The regulation of sympathetic nerve activity in chronic heart failure (CHF) has been an area of renewed investigation. Understanding the central mechanisms that are responsible for sympatho-excitation in this disease state may help in reducing the deleterious effects of chronic sympatho-excitation. This review will summarize our understanding of abnormal reflex control of the circulation in CHF. The roles of the arterial baroreflex, the chemoreflex, the cardiac sympathetic afferent reflex and the cardiopulmonary reflex are discussed. New experimental techniques that allow genetic manipulation of substances such as nitric oxide synthase in discrete areas of the brain aid in clarifying the role of NO in the modulation of sympathetic tone in the CHF state. Lastly, clinical implications of this work are discussed.

The origin of sympathetic outflow in heart failure: The roles of angiotensin II and nitric oxide

A first-time parachute jump was chosen as a model to evaluate the endocrine response to acute psychological stress. In 43 inexperienced tandem parachutists, blood was drawn continuously from 2 h before to 1 h after the jump and analyzed at 10-min intervals for plasma concentrations of epinephrine (E), norepinephrine (NE), cortisol, GH, PRL, and TSH. In addition, heart rate was recorded throughout the experiment. There was a significant increase in heart rate and E concentrations during the jump itself. NE, cortisol, GH, PRL, and TSH peaked with a latency of 10-20 min. Apart from cortisol and TSH concentrations, which were still elevated 1 h after the stress event, plasma levels of the other endocrine variables normalized within 1 h following the jump. Statistically significant cross-correlations could be observed between E and NE (r = 0.60, no time lag) and between E and PRL (r = 0.58, 10-min time lag) only. Even in a very homogenous group of subjects and under well-controlled conditions, endocrine responses to acute psychological stress show considerable variations.

Time kinetics of the endocrine response to acute psychological stress.

William James’s theory of emotion has been controversial since its inception, and a basic analysis of Cannon’s critique is provided. Research on the impact of facial expressions, expressive behaviors, and visceral responses on emotional feelings are each reviewed. A good deal of evidence supports James’s theory that these types of bodily feedback, along with perceptions of situational cues, are each important parts of emotional feelings. Extensions to James’s theory are also reviewed, including evidence of individual differences in the effect of bodily responses on emotional experience.

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Bodily Influences on Emotional Feelings: Accumulating Evidence and Extensions of William James’s Theory of Emotion

Acute and delayed effects of alprazolam on flight phobics during exposure.

We investigated the effect of raising arterial plasma epinephrine within the lower pathophysiological concentration range on various indicators of blood platelet function and hematocrit. Epinephrine was raised over 60 minutes by a stepwise increasing intravenous infusion in 40 healthy men aged 20 to 40 years. Platelet count increased progressively with increasing arterial epinephrine to a maximal change of 69 +/- 6 x 10(9)/L in EDTA-anticoagulated blood and a maximal change of 42 +/- 6 x 10(9)/L in acid-citrate-dextrose (ACD)-anticoagulated blood, and the weight of circulating platelets increased by 29% (P < .001). Platelet size increased significantly in EDTA and decreased in ACD, and the difference between EDTA and ACD was significant (P < .0001) for both count and size, suggesting that epinephrine not only recruits platelets into the circulation but also induces some microaggregation in vivo or adhesion ex vivo. Aggregation of platelets in vitro induced by epinephrine decreased (P < .003 for delta optical density and P = .038 for maximal optical density) after epinephrine infusion compared with saline but did not change when stimulated with ADP or collagen. These findings suggest a selective downregulation of the epinephrine-activating mechanisms concomitant with a rise in the platelet content of epinephrine by 81% (P < .001) and no change in the platelet sodium-proton membrane exchange. The release of granular content (beta-thromboglobulin and platelet factor 4) to the circulation in response to epinephrine was not significant. Thus, under acute conditions it seems that the platelets may protect themselves against inappropriate overstimulation by epinephrine. The importance of platelet epinephrine uptake is still unknown, but sodium-proton exchange does not seem to be involved in regulating the effects of circulating epinephrine on platelet function. Epinephrine has a pronounced effect on raising hematocrit (maximal change of 1.74 +/- 0.13 x 10(-2), P < .0001).

Effect of Circulating Epinephrine on Platelet Function and Hematocrit

Exposure of phobic subjects to real-life psychological stress may induce a high level of anxiety and be better than laboratory experiments for studies of physiological responses to psychological stress in human research. Therefore, by introducing natural psychological stress, i.e. actual flying in subjects with flight phobia (n=23), the present study aimed at testing the hypothesis that there is, during mental stress, a direct relationship between the level of anxiety and the responses in the physiological variables blood pressure, heart rate and plasma catecholamines. Plasma adrenaline, heart rate, blood pressure and perceived anxiety measured by three different scales increased highly significantly during flight whereas plasma noradrenaline did not change. No direct relationship was found between the physiological and psychological variables. Thus, the physiological responses to natural psychological stress in terms of phobic anxiety may be definite, but the way the responses are related is less clear.

Correlations between psychological and physiological responses to acute flight phobia stress.

The present study is aimed at studying the effects of selective beta-adrenoceptor blockade on anxiety in subjects with flight phobia. Using an incomplete block design subjects received a beta-1 (atenolol 2 x 50 mg), a beta-2 (ICI 118 551 3 x 50 mg) selective blocking drug, or placebo on three occasions over a 16 h period under double-blind conditions prior to a 1/2 h flight. The same procedure was repeated 4 weeks later. Thirty-four subjects completed this double-blind, two-period crossover study. Self-reporting by the Alderley Park State Anxiety Questionnaire, Global Flight Anxiety and Treatment Preference showed a moderate but significant effect of atenolol in alleviating especially somatic symptoms of flight anxiety in addition to an overall effect in the treatment of this entity (p<0.01). ICI 118 551 was ineffective in alleviating any of the important symptoms of flight phobia. These results may imply that the effect of beta-adrenoceptor blockade in reducing phobic anxiety may be more a result of beta-1 than of beta-2 blockade. Beta-1 adrenoceptor blockade may be an alternative treatment of flight phobia, particularly when the symptoms are of somatic character and when intellectual performance is expected shortly after the flight.

D.T. Greenwood

Papers

Correlations between psychological and physiological responses to acute flight phobia stress.

Effects of selective beta-adrenoceptor blockade on anxiety associated with flight phobia: