Figures & data
Figure 1 A systems definition of stress.
Figure 2 Twenty-four hour ambulatory blood pressure monitoring records for a control subject and three patients (Pt) with baroreflex failure as a late sequela of neck irradiation.
Figure 3 Values for arterial plasma adrenaline (EPI), noradrenaline (NE), forearm vascular resistance (FVR) and mean arterial pressure (MAP) in a patient with tilt-induced syncope. Grey arrows highlight changes in EPI and FVR preceding hypotension and syncope.
Figure 4 Overview of thermoregulatory mechanisms. SCS = sympathetic cholinergic system; SNS = sympathetic noradrenergic system.
Figure 5 Hypothetical changes associated with heat shock. AHS = adrenomedullary hormonal system. Note positive feedback loop, indicated by a circuit with all (+) signs, as well as interference with a negative feedback loop, indicated by an even number of ( − ) signs.
Figure 6 Model of compensatory activation of the sympathetic noradrenergic system (SNS) by thyroidectomy. THY: thyroid; TEMP: temperature.
Figure 7 Relative intensities of activation of the HPA axis, adrenomedullary hormonal system (AHS) and sympathetic noradrenergic system (SNS) during exposure to different stressors, based on literature review.
Figure 8 Model of effector sharing. The “barostat” and “osmostat” share the arginine vasopressin (AVP) effector.
Figure 9 Plasma concentrations of corticotropin (ACTH) and adrenaline before and at 150 minutes after injection of 2-deoxyglucose into healthy volunteers, in the context of pretreatment with placebo or alprazolam. Differences between placebo and alprazolam conditions might reflect distress (gray rectangles).
Figure 10 Predicted effects of stress and aging on allostatic load and clinical status, based on a kinetic model.
