OBJECTIVE: To develop a laboratory paradigm for assessing the tendency to amplify somatic symptoms and report bodily distress. METHOD: Reports of four different cardiopulmonary symptoms were obtained during standardized, treadmill exercise, while the physiological parameters which induce these symptoms were simultaneously measured. Two indices were developed to compare symptom reporting across patients: symptom severity after reaching 80% of predicted, maximal exercise capacity; and the magnitude of physiological arousal necessary to induce an initial sensation of discomfort. RESULTS: Fifty-one medical outpatients with a chief complaint of palpitations were studied. Symptom distress at 80% of maximal exercise capacity was significantly associated with state anxiety and daily life stress. The complaint of "heart racing" first occurred at a significantly lower heart rate for patients who were older, more anxious, and reported more daily life stress. Measures of hypochondriasis, somatization, bodily amplification, and bodily absorption were not significantly associated with either symptom measure. CONCLUSIONS: Standardized exercise testing may provide a suitable paradigm with which to study the tendency to amplify symptoms and to somatize. The distress reported by different subjects at 80% of maximal exercise capacity may be considered an index of the discomfort engendered by a standardized stimulus, whereas the point of onset of discomfort may be a measure of the patient's threshold for becoming symptomatic. These findings are not conclusive, but do suggest that patients who are more anxious and under more stress tend to report more intense cardiopulmonary symptoms at comparable levels of physiological arousal, and to have a lower threshold for experiencing discomfort.

Adult↗

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Acute hypertension in a nonhuman primate: humoral and hemodynamic mechanisms.

The present study assessed the contribution of the renin-angiotensin system (RAS), dietary sodium, and cardiac output (CO) to the genesis of primate hypertensin in a one-kidney model which was developed to test species-specific renin inhibitors. Reduction of renal perfusion pressure increased mean arterial pressure (MAP) from 105 +/- 4 to 127 +/- 3 mm Hg (p less than 0.0005), associated with increased plasma renin activity (PRA) from 4.9 +/- 0.7 to 13.8 +/- 1.1 ng. ml-1.hr-1 (p less than 0.0005). Correlation of MAP with PRA yielded an r value of 0.662 (p less than 0.0005). Significant blood pressure elevation was obtained with both regular (R) and low sodium (LS) diet (p less than 0.0005), although the MAP change was greater with LS. With both R and LS diet, hypertension was associated with increased PRA (p less than 0.0005), and normotensive pressures were achieved with converting enzyme inhibitor (teprotide). The hemodynamic change with hypertension was an increase of systemic vascular resistance (SVR) from 0.89 +/- 0.12 to 1.17 +/- 0.09 units (p less than 0.05); cardiac output (CO) and central blood volume did not change significantly. Thus, acute hypertension, mediated by the RAS, was developed in a one-kidney primate model. The hemodynamic correlate of hypertension was increased SVR; CO and volume redistribution were not initiating factors.

Angiotensin-Converting Enzyme Inhibitors↗