01 (0.07) 0.01 (0.06) 0.00 (0.08) −0.00 (0.06) Amp −0.3 (0.7) −0.2 (0.7) −0.1 (0.4) −0.1 (0.5) −0.0 (0.6) 0.0 (0.6) −0.2 (0.6) 0.0 (0.8) −0.3 (0.9) −0.0 (1.4) PetCO2 0.4 (0.9) 0.1 (0.9) −0.1 (1.5) 0.4 (0.8) −0.1 (1.3) 0.3 (0.8) 0.2 (1.4) −0.0 (1.2) 0.2 (1.3) −0.0 (1.5) Note: Ttot, respiratory cycle time (s); Ti, inspiratory time (s); Te, expiratory time (s); Pexpin, post-expiratory pause duration (s); Amp, respiratory amplitude (standardized within subjects); Ti/Ttot, inspiratory duty time (%); PetCO2, end-tidal carbon dioxide (mmHg). Table options A significant conditioning effect was also found for inspiratory duty cycle time: the relative inspiratory time increased more in response to the CS+ than to the CS−, F(1, 33) = 4.77, p < .05, View the MathML sourceηp2=.13, see Table 1. No significant-conditioning effects were found for the subcomponents of the respiratory cycle time (inspiratory and expiratory time, and end-expiratory pause), or for amplitude measures. For PetCO2, a significant CS × Block interaction was present during acquisition (F(2, 66) = 4.06, p < .05, ɛ = .99, View the MathML sourceηp2=.11; see Table 1). Compared to the CS−, a significant decrease in response to the CS+ was present in the second and third (F(1, 33) = 4.70, p < .05), but not in the first (F(1, 33) = 2.37, n.s.) acquisition block. No significant effects were found for the extinction data. 3.2. Heart rate No significant effects on any of the heart rate components (initial and secondary deceleration and midinterval acceleration) were observed during acquisition. During extinction, heart rate increased more in response to the CS+ than to the CS− in the first (F(1, 37) = 6.23, p < .05), but not in the second block of extinction (F(1, 37) = 0.01, n.s.; CS × Block interaction: F(1, 37) = 4.21, p < .05, View the MathML sourceηp2=.10; see Table 2). No significant effects were found for the initial or secondary deceleration during extinction. Table 2. Mean (S.D.) heart rate responses during each block of acquisition and extinction. Acquisition Extinction Block 1 Block 2 Block 3 Block 1 Block 2 CS+ CS− CS+ CS− CS+ CS− CS+ CS− CS+ CS− D1 −4.6 (6.0) −3.4 (3.2) −3.8 (5.5) −2.0 (3.5) −3.6 (5.0) −3.2 (4.2) −2.7 (4.5) −4.7 (6.0) −3.3 (4.6) −3.6 (4.9) A 1.1 (7.0) 2.5 (7.0) 3.5 (7.7) 4.3 (5.9) 5.6 (6.0) 3.1 (5.6) 4.8 (5.9) 1.4 (7.9) 2.9 (7.7) 2.9 (5.3) D2 −5.9 (5.7) −5.5 (6.0) −4.0 (7.3) −3.9 (5.2) −4.0 (7.4) −5.9 (6.0) −6.5 (6.5) −8.8 (7.6) −7.4 (7.6) −6.5 (8.0) Note: D1, initial cardiac deceleration (bpm); A, midinterval cardiac acceleration (bpm); D2, late cardiac deceleration (bpm). Table options 3.3. Subjective ratings Compared to the pre-experimental ratings, participants rated the CS+, but not the CS− as more unpleasant following conditioning, compared to these ratings prior to conditioning (Time × CS, F(1, 40) = 23.09, p < .01, View the MathML sourceηp2=.37). Furthermore, participants rated the CS+ picture higher in arousal than the CS− picture following, but not prior to the experiment (Time × CS, F(1, 40) = 23.07, p < .01, View the MathML sourceηp2=.37). 3.4. Clustering by PetCO2 response 3.4.1. Cluster analysis Two clusters were identified based on PetCO2 responses to both CSs in the last two acquistion blocks. Table 3 displays the descriptive statistics of the PetCO2 responses averaged over the last two acquistion blocks for each cluster. In the first cluster (n = 14), participants showed minor, non-differential increases in PetCO2 to both CSs; this group will be further called hypoventilators. In the second cluster (n = 19), participants showed a marked decrease in PetCO2 in response to the CS+, but not to the CS−; this cluster will be further labeled hyperventilators. The clusters’ labeling refers to a response tendency and does not reflect a clinically significant state of hypo- or hyperventilation, which would imply more pronounced and sustained PetCO2 responses. Table 3. Mean, S.D. and range of PetCO2 responses to CS+ and CS− during the last two blocks of acquisition for hypoventilators (N = 14) and hyperventilators (N = 19). Acquisition Block 2 Acquisition Block 3 CS+ CS− CS+ CS− Hypoventilators Mean 0.5 0.6 0.8 0.3 S.D. 0.7 0.7 1.1 0.7 Range −0.7 to 1.5 −0.6 to 1.5 −0.4 to 4.2 −0.9 to 1.8 Hyperventilators Mean −0.8 0.2 −0.8 0.3 S.D. 0.9 0.8 0.9 0.9 Range −2.6 to 0.7 −1.1 to 1.9 −3.4 to 0.5 −0.9 to 2.5 Table options 3.4.2. Respiration During acquisition, a significant Cluster × CS × Block interaction: F(2, 62) = 4.00, p < .05, ɛ = .96, View the MathML sourceηp2=.11) was present for PetCO2, reflecting the clustering procedure. No differences were observed for PetCO2 responses during extinction. During acquisition, hyperventilators had a shorter expiration in response to the CS+ compared to the CS− (F(1, 29) = 8.37, p < .01; means (S.D.) were −0.08 (0.25) and −0.22 (0.28), respectively), whereas expiratory time during CS+ versus CS− did not differ for the hypoventilators (F(1, 29) = 1.17, n.s.; means (S.D.) were 0.15 (0.18) and 0.13 (0.23), respectively). The overall Cluster × CS × Block interaction for expiratory time was significant, F(1, 29) = 7.34, p < .05, ɛ = .96, View the MathML sourceηp2=.11. Also during acquisition, hyperventilators learned to respond with an increased inspiratory duty time in response to the CS+, but not to the CS− (linear trends were F(1, 31) = 5.47, p < .05 and F(1, 31) = 0.11, n.s., respectively). No such increases were observed for the hypoventilators (CS+: F(1, 31) = 0.31, n.s.; CS−: F(1, 31) = 1.01, n.s.). Fig. 1 displays the Cluster × CS × Block interaction for responses in inspiratory duty time during acquisition, F(2, 58) = 3.73, p < .05, ɛ = .81, View the MathML sourceηp2=.11. Changes in inspiratory duty time (means and standard errors) in response to CS+ ... Fig. 1. Changes in inspiratory duty time (means and standard errors) in response to CS+ and CS− during three acquisition blocks for each cluster (hypoventilators/hyperventilators). Figure options During extinction, a differential increase in inspiratory duty time in response to the CS+ tended to be present for the hyperventilators (F(1, 31) = 3.64, p < .07), but not for the hypoventilators (F(1, 31) = 0.58, n.s.). The overall Cluster × CS interaction was only marginally significant (F(1, 31) = 3.32, p < .08). 3.4.3. Heart rate Participants in the two clusters differed in their conditioned midinterval cardiac acceleration during the acquisition phase (Cluster × CS × Block interaction, F(2, 62) = 4.20, p < .05, View the MathML sourceηp2=.12; see Fig. 2). Only hyperventilators showed a progressive increase across acquisition blocks in midinterval cardiac acceleration in response to the CS+ (linear trend: F(1, 31) = 11.89, p < .01). This did not happen for the CS− (F(1, 31) = 0.05, n.s.). No significant effects were found for the initial or secondary deceleration components. Changes in heart rate per second during the 8s presentation of the CS pictures ... Fig. 2. Changes in heart rate per second during the 8 s presentation of the CS pictures for each cluster (hypoventilators/hyperventilators). Figure options For extinction, no significant effects involving the Cluster variable were observed. 3.4.4. Subjective ratings No differences in ratings of pleasantness and arousal were found as a function of cluster membership.

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