Summary: The possible involvement of an adrenergic-endorphin system in the mediation of the pressor response to isometric muscular contraction was studied in cats. Fatiguing contractions of the gastrocnemius and plantaris muscles caused an increase in the mean arterial blood pressure by 35 to 70 mmHg. Intravenous infusion (30 μg·kg-1) as well as intracisternal injection (2.5 μg) of clonidine-HCl eliminated the pressor response to muscular contraction. In both sets of experiments, the mean blood pressure remained at the resting level throughout the duration of the isometric contraction. Injection of naloxone (0.5 μmol·litre-1) into the cisterna magna did not alter the resting blood pressure and did not affect the rise in mean arterial pressure during muscle contractions. Intracisternal injection of naloxone (0.5 μmol·litre-1) prior to an intracisternal injection of clonidine (2.5 μg) did not alter the resting blood pressure but effectively antagonised the anti-pressor effects of clonidine during fatiguing isometric contractions. These data may indicate that activation of muscle "ergoreceptor" afferents (group III and IV fibres) during muscular contraction may cause an increase in the arterial blood pressure by interfering with an inhibitory adrenergic-endorphinergic pathway in the brainstem.

Defensive hostility has been attributed as an early risk factor of coronary heart disease. The autonomic characteristics of high defensive, high hostile (HD) and low defensive, high hostile (LD) men and women were assessed with a variety of cardiovascular (CV) measures. Reactivity and recovery to an active laboratory stressor (video game, VG) and a passive laboratory stressor (hand cold pressor, CP) of 15 HD men, 16 LD men, 16 HD women, and 16 LD women were recorded. It was predicted that the CV patterning associated with the HD participants would display more sympathetic and less vagal control as well as the least pronounced recovery from the stressors in comparison to LD participants. Results revealed differential CV responses to the lab tasks by group. HD women displayed consistently high levels of low frequency power heart rate variability (HRV) during baseline and across conditions. HD men exhibited significantly pronounced heart rate reactivity and reduced high frequency power HRV to the CP task in comparison to LD men. Interestingly, LD women displayed weaker blood pressure (BP) recovery to the VG in comparison to HD women, whereas the opposite pattern was observed in BP recovery to the CP. These results suggest that defensiveness and sex may moderate the CV reactivity and recovery to different types of stressors in hostile participants. / Master of Science

Pain perception can be drastically affected by external factors in the surrounding environment. Previous studies relying on subjective ratings of pain have shown that guided meditations supplemented by virtual reality (VR) can reduce the perception of pain more successfully than the audio alone. The research question for this study was: How does the efficacy of meditation as a means of pain mitigation differ with and without the application of VR? To answer this question, we used fNIRS to visualize changes in the dorsolateral prefrontal cortex (DLPFC), which has been shown to play a role in the larger pain matrix in the brain. To induce discomfort, we used a Cold Pressor Arm Wrap (CPAW), which is a variation of the more common Cold Pressor Task (CPT). This study was a within-subjects design where in each of the three conditions participants experienced CPAW. The three conditions were: (1) control (no VR & no audio), (2) audio (audio only), and (3) VR (audio + VR). We hypothesized that there would be a decrease in cortical activity in the DLPFC during CPAW when supplemented by VR meditation compared to audio-led meditation and no meditation, due to a decrease in perceived pain in the VR condition. Our results showed that VR meditation did significantly reduce perceived pain, according to the subjective pain ratings. Participants rated their discomfort the lowest in the VR condition, slightly higher in the audio condition, and highest for the control condition (in the absence of meditation). However, there were no significant differences in activity in the DLPFC between the conditions. The lack of any significant findings with the fNIRS data could be the result of many issues, including not having a large enough sample, physiological noise, improper localization of the pain ROIs, and not having a strong enough discomfort stimulus. The future directions for this study would seek to remedy these issues in order to obtain more informative fNIRS results. Overall, this study did show that VR meditation does effectively reduce pain perception and is therefore a promising tool for nonpharmacological pain management.

The bond between pet and owner has been shown to decrease stress-related physical, mental, and emotional disorders by lowering blood pressure and heart rate. The purpose of this study was to examine whether a nonpet canine would have the same effect in reducing physical symptoms of stress as a known dog. Human-animal bond theory, Human pressor test. Data were analyzed using repeated measures, analyses of variance, and t tests. Results indicated that interaction with a strange dog lowered heart rate and blood pressure significantly faster in the experimental group than in the control group. The positive social change implications of this research include policy and procedural accommodations for the use of canines as comfort animals for individuals in stressful conditions.

Vor allem in der Schmerzforschung spielt eine Erfassung der Schmerztoleranzschwellen eine große Rolle. Ziel unserer Studie war es, die ideale Stimulationstemperatur zur Messung der Schmerztoleranz zu erarbeiten. In älteren Studien wurden diese Methoden bereits untersucht, entsprachen aber nicht den Kriterien evidenzbasierter Forschung. Zu diesem Zweck wurde eine randomisierte, kontrollierte Studie an 100 Probanden durchgeführt. Eine Verblindung fand nicht statt. Zum Einsatz kamen fünf Tests, zum einen der „cold-pressor“-Test, der Elektrostimulationstest, sowie drei „hot-pressor“-Tests bei 45°C, 47°C und 49°C. Die Studie fand bei standardisierten Testbedingungen im Rahmen von insgesamt fünf Sitzungen statt, in denen je einer der oben genannten Tests durchgeführt wurde. Potentielle Beeinflussung der nicht-gewünschten Umgebungsfaktoren auf die Studienergebnisse wurde durch standardisierte Testbedingungen so weit wie möglich minimiert. Insgesamt gab es bei keinem der Probanden unter den oben genannten maximalen Schmerzstimulationsexpositionen lang anhaltende unerwünschte Nebenwirkungen oder sensorische Störungen. Im Vergleich zu früheren Studien konnten bei einer deutlich höheren Probandenzahl die Kälteschmerztoleranzschwellenwerte bestätigt werden. Zu erkennen ist, dass die Variabilität der Inter-Probanden-Schwellenwerte bei elektrischen Reizen am niedrigsten ist, wahrscheinlich aber bedingt durch die Tatsache, dass viele Probanden maximal erlaubte Stromstärke tolerierten. Eine Heißwasserbadtemperatur von 45°C wird auch bei mehr als 60% der Probanden bis zu unserer gemessenen Maximaldauer von 300 Sekunden toleriert und bei einer Temperatur von 47°C von fast 10% der Probanden problemlos toleriert. Eine Wärmestimulation („hot-pressor“-Test) des Unterarmes im Heißwasserbad mit 49°C wird bei nur einem von 100 Probanden in der maximal erlaubten Zeit der Stimulation toleriert. Die Inter-Probanden-Variabilität ist vergleichbar zur Kaltwassertoleranz, jedoch ohne Korrelation der beiden Tests zueinander. Die gefundene hohe Variabilität der NRS-Werte bei allen Schmerzstimulationen hebt die Notwendigkeit einer detaillierten Definition der „tolerierten Schmerzintensität“ bei diesen Studien hervor.

Background: Isometric handgrip (IHG) exercise increases heart rate (HR) and mean arterial pressure (MAP); MAP can be sustained after exercise via post-exercise ischemia (PEI). HR and MAP responses are mediated by feed-forward cortical signals (central command, CC) and neural feedback from active muscles (exercise pressor reflex, EPR). Purpose: Differentiate between cortical regions involved with CC versus the EPR via changes in alpha (8-12Hz) and beta (13-30Hz) power using magnetoencephalography (MEG). Methods: Participants (n=11, 22 ± 2 years) completed a repeated IHG and PEI protocol at 5% (control) and 40% maximum force. Results: HR and MAP increased (p<0.04) early during IHG (CC only), while MAP increased further (p=0.03) as IHG continued (CC & EPR). The MAP response persisted during PEI (EPR, p=0.07). During IHG, alpha and beta power decreased within the contralateral sensorimotor cortex. Power increased within MEG sensors associated with the ipsilateral (IHG-alpha) and contralateral (IHG-beta and PEI-beta) insular cortex.

Master of Science / Department of Kinesiology / Steven W. Copp / Mechanical signals within contracting skeletal muscles contribute to the generation of the exercise pressor reflex; an important autonomic and cardiovascular control mechanism. In decerebrate rats, GsMTx4, a mechanically–activated channel inhibitor that is partially selective for piezo channels, was found recently to reduce the pressor response during static hindlimb muscle stretch; a maneuver used to investigate the mechanical component of the exercise pressor reflex (i.e., the mechanoreflex). However, the effect was found only during the very initial phase of the stretch when muscle length was changing which may have reflected the inhibition of rapidly-deactivating piezo 2 channels and the fact that different mechanically-activated channels with slower deactivation kinetics evoked the pressor response during the static phase of the maneuver. We tested the hypothesis that in decerebrate, unanesthetized rats, GsMTx4 would reduce the pressor response throughout the duration of a 30 second, 1 Hz dynamic hindlimb muscle stretch protocol. We found that the injection of 10 µg of GsMTx4 into the arterial supply of a hindlimb reduced the peak pressor response (control: 15±4, GsMTx4: 5±2 mmHg, p<0.05, n=8) and the pressor response at multiple time points throughout the duration of the stretch. GsMTx4, however, had no effect on the pressor response to the hindlimb arterial injection of lactic acid. Moreover, the injection of GsMTx4 into the jugular vein (a systemic control, n=5) or the injection of saline into the hindlimb arterial supply (a vehicle control, n=4) had no effect on the pressor response during dynamic stretch. We conclude that GsMTx4 reduced the pressor response throughout the duration of a 1 Hz dynamic stretch protocol which may have reflected the inhibition of piezo 2 channels throughout the dynamic stretch maneuver.

Experiments were performed to determine to what extent increments in esophageal and abdominal pressure would have on arterial blood pressure during fatiguing isometric exercise. Arterial blood pressure was measured during handgrip and leg isometric exercise performed with both a free and occluded circulation to active muscles. Handgrip contractions were exerted at 33 and 70% MVC (maximum voluntary contraction) by 4 volunteers in a sitting position and calf muscle contractions at 50 and 70% MVC with the subjects in a kneeling position. Esophageal pressure measured at the peak of inspirations did not change during either handgrip or leg contractions but peak expiratory pressures increased progressively during both handgrip and leg contractions as fatigue occurred. These increments were independent of the tensions of the isometric contractions exerted. Intra-abdominal pressures measured at the peak of either inspiration or expiration did not change during inspiration with handgrip contractions but increased during expiration. During leg exercise, intraabdominal pressures increased during both inspiration and expiration, reaching peak levels at fatigue. The arterial blood pressure also reached peak levels at fatigue, independent of circulatory occlusion and tension exerted, averaging 18.5-20 kPa (140-150 mm Hg) for both handgrip and leg contrations. While blood pressure returned to resting levels following exercise with a free circulation, it declined by only 2.7-3.8 kPa after leg and handgrip exercise, respectively, during circulatory occlusion. These results indicate that straining maneuvers contribute 3.5 to 7.8 kPa to the change in blood pressure depending on body position.

The purpose of this study was to examine the effects of the cold pressor test on skin temperature, natural killer cell activity, plasma concentrations of interleukin-1 and cortisol, and the numbers of white blood cells, CD3+ cells, CD4+ cells, CD8+ cells, and CD56+ cells in the peripheral blood. In addition, the study examined whether thermal biofeedback, when presented following the cold pressor tests, would mitigate the effects of the cold pressor tests. Four male university students completed pretest psychological inventories and were pretrained during nine laboratory sessions to increase their skin temperature to 95 degrees Fahrenheit. During the experiment, blood samples were collected at 5-minute intervals and before and after the 1-minute cold pressor tests through an 18-mm catheter inserted into each subject's arm. Subjects were randomly assigned to a matched pair and to the order of experimental conditions, including baseline, the initial cold pressor test, return to baseline, the second cold pressor test, and thermal biofeedback. Each matched pair experienced the conditions in a multiple baseline fashion across subjects during the individual 1.5-hour experimental sessions. Following the experiment, subjects completed posttest psychological inventories, exit interviews, and consumer satisfaction surveys. All subjects demonstrated a decrease in skin temperature ranging from 1 to 1.4 degrees Fahrenheit during the 1-minute cold pressor tests in a multiple baseline fashion, and repeated the temperature decreases within-subjects during the second cold pressor test. Increases in natural killer cell activity ranged from 1% to 14% during the cold pressor tests. For all subjects, both cold pressor tests were associated with increased plasma concentrations of interleukin-1, ranging from 2 to 69 pg/ml. The initial cold pressor tests were associated with increases in all cell numbers in a multiple baseline fashion, but cell numbers varied during the second cold pressor tests. For all subjects, average skin temperatures during the thermal biofeedback conditions were from .3 to .9 degrees higher than during the return to baseline conditions. For all subjects, thermal biofeedback conditions were associated with from 2 to 8 (10^4 cells/ml) higher mean numbers of CD56+ cells than the return to baseline conditions. For 3 subjects, the thermal biofeedback conditions were associated with higher numbers of white blood cells, CD3+ cells, CD4+ cells, and CD8+ cells than the return to baseline conditions. Thermal biofeedback was associated with reductions of from .2 to 26 in the standard deviations of interleukin-1 values, and with a reduced range of cortisol values following the cold pressor tests. Few changes occurred in scores from pre- to posttest on the psychological tests. Subjects rated the goal of learning to relax as very important. All of the subjects stated that they would seek relaxation training for the treatment of a medical or psychological disorder if prescribed. Implications are discussed for design of research in psychoneuroimmunology, for measurement of immune system variables, and for potential clinical applications of these data.

Various opioids were used to investigate the role they might play in the cardiovascular responses to fatiguing isometric contractions. Changes in blood pressure were measured in cats anaesthetised with α-chloralose. Fatiguing isometric contractions of the hind limb muscles (ergoreceptor activation) were generated using a microprocessor controlled stimulator (50 Hz, 0.2 ms, 200-800 mV). Baroreceptor inactivation was elicited by carotid artery occlusion. Muscle contraction caused an increase in mean arterial pressure of 51 (SEM 12) mm Hg and carotid occlusion an increase of 56(9) mm Hg above resting levels in control conditions. Injection of dynorphin (0.5-5.0 μg·5 μl-1) into the cerebral aqueduct just rostra1 to the 4th ventricle eliminated the pressor response to muscular contraction (mean arterial pressure at rest, 80-118 mm Hg: on fatigue, 72-129 mm Hg) but did not affect the pressor response to carotid occlusion in the same cats. Similarly, injections of met-enkephalin (1-100 μg·5 μl-1) or β-endorphin (10-100 μg·5 μl-1) eliminated the ergoreceptor induced changes in mean arterial pressure during isometric contractions but had no effect on the changes caused by carotid occlusion. Pressor responses to nerve crush were not eliminated. These results support the suggestion that a catecholaminergic-opioidergic pathway in part mediates the cardiovascular responses to ergoreceptor afferent but probably not baroreceptor afferent input.