Sadness and broken hearts: neurohumoral mechanisms and co-morbidity of ischemic heart disease and psychological depression

• Autorzy: Johnson A.K. , Grippo A.J.
• Języki publikacji: EN

Abstrakty

EN

Heart disease and depression are highly co-morbid. Clinical and experimental research over the past 70 years has led to several neurohumoral hypotheses of causative factors present under the conditions of either heart failure or of psychological depression. Some of these hypothesized factors are common to both disorders and are therefore attractive candidates to account for the high incidence of co-occurrence of depression and heart disease. One experimental approach to study the co-morbidity of heart failure and depression has been to study the behavioral, biochemical and physiological changes in a chronic mild stress model of depression and in heart failure induced by experimental myocardial infarction. Our studies have led us to focus on the pro-inflammatory cytokines, in particular tumor necrosis factor (TNF)-alpha, and the renin-angiotensin-aldosterone system. Both of these families of humoral factors are elevated in human heart failure and in depression and the two experimental models we have studied. The demonstrated validity of each of these models will be of great value in elucidating the nature of the actions and interactions of these humoral agents as they contribute to the co-morbid conditions of heart failure and depression.

Słowa kluczowe

EN

sadness; broken heart; neurohumoral mechanism; ischaemic heart disease; heart disease; psychological depression; depression; renin-angiotensin-aldosterone; proinflammatory cytokine; myocardial infarction; heart failure; tumour necrosis factor-alpha; hypothalamic-pituitary-adrenal axis; brain amine system

• Wydawca: -
• Czasopismo: Journal of Physiology and Pharmacology. Supplement
• Rocznik: 2006
• Tom: 57
• Numer: 11
• Opis fizyczny: p.5-29,fig.,ref.

Twórcy

autor

Johnson A.K.

• University of Iowa, Iowa City, IA 52242-1407, USA

autor

Grippo A.J.