This study examined the cardiovascular mechanisms governing differential blood pressure changes during the emotions of joy, sadness, fear, and anger. Heart rate, blood pressure, stroke volume, peripheral vascular resistance, cardiac output, and indices of myocardial contractility were measured during fear, anger, joy, sadness, physical action, and neutral imagery conditions in 27 right-handed male volunteers screened for imagery ability, alexithymia, anxiety, and depression. Anger imagery, rather than fear, was accompanied by the largest effects on the cardiovascular system. Increased diastolic blood pressure in anger was associated with maintained levels of peripheral vascular resistance and increased cardiac output and heart rate compared with changes during neutral imagery. Sadness produced a distinct pattern with moderate increases in blood pressure and vascular resistance and a decrease in cardiac output compared with changes during neutral imagery. Fear, action, and joy produced similar blood pressure changes in which systolic pressure increased and diastolic pressure was relatively unchanged. The measurement of cardiac output and determination of vascular resistance changes during emotional imagery demonstrate that previously observed emotion-specific blood pressure responses are produced by underlying patterns of cardiovascular activation, which differ between the major categories of emotions.

Our research program has investigated neurocognitive deficits in sober alcoholics for several decades. We have shown that both male and female adult alcoholics--compared with peer nonalcoholic controls--have deficits on tests of learning, memory, abstracting, problem-solving, perceptual analysis and synthesis, speed of information processing, and efficiency. The deficits are equivalent to those found in patients with known brain dysfunction of a mild to moderate nature. Attempts to identify factors other than alcoholism to account for these differences have been unsuccessful. The deficits appear to remit slowly over 4 to 5 years. Relapse of recovering alcoholics is predicted by behavioral (e.g., depressive symptoms and neurocognitive performance) and biological measures (e.g., event-related potentials) obtained at the end of treatment. Results of recent studies support the hypothesis of a continuum of neurocognitive deficits ranging from the severe deficits found in Korsakoff patients to moderate deficits found in alcoholics and moderate to mild deficits in heavy social drinkers (more than 21 drinks/week). Individual differences in the presence and magnitude of neurocognitive deficits in social drinkers and alcoholics are hypothesized to be due, in part, to individual differences in vulnerability of the brain to alcohol or its metabolites' toxic effects.

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Previous research has demonstrated neuropsychological deficits in moderately to severely hypoxemic chronic obstructive pulmonary disease (COPD) patients. The present article reports on the neuropsychological functioning of mildly hypoxemic COPD patients. One hundred patients and 25 controls matched on relevant variables were given extensive neuropsychological tests. Mild neuropsychological impairment was observed in the COPD patients with overall indexes of neuropsychological dysfunction correlating with resting partial pressure of oxygen. Depression and motivation to perform could not account for the results. Long-term reduced oxygen supply to the brain may account for these observed deficits.Patients with chronic obstructive pulmonary disease (COPD) and hypoxemia have been reported to show neuropsychological impairment (Grant, Heaton, McSweeney, Adams, & Timms, 1980;Krop, Block, & Cohen, 1973). They also have complaints of depression and associated worries about bodily functioning (Cummings, Godfrey, & Burrows, 1969; DeCensio, Leshner, & Leshner, 1968). Presumably, chronic reduction of the partial pressure of oxygen (PaO 2 ) significantly contributes to these psychiatric com-