Neural Factors Contribute to Atherogenesis

Gutstein, William H.; Harrison, John; Parl, Fritz F.; Ku, George; Avtable, Matt

doi:10.1126/science.619468

Cited by 33 publications

(10 citation statements)

References 12 publications

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“…Evidence suggesting an important role of neuropsychologic aberrations in the development and, perhaps more importantly, in the clinical expression of human atherosclerosis has been reviewed. 133 ' 134 In an animal model, Gustein et al 135 have shown the development of coronary lesions, morphologically resembling human atheroma, by a sustained electric stimulation of the lateral hypothalamus in the absence of changes in lipids or blood pressure. Based on such observations, some investigators expressed skepticism over the role of other risk factors.…”

Section: Stress and Personalitymentioning

confidence: 98%

Pathogenesis of Macrovascular Disease in the Human Diabetic

Ganda

1980

Diabetes

150

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Section: Stress and Personalitymentioning

confidence: 98%

Pathogenesis of Macrovascular Disease in the Human Diabetic

Ganda

1980

Diabetes

150

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“…An interesting model capable of inducing endothelial cell degeneration and cell loss in the aorta and coronary vessels is brief electrical stimulation of the lateral hypo thalamus [21], while continuous stimulation leads to the development of intimal lesions rich in smooth muscle cells and collagen [22], Vasospasm induced by application of an electric cur rent to the vessel wall of the common carotid artery in rabbits has been shown to induce atherosclerotic lesions and foci of smooth muscle cell hyperplasia [23]. Similarly, aortic vasoconstriction, induced by noradrenaline admin istered to rabbits, was associated to the appearance of ath erosclerotic lesions in the affected vessels [24], Hanke et al [25] produced an atheromatous lesion in the rabbit carotid artery by electrical stimulation and by maintain ing the integrity of the endothelial lining in the stimulated area.…”

Section: Animal Models Of Atherosclerosismentioning

confidence: 99%

The Adventitia, Endothelium and Atherosclerosis

Loo

Martin²

1997

Int J Microcirc

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Despite many theories, the initiating circumstances for the development of atherosclerosis remain obscure. The development of animal models of atherosclerosis was based upon the different theories of the origins of atherosclerosis which suggested that it originates at the intimal surface of the vessel. A more recent model of atherosclerosis involves perivascular manipulation of the vessel by positioning of a hollow silastic collar around the artery. In this model, several of the features seen in early human atherosclerosis are generated within a period of 7 days. It is hypothesized that arterial wall hypoxia following occlusion of the vasa vasorum may be the initial lesion of atherosclerosis, and hence that in some cases atherosclerosis is a disease of the outer layers of the arterial wall.

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“…It activates the sympathetic nervous system (and the HPA axis) via hypothalamic pathways [247,[497][498][499][500][501]. Consciousness interprets nociception as pain [265,459,497,498,502,503].…”

Section: The Cognitive Pathwaymentioning

confidence: 99%

A Stress Repair Mechanism That Maintains Vertebrate Structure During Stress

Coleman

2010

CHDDT

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Based on Capillary Gate Theory and Tissue Repair Theory, this paper describes the "Stress Repair Mechanism" (SRM) that maintains and repairs vertebrate tissues. It accounts for most of the mysterious manifestations of allostasis that remain unexplained by Hypothalamic-Pituitary-Axis (HPA) hormones and thereby enables the Universal Theory of Medicine predicted by Hans Selye. SRM activity explains hemodynamic physiology, capillary hemostasis, infarction, Korotkoff sounds, blood pressure, hypertension, diabetes, allostasis, allostatic load, anesthesia, analgesia, atherosclerosis, apoptosis, malignancy, eclampsia, sepsis, Multi-System Organ Failure (MSOF), the surgical stress syndrome, the fight or flight response, and numerous other manifestations of physiology and pathology. SRM function comprises the autonomic nervous system, the vascular endothelium, and the dynamic enzymatic interaction of blood-borne hepatic Factors VII, VIIIC, IX and X that produces thrombin, soluble fibrin and insoluble fibrin, whose combined effects account for all SRM manifestations. The vascular endothelium is a diaphanous neuroendocrine organ that lines all blood vessels and is the sole constituent of capillary walls. It secretes tissue factor into extravascular tissues, and insulates those tissues from the hepatic enzymes, so that tissue disruption exposes tissue factor to the enzymatic interaction and activates tissue repair. The vascular endothelium also releases nitric oxide and von Willebrand Factor into blood in accord with autonomic balance to regulate the enzymatic interaction to govern tissue perfusion and organ function. Therefore, continuously fluctuating combinations of nervous stimuli that affect autonomic balance and forces that disrupt tissues determine SRM activity.

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Neural Factors Contribute to Atherogenesis

Cited by 33 publications

References 12 publications

Pathogenesis of Macrovascular Disease in the Human Diabetic

Pathogenesis of Macrovascular Disease in the Human Diabetic

The Adventitia, Endothelium and Atherosclerosis

A Stress Repair Mechanism That Maintains Vertebrate Structure During Stress

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