Unstable angina, myocardial infarction and sudden death after an exercise stress test

Ciampricotti, Renzo; Gamal, M. I. H. El

doi:10.1016/0167-5273(89)90306-9

Cited by 18 publications

(10 citation statements)

References 25 publications

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“…Aged subjects may have lower tolerance to stress [2][3][4][5] and be more susceptible to thrombotic diseases caused by a variety of stressors than the young. 13,14 We previously showed that the expression of PAI-1 was also induced by restraint stress and that this response was exacerbated by aging. 23 In this study, we demonstrated the induction of TF mRNA in several tissues by restraint stress was substantially higher in aged mice than in young mice (Figures 2-4).…”

Section: Discussionmentioning

confidence: 99%

“…10 In this context, aged animals [2][3][4][5] and/or obese mice 11,12 may have lower tolerance to stress insults. Clinically, older and obese individuals are susceptible to the stress-mediated pathologic changes, including thrombotic complications, 13,14 possibly because of the stress-induced imbalance in the coagulation and fibrinolytic system.…”

Section: Introductionmentioning

confidence: 99%

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Aging and obesity augment the stress-induced expression of tissue factor gene in the mouse

Yamamoto

Shimokawa

et al. 2002

Blood

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Aging and obesity augment the stress-induced expression of tissue factor gene in the mouse

Yamamoto

Shimokawa

et al. 2002

Blood

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“…Because aged subjects may have lower tolerance to stress (10,40,41) and be susceptible to thrombosis caused by a variety of stressors (42,43), we compared the stress-induced PAI-1 expression and tissue microthrombosis between young and aged mice. The induction of PAI-1 expression by stress was shown to be much more dramatic in aged mice in most tissues examined.…”

Section: Discussionmentioning

confidence: 99%

“…The induction of PAI-1 was regulated in a tissue-specific and cell type-specific manner in the restraint model. Because aged subjects may have lower tolerance to stress (10,40,41) and be more susceptible to thrombosis caused by stress (42,43), we also compared the magnitude of stress-induced PAI-1 expression and evaluated tissue thrombosis in young and aged mice in vivo.…”

mentioning

confidence: 99%

Plasminogen activator inhibitor-1 is a major stress-regulated gene: Implications for stress-induced thrombosis in aged individuals

Yamamoto

Takeshita

Shimokawa

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

148

127

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Plasminogen activator inhibitor-1 (PAI-1) is one of the primary inhibitors of the fibrinolytic system and has been implicated in a variety of thrombotic disorders. In this report, stress-induced changes in murine PAI-1 gene expression were investigated to study the role of this inhibitor in the development of stress-induced hypercoagulability. Restraint stress led to a dramatic induction of plasma PAI-1 antigen and of tissue PAI-1 mRNA with maximum induction in adipose tissues. In situ hybridization analysis of the stressed mice revealed that strong signals for PAI-1 mRNA were localized to hepatocytes, renal tubular epithelial cells, adrenomedullar chromaffin cells, neural cells in the paraaortic sympathetic ganglion, vascular smooth muscle cells, and adipocytes, but not to endothelial cells. These observations indicate that the stress induces the PAI-1 gene expression in a tissue-specific and cell type-specific manner. The induction of PAI-1 mRNA by restraint stress was greater than that observed for heat shock protein, a typical stress protein, suggesting that PAI-1 is one of the most highly induced stress proteins. Importantly, the magnitude of induction of PAI-1 mRNA by stress increased markedly with age, and this increase in PAI-1 correlated with tissue thrombosis in the older stressed mice. Moreover, much less tissue thrombosis was induced by restraint stress in young and aged PAI-1-deficient mice compared with agematched wild-type mice. These results suggest that the large induction of PAI-1 by stress increases the risk for thrombosis in the older populations, and that the adipose tissue may be involved.

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“…In humans, it is one of the triggers of unstable angina, myocardial infarction, and sudden death. [22][23][24] The levels of several coagulation or fibrinolytic factors-including von Willebrand factor, factor VIII, factor VII, 13 or plasminogen activator inhibitor-1 (PAI-1) 14 appear to increase in response to mental stress, suggesting the possibility that prothrombic potential may be increased, thus promoting thrombotic complications under stressful conditions. In this study, as an alternative thrombogenic challenge, we exposed ATϩ/ϩ and ATϩ/Ϫ mice to 20 hours of restraint stress.…”

Section: Discussionmentioning

confidence: 99%

Impact of antithrombin deficiency in thrombogenesis: lipopolysaccharide and stress-induced thrombus formation in heterozygous antithrombin-deficient mice

Yanada

Kojima

Ishiguro

et al. 2002

Blood

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Unstable angina, myocardial infarction and sudden death after an exercise stress test

Cited by 18 publications

References 25 publications

Aging and obesity augment the stress-induced expression of tissue factor gene in the mouse

Aging and obesity augment the stress-induced expression of tissue factor gene in the mouse

Plasminogen activator inhibitor-1 is a major stress-regulated gene: Implications for stress-induced thrombosis in aged individuals

Impact of antithrombin deficiency in thrombogenesis: lipopolysaccharide and stress-induced thrombus formation in heterozygous antithrombin-deficient mice

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