Search PubMed⌕ Search

Biomedical subjects

S M Monroe

Publications and source records attributed to S M Monroe.

At least 55 records · Page 3Linked to original sources
PubMed1993

Cognition and life stress in depression: cognitive factors and the definition, rating, and generation of negative life events.

The relationship between cognitive factors and different conceptualizations and measures of life stress poses important questions for contemporary theories of depression. We examined whether cognitive factors (dysfunctional attitudes and attributional style) are related to the definition, rating, and generation of negative life events. Life events were assessed with both subjective self-report and more objective interview-based methods in endogenously depressed outpatients. The results partially support the hypothesis that cognitive factors are related to definition and severity ratings of self-report measures of particular types of life events. These relationships held primarily for achievement, as compared with interpersonal, events. The results also support the hypothesis that elevated scores on measures of cognition are associated with the number of objectively defined events occurring prior to the onset of depression, suggesting that some patients may generate the life events that in turn may initiate a depressive episode.

Adult↗
PubMed1992

Social factors and the psychobiology of depression: relations between life stress and rapid eye movement sleep latency.

We examined psychosocial factors (i.e., life stress) and biological factors (i.e., REM sleep latency) that are hypothesized to be of complementary importance for defining depressive subtypes in a sample of 61 nonpsychotic, endogenous major depressives. Subjects were evaluated on several diagnostic scales for life stress, on electroencephalographic sleep data, and on 2 symptom measures for depression. As predicted, persons with severe stress that occurred shortly before depression onset had essentially normal REM latency values; patients without such stress had reduced REM latency values. Both stress and REM latency were also associated with greater severity of self-reported depressive symptoms. Alternative explanations of these findings are discussed, with particular emphasis on different roles of pre-onset and post-onset stressors.

Adaptation, Psychological↗
PubMed1992

Life stress and treatment course of recurrent depression: 1. Response during index episode.

Research on treatment course and outcome in depression is mixed with respect to the implications of life stress. Several concerns are addressed in a prospective study of 91 individuals treated for recurrent depression. Specific forms of stress occurring before treatment entry predicted a poor clinical response both after 16 weeks and after a more extended intervention period. Specific forms of stress occurring during the 1st 6 weeks of treatment also predicted poor response after 16 weeks and after the extended intervention period. Severe stress occurring early in treatment predicted a longer time to attain relief for treatment responders. Concepts underlying the idea that stress-related disorders have a better clinical outcome are discussed, and it is proposed that life stress has different implications for individuals with and without recurrent depression.

Adjustment Disorders↗
PubMed1992

Vulnerable self-esteem and depressive symptoms: prospective findings comparing three alternative conceptualizations.

Across diverse theoretical orientations, vulnerable self-esteem (SE) is thought to act as a diathesis for depression after life stress. In the present study, the roles of trait-level SE, low SE primed by depressed mood, and labile SE in prospectively predicting changes in depressive symptoms in a nonclinical sample (n = 192) were examined. Results indicated that labile SE predicted increases in symptoms. Furthermore, a 3-way interaction (Labile SE x Academic Stress x Initial Depression) suggested that in Ss who were initially asymptomatic, lability made Ss differentially vulnerable to increases in depressive symptoms after stress. In contrast to labile SE, trait-level SE and priming of low SE were relatively weak predictors of changes in depressive symptoms and did not interact with stress.

Achievement↗
PubMed1991

Onset of depression and time to treatment entry: roles of life stress.

Patients with depression vary greatly in the time between onset of disorder and entry into treatment. Few data exist on the dimensions of this time interval and the forces that influence it. The present article outlines considerations for research on this topic and presents findings for outpatient depressives (N = 61) on life stress and the time lag between onset and treatment entry. Results indicate that life stress occurring before the onset of depression is highly predictive of time to treatment entry. In marked contrast, stress occurring after onset is not associated with this time interval. Further analyses suggest different mechanisms of association between different stress variables and time to treatment entry. The clinical implications for alleviating suffering from a depressive episode and for decreasing the likelihood that depression will lead to disruption in other spheres of the person's life are discussed. Overall, the results add to the emerging literature on life stress and depression, enlarging the scope to include forces operative in seeking formal treatment.

Adult↗
PubMed1991

Diathesis-stress theories in the context of life stress research: implications for the depressive disorders.

Advances in the conceptualization and measurement of life stress in the past 2 decades raise several questions concerning traditional diathesis-stress theories of psychopathology. First, comprehensive measures of life stress force investigators to become more precise about the particular stressful circumstances hypothesized to interact with diatheses. Second, the influence of the diathesis on a person's life is typically ignored, which results in several types of possible bias in the assessment of life stress. Finally, information is available on diatheses and stress for specific disorders to provide a foundation for more empirically based hypotheses about diathesis-stress interactions. This possibility is outlined for depression. Such an approach provides the basis for developing broader, yet more specific, frameworks for investigating diathesis-stress theories of psychopathology in general and of depression in particular.

Depressive Disorder↗
PubMed1991

Comparison of halothane, enflurane, and isoflurane with nitrous oxide on contractility and oxygen supply and demand in isolated hearts.

The authors' aim was to examine direct cardiac responses to isoflurane, enflurane and halothane, as altered during mild hypoxia by the substitution of nitrogen (N2) for oxygen (O2), and additionally by the substitution of nitrous oxide (N2O) for N2. Heart rate, atrioventricular conduction time, left ventricular pressure (LVP), peak positive and negative derivatives of LVP (dLVP/dtmax), coronary flow, O2 delivery (DO2), percent O2 extraction, and myocardial O2 consumption (MVo2) were examined in 47 isolated guinea pig hearts. Changes in the ratio of DO2 to MVO2 indicated the relationship of autoregulation of coronary flow to myocardial O2 utilization. Each heart was first exposed to 96% O2 and then randomly exposed to 48% N2 and 48% N2O alone and with three equivalent concentrations of one of three volatile anesthetics: isoflurane (n = 15), halothane (n = 16), or enflurane (n = 16). Results were as follows: 1) N2 alone significantly decreased LVP, +dLVP/dtmax and -dLVP/dtmax, DO2 and MVO2; increased coronary flow; and produced no change in heart rate, atrioventricular conduction time, percent O2 extraction, or the DO2/MVO2 ratio. 2) Compared to N2, N2O alone only produced additional significant decreases in LVP and +dLVP/dtmax. 3) In the presence of N2 or N2O, each volatile anesthetic caused significant stepwise decreases in heart rate, LVP, +dLVP/dtmax and -dLVP/dtmax, MVO2, and percent O2 extraction; no additional change in coronary flow or DO2; and a stepwise increase in the DO2/MVO2 ratio. The effects of halothane and enflurane were generally greater than those of isoflurane. 4) Each volatile anesthetic caused an additive, parallel depression of LVP and percent O2 extraction as a function of MAC with N2O compared to N2. This study demonstrates that the direct negative inotropic effects of halothane and enflurane are more pronounced than those of isoflurane and are accompanied by a greater reduction in O2 utilization by halothane and enflurane than by isoflurane in the presence of mild hypoxia alone or with the addition of N2O. The study also demonstrates that N2O accentuates the negative inotropic effects of volatile anesthetics during reduced O2.

Animals↗
PubMed1990

Effects of nitrous oxide on contractile function and metabolism of the isolated heart.

Nitrous oxide has a long clinical history, but its effects on the heart remain controversial. The direct effects of N2O on global myocardial function have not been reported. The authors' aim was to examine the inotropic, chronotropic, dromotropic, and vascular effects of N2O, compared with its N2 control, on hearts isolated from the guinea pig. Hearts (N = 31) were isolated and perfused at 37 degrees C with Krebs-Ringer solution at constant pressure. Isovolumetric left ventricular pressure (LVP) and its derivative (maximum rate of tension development [dP/dtmax]) were measured by placing a saline-filled, latex balloon into the left ventricle. Bipolar electrodes were placed in the right atrium and right ventricle for measurement of heart rate (HR) and atrioventricular conduction time (AVCT). The venae cavae were ligated, and the right ventricle was cannulated through the pulmonic valve to collect coronary sinus effluent for measurement of coronary outflow O2 tension, adenosine, and inosine. After stabilization and perfusion with 96% O2 (plus 4% CO2), each heart was exposed for 10 min either to 48% N2O or to 48% N2 with 48% O2. After repeated perfusion with 96% O2 for 10 min, hearts were exposed in the reverse order to 48% N2O or 48% N2. In the postcontrol period, hearts were again exposed to 96% O2. Inflow Po2 (in mmHg) was 506 +/- 5 (standard error of the mean [SEM]) during 96% O2 and 258 +/- 5 during both 48% N2 and 48% N2O. Effluent Po2 was 155 +/- 7 during 96% O2, 81 +/- 5 during 48% N2, and 83 +/- 5 during 48% N2O.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗