Examining the Role of Trait Resilience and Self-Compassion in Adaptive Responses to Stress: A Physiological Stress Response Study

Psychological resilience is concerned with adaptive functioning in the face of stress, adversity, or trauma (Davydov, Stewart, Ritchie, & Chaudieu, 2010; Windle, 2011). Trait level psychological resilience refers to characteristics that may predispose adaptive responses to stress, trauma, and adversity (e.g., Connor & Davidson, 2003). Despite work suggesting the benefits of trait resilience (e.g., Hu, Zhang, & Wang, 2015), there are multiple self-report measures in existence with no identified measurement standard (Windle et al., 2011). Given differing conceptualizations of trait resilience, physiological measurement of stress response represents a viable and objective approach to examine psychological resilience (Walker, Pfingst, Carnevali, Sgoifo, & Nalivaiko, 2017), with some work suggesting that those high in trait level resilience exhibit an adaptive and flexible physiological stress response to induced stressors (Lü, Wang, & You, 2016; Tugade & Fredrickson, 2004). However, findings have been mixed, in part due to the utilization of measures across studies that differ in their conceptualization of trait resilience. Further, research has not examined other variables with empirical and conceptual links to trait resilience within this context; such as self-compassion (e.g., Arch et al., 2014). The first chapter of this dissertation provides a review of the differing conceptualizations of psychological resilience and potential resilience enhancing interventions. The second chapter of this dissertation comprises a study that aimed to examine the relationship between four self-report measures of trait resilience and several cardiovascular indices of physiological stress response in order to determine which measure best captured an objective ability to adaptively respond to stress. Self-compassion was measured in order to examine the potential additive role of this variable. Despite the hypothesis that multiple measures of trait resilience would correlate significantly with an adaptive stress response and subsequently predict adaptive stress response in a simultaneous multiple regression model, results indicated non-significant relationships between all self-report measures and physiological indices. Subsequent analyses examining additional cardiovascular indices and curvilinear analyses were also non-significant. Implications, limitations, and directions for future research are discussed

The effects of trait anxiety, potentially traumatic events, and psychological adjustment on attentional threat bias in college students

Attentional biases towards threatening information are considered a highly adaptive process(e.g., Boyer & Bergstrom, 2011). However, differential processing of threat as a result ofindividual differences can result in attentional mechanisms that are biased towards threateninginformation at a level that is considered maladaptive. Previous research has suggested that individuals with high levels of trait anxiety and individuals who exhibit trauma symptomatology as a result of a potentially traumatic event (PTE) exhibit this maladaptive level of attentional threat bias that may in turn result in the maintenance of anxious states and debilitating trauma symptomatology, respectively (Ehlers & Clark, 2000; Kimble et al., 2014). The present study aimed to further explore trait anxiety and trauma symptomatology as they relate to attentional threat bias by examining trait anxiety and trauma symptomatology as predictors of attentional threat bias. A non-clinical sample was given self-report measures to assess trait anxiety, PTEs, and trauma symptomatology, and completed an eye-tracking paradigm to assess attentional threat bias. Though no relationship between trait anxiety and attentional threat bias was found, results suggest a significant relationship between trauma symptomatology and attentional threat bias

Platelet Function in Acute Experimental Pancreatitis

Acute pancreatitis (AP) is characterized by disturbances of pancreatic microcirculation. It remains unclear whether platelets contribute to these perfusion disturbances. The aim of our study was to investigate platelet activation and function in experimental AP. Acute pancreatitis was induced in rats: (1) control (n = 18; Ringer’s solution), (2) mild AP (n = 18; cerulein), and (3) severe AP (n = 18; glycodeoxycholic acid (GDOC) + cerulein). After 12 h, intravital microscopy was performed. Rhodamine-stained platelets were used to investigate velocity and endothelial adhesion in capillaries and venules. In addition, erythrocyte velocity and leukocyte adhesion were evaluated. Serum amylase, thromboxane A2, and histology were evaluated after 24 h in additional animals of each group. Results showed that 24 h after cerulein application, histology exhibited a mild AP, whereas GDOC induced severe necrotizing AP. Intravital microscopy showed significantly more platelet–endothelium interaction, reduced erythrocyte velocity, and increased leukocyte adherence in animals with AP compared to control animals. Thromboxane levels were significantly elevated in all AP animals and correlated with the extent of platelet activation and severity of AP. In conclusion, platelet activation plays an important role in acute, especially necrotizing, pancreatitis. Mainly temporary platelet–endothelium interaction is observed during mild AP, whereas severe AP is characterized by firm adhesion with consecutive coagulatory activation and perfusion failure

Cyclical coronary flow reductions in conscious dogs equipped with ameroid constrictors to produce severe coronary narrowing

In conscious dogs equipped with ameroid constrictors to produce gradual coronary occlusion, coronary flow velocity was monitored prior to complete occlusion when coronary constriction was severe (resting flow velocity reduced by 10–50% from control recordings made 7–10 days after ameroid implantation). In six of the ten dogs, we observed spontaneous cyclical variations in coronary flow velocity, characterized by gradual reduction in flow followed by very abrupt restoration of flow. The cyclic coronary flow reductions were observed between 20 and 31 days after ameroid implantation. These changes in flow bear striking similarity to those observed by previous investigators using anesthetized, open-chest canine preparations, in which the role of platelets was clearly demonstrated. Consequently, we hypothesize that spontaneous platelet aggregation and de-aggregation within the severely narrowed coronary lumen (enclosed by the ameroid constrictors) could account for our observations.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/41746/1/395_2005_Article_BF01906748.pd