Abstract 3741: Stress Promotes Arterial Thrombosis through Activation of the Sympathetic Nervous System

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Simon F Stampfli ◽  
Giovanni G Camici ◽  
Irene Garcia ◽  
Thomas F Luscher ◽  
Felix C Tanner
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Tissue Factor ◽  
Arterial Thrombosis ◽  
Cardiovascular Events ◽  
Bleeding Time ◽  
Thrombus Formation ◽  
Factor Activity ◽  
Tissue Factor Activity ◽  
Sympathetic Nervous

Background: Several lines of evidence demonstrate a correlation between stress and cardiovascular mortality and morbidity. Myocardial infarction can be triggered by life threatening events such as earthquakes or missile attacks, and even every day stressful situations such as anger were shown to correlate with adverse cardiovascular events, primarily caused by arterial thrombus formation. The sympathetic nervous system is known to mediate various stress-related effects; however, a mechanism linking stress and thrombosis has not been described. Methods: To investigate the influence of acute stress on arterial thrombosis, mice were subjected to a restraint stress protocol for 20 hours. Subsequently, arterial thrombosis was induced by photochemical injury in vivo . Furthermore, coagulation times (PT, aPTT) and tissue factor activity were assayed in plasma and carotid artery, respectively. In addition, tail bleeding time was assessed. To investigate the role of the sympathetic nervous system, chemical sympathectomy was performed by treating mice with 6-Hydroxydopamine (OHDA) or control vehicle, respectively. Results: Time to thrombotic occlusion was significantly decreased in stressed mice as compared to controls (−26.7 ± 4.0 minutes, p<0.001, n=5). In sympathectomized mice stress failed to decrease time to occlusion (−8.1 ± 5.6 minutes, n.s., n=5); Sympathectomy alone had no effect on time to occlusion as compared to vehicle treatment. Tissue factor activity, tail bleeding time, and coagulation times remained unchanged under all conditions, indicating an unaltered state of vessel wall tissue factor, systemic coagulation and platelet function, respectively. Conclusions: Stress enhances arterial thrombosis via the sympathetic nervous system. The link between increased sympathetic activity and thrombus formation is still under investigation. These findings may open novel perspectives for the understanding of stress-induced cardiovascular events.

The MAP kinase JNK2 mediates cigarette smoke-induced arterial thrombosis

2017 ◽  
Vol 117 (01) ◽  
pp. 83-89 ◽  
Author(s):  
Simon F. Stämpfli ◽  
Martin F. Reiner ◽  
Yi Shi ◽  
Stephan Keller ◽  
Alexander Akhmedov ◽  
...  
Keyword(s):  
Map Kinase ◽  
Tissue Factor ◽  
Cigarette Smoke ◽  
Arterial Thrombosis ◽  
Molecular Mechanisms ◽  
Public Awareness ◽  
Smoking Ban ◽  
Factor Activity ◽  
Wild Type ◽  
Tissue Factor Activity

SummaryDespite public awareness of its deleterious effects, smoking remains a major cause of death. Indeed, it is a risk factor for atherothrombotic complications and in line with this, the introduction of smoking ban in public areas reduced smoking-associated cardiovascular complications. Nonetheless, smoking remains a major concern, and molecular mechanisms by which it causes cardiovascular disease are not known. Peripheral blood monocytes from healthy smokers displayed increased JNK2 and tissue factor (TF) gene expression compared to non-smokers (n=15, p<0.05). Similarly, human aortic endothelial cells exposed to cigarette smoke total particulate matter (CS-TPM) revealed increased TF expression mediated by JNK2 (n=4; p<0.05). Wild-type and JNK2−/− mice were exposed to cigarette smoke for two weeks after which arterial thrombosis was investigated. Wild-type mice exposed to smoke displayed reduced time to thrombotic arterial occlusion (n=8; p<0.05) and increased tissue factor activity (n=7; p<0.05) as compared to wild-type controls (n=6), while JNK2−/− mice exposed to smoke maintained an unaltered thrombotic potential (n=8; p=NS) and tissue factor activity (n=8) comparable to that of JNK2−/− and wild-type controls (n=6; p=NS). Smoking caused an increased production of reactive oxygen species (ROS) in wild-type but not in JNK2−/− mice (n=7; p<0.05 for wild-type mice and n=5–6; p=NS for JNK2−/− mice). In conclusion, the MAP kinase JNK2 mediates cigarette smoke-induced TF activation, arterial thrombosis and ROS production. These results underscore a major role of JNK2 in smoke-mediated thrombus formation and may offer an attractive target to prevent smoke-related thrombosis in those subjects which do not manage quitting.

Thyroid hormone-catecholamine interrelationships during exposure to cold

1981 ◽  
Vol 97 (1) ◽  
pp. 91-97 ◽  
Author(s):  
H. Storm ◽  
C. van Hardeveld ◽  
A. A. H. Kassenaar
Keyword(s):  
Nervous System ◽  
Plasma Concentration ◽  
Thyroid Hormone ◽  
Sympathetic Nervous System ◽  
Plasma Levels ◽  
Surgical Procedure ◽  
Exposure To Cold ◽  
Basal Plasma ◽  
Sympathetic Nervous

Abstract. Basal plasma levels for adrenalin (A), noradrenalin (NA), l-triiodothyronine (T3), and l-thyroxine (T4) were determined in rats with a chronically inserted catheter. The experiments described in this report were started 3 days after the surgical procedure when T3 and T4 levels had returned to normal. Basal levels for the catecholamines were reached already 4 h after the operation. The T3/T4 ratio in plasma was significantly increased after 3, 7, and 14 days in rats kept at 4°C and the same holds for the iodide in the 24-h urine after 7 and 14 days at 4°C. The venous NA plasma concentration was increased 6- to 12-fold during the same period of exposure to cold, whereas the A concentration remained at the basal level. During infusion of NA at 23°C the T3/T4 ratio in plasma was significantly increased after 7 days compared to pair-fed controls, and the same holds for the iodide excretion in the 24-h urine. This paper presents further evidence for a role of the sympathetic nervous system on T4 metabolism in rats at resting conditions.

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