Conrad Droste

Experimental pain thresholds and plasma beta-endorphin levels during exercise

Experimental pain thresholds (electrical intracutaneous finger and dental pulp stimulation) and plasma hormone levels (beta-endorphin, cortisol, and catecholamines) were measured in ten healthy sportive men before, during, and after progressively more strenuous physical exercise. In a double-blind study conducted on two different days, 20 mg of the opioid-antagonist naloxone or placebo was administered prior to exercise. A significant pain threshold elevation was found during exercise for finger (ANOVA, P less than 0.004) and dental pulp stimulation (P less than 0.01). Pain threshold elevation was most pronounced during maximal exertion, at which time the subjects reported the greatest subjective fatigue. Thresholds remained elevated 10-15 min after the end of exercise, and, 60 min after exercise, thresholds returned to baseline values. The subjective magnitude estimation of suprathreshold stimuli was significantly reduced (P less than 0.0001) 5-10 min after exercise. Plasma beta-endorphin, cortisol, and catecholamines increased significantly (P less than 0.0005, all values) during exercise. Plasma beta-endorphin levels did not correlate significantly with pain thresholds (r = -0.37, NS). Naloxone failed to affect pain thresholds, although beta-endorphin and cortisol increased significantly more (P less than 0.02) during exercise after naloxone. It is concluded that short-term, exhaustive physical exercise can evoke a transient elevation in pain thresholds. This exercise-induced elevation in pain threshold does not, however, appear to be directly related to plasma endorphin levels.

Baroreceptor stimulation: Pain perception and sensory thresholds

Baroreceptor activity has been implicated in the modulation of pain. Sensory detection thresholds and pain ratings were measured in a group of 28 men during carotid baroreceptor manipulation with the PRES (phase-related external suction) neck suction technique. Brief, cardiac phase-related electrical impulses were delivered intracutaneously to the finger. The results indicate that minimum baroreceptor activity was associated with more severe pain, but had no effect on sensory detection threshold. The results are discussed in terms of the learned model of hypertension.

A defective angina pectoris pain warning system: experimental findings of ischemic and electrical pain test.

&NA; Ischemic pain threshold and tolerance levels using the tourniquet pain technique and electrical cutaneous pain thresholds were measured in patients with asymptomatic ischemie heart disease. Thirty asymptomatic patients, who repeatedly exhibited no angina pectoris pain during the occurrence of exercise‐induced coronary ischemia (≥ 0.1 mV ST segment depression in exercise ECG) were compared to 30 randomly selected symptomatic control patients. In a smaller patient group (6 symptomatic, 6 asympatomatic) the degree of forearm ischemia during the tourniquet test was determined non‐invasively by monitoring transcutaneous pO2. Results indicated that asymptomatic patients needed significantly more time to reach pain threshold following occlusion of forearm blood flow and exhibited significantly lower tcpO2 values at threshold than symptomatic patients. Electrical pain thresholds were also elevated in the asymptomatic group. These findings indicate that the phenomenon of asymptomatic myocardial ischemia can be explained by an extracardiac pain modifying mechanism.

Symptomatic myocardial ischemia and everyday life: Implications for clinical use of interactive monitoring

In coronary heart disease (CHD), pathological myocardial ischemic changes do not always occur with the symptom of heart pain. Methodological problems make it difficult to examine the factors that influence silent and symptomatic myocardial ischemia in everyday life. This study uses a computer-assisted monitoring system with an interactive Holter ECG, an actometer, and an electronic diary. Self-report measurements indicate that symptomatic patients tend toward increased neuroticism, whereas asymptomatic patients engage in beneficial and active coping skills more frequently. The results of the monitoring study demonstrate the same degree of ischemia in silent and symptomatic episodes. However, these episodes show differences in certain psychological context variables. Symptomatic episodes are linked to high subjective strain and severe tension. Because angina pectoris is not a reliable warning signal of myocardial ischemia, the use of the interactive monitoring system is recommended for educating CHD patients on how to cope with excessive strain in everyday life.

Blood pressure changes validate phase related external suction, a controlled method for stimulation of human baroreceptors

SummaryPhase related external suction (PRES), a new controlled method for manipulating activity in human baroreceptors, applies precisely timed bursts of suction and pressure within the cardiac cycle through an external neck cuff. Seven healthy adult men participated in 32 pseudo-random trials of baroreceptor stimulation and inhibition. Blood pressure was assessed both intra-arterially and with a noninvasive device. In the present study, PRES baroreceptor stimulation elicited invasively measured blood pressure decreases of about 2.5 mmHg (0.33 kPa) and heart rate decreases of about 5 beats · min−1, while baroreceptor inhibition increased invasively measured blood pressure by about 1.5 mmHg (0.20 kPa) and heart rate about 2.5 beats · min−1. It was concluded that PRES is an effective method for baroreceptor manipulation with weaker size effect but better control of nonspecific factors in human subjects than other baroreceptor manipulation techniques. The noninvasive blood pressure measurement device was less sensitive to experimental variation than was the invasive device.

Development of angina pectoris pain and cardiac events in asymptomatic patients with myocardial ischemia

A total of 389 patients with angiographically determined coronary artery disease, who exhibited a complete absence of angina pectoris in the presence of reproducible myocardial ischemia, were studied in a follow-up investigation. After an initial coronary angiogram, anti-ischemic medication was prescribed as treatment. After a mean follow-up time of 4.9 years (maximum 13.4 years) patients were sent a questionnaire that assessed any new development of angina pectoris pain and cardiac events. In 48 of these patients a second angiogram was recorded after a mean period of 4.2 years. Asymptomatic patients had a worse prognosis than an age-adjusted normal population. After 5 and 10 years, 9 and 26% of the patients, respectively, had died, nonfatal cardiac events (myocardial infarction, bypass surgery or percutaneous transluminal coronary angioplasty) occurred after 5 and 10 years in 19 and 46%, respectively. A large number of initially asymptomatic patients developed angina pectoris pain over the follow-up period (34% after 5 years, 58% after 10 years). Novel angina pectoris pain often preceded cardiac events by months to years. Multivariate analysis indicated that vessel disease (p = 0.0001) and degree of ischemia (defined by ST-segment depression free exercise tolerance, p = 0.04) proved to have independent predictive value with respect to mortality rate. Newly developed angina pectoris was associated with an increase in objective signs of myocardial ischemia and a progression in coronary stenosis. The results indicate that patients who originally had myocardial ischemia with a marked absence of pain can develop angina pectoris over the course of years and that newly developed pain often precedes cardiac events.

Pain threshold elevation during physical exercise — correlation to serum beta-endorphin and effect of naloxone

AIM OF INVESTIGATION: Determination of pain threshold elevation during exercise, relationship to concomitant changes in beta endorphin, effect of naloxone. METHODS: Double blind study (placebo vs. 20 mg naloxone i.v.) in 10 healthy sportive men. Measurement of serum hormone levels (beta endorphin, cortisol, catecholamines), experimental pain thresholds (electrical [dental pulp, intracutaneaous on finger tip], criterion free psychometric [two interval forced choice] procedure) and subjective magnitude estimation of suprathreshold stimuli before, during and after exercise on bicycle ergometer. RESULTS: A significant pain threshold elevation was found during exercise for finger (30% above baseline level, ANOVA p<O.O05) and dental pulp stimulation (16% above baseline, ANOVA p<O.O2). Subjective magnitude estimation of suprathreshold stimuli was significantly lowered (p<O.OOOl) 5-10 min after exercise. Serum beta-endorphin, cortisol and catecholamines increased significantly (p<O.O005) during exercise. Serum beta-endorphin levels did not correlate signifcantly with pain threshold (r--0.37, n.s.). Naloxone failed to ef feet pain thresholds, although beta endorphin and cortisol increased significantly more (p<O,O2) after naloxone. Beta endorphin and pain thresholds showed different time courses and different correlational patterns to other exercise parameters. CONCLUSION: Short term physical exercise can induce transient elevation of pain thresholds not influenced by (20 mg) of naloxone. Although serum betaendorphin also increased during exercise these factors are not causally related to each other. Parallels to TENS will be discussed.