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 Physiology and Pathophysiology of Blood Vessels

1. Physiology

  • Circumferential, longitudinal and radial deformation and stresses of blood vessels.
  • Properties of collagen, elastin and glycosaminoglycan ground substance.
  • The length-active stress curve of the vascular muscle.
  • Changes induced by aging.

2. Pathophysiology

  • Aneurysms
  • Histological changes
  • Causes of aneurysms (including the role of proteases, inflammation, autoimmunity and atherosclerosis)
  • Mechanisms preventing instantaneous enlargement of aneurysms.

3. Poststenotic dilatation

  • Histological changes.
  • Mechanisms for poststenotic dilatation.

4. Autogenous vein grafts

  • Histological changes.
  • Mechanisms for the beneficial effects of vein grafts.
  • Distribution and causes of intimal hyperplasia in end-to-side vascular anastomoses.

5. Arteries of hypertensive subjects

  • Histological changes.
  • Behavior and control of the precapillary resistance vessels.
  • Atherosclerotic arteries.
  • Histological and mechanical changes.
  • Distribution of vasa vasorum.

References

1. Dobrin PB, Baker WH, Gley WC. Elastolytic and collagenolytic studies of arteries. Implications for the mechanical properties of aneurysms. Arch Surg 1984;119:405-409.

Results of elastolytic and collagenolytic studies on canine and human arteries are presented. Treatment with elastase caused the vessels to dilate but to remain intact, while all vessels treated with collagenase ruptures. The authors conclude that wall integrity depends on intact collagen rather than elastin.

2. Dobrin PB. Poststenotic dilatation. Surg Gynecol Obstet 1991;172:503-508.

This paper presents the pathogenetic mechanisms of poststenotic dilatation. According to experimental studies, shear stress and turbulence are the most likely causes. Whatever the flow disturbance, it must may the wall vibrate to produce poststenotic dilatation. Vibrations are thought to produce alterations in wall elastic and possibly in vascular smooth muscle tone.

3. Dobrin PB, Littooy FN, Endean ED. Mechanical factors predisposing to intimal hyperplasia and medial thickening in autogenous vein grafts. Surgery 1989;105:393-400.

This paper presents experimental data showing that intimal hyperplasia is best associated with low flow velocity, a factor correlated with low blood-artery shear stress. By contrast, medial thickening is best associated with increased deformation of the vein wall in the circumferential direction (increased diameter). These findings correlate with clinical responses of vein grafts.

4. Zarins CK, Weisenberg E, Kolettis G, Stankunavicius R, Glagov S. Differential enlargement of artery segments in response to enlarging atherosclerotic plaques. J Vasc Surg 1988;7:386-394.

This is a study of the response of artery segments to enlarging atherosclerotic plaques. It shows that coronary arteries enlarge in response to increasing atherosclerotic plaque and that such enlargement can prevent narrowing of the lumen. However, differential segments of the same artery may respond differently. Local differences in the relative rates of plaque growth and artery enlargement may determine progression to stenosis, preservation of normal lumen area, or enlargement.

5. Dobrin PB. Mechanical factors associated with the development of intimal and medial thickening in vein grafts subjected to arterial pressure. A model of arteries exposed to hypertension. Hypertension 1995;26:38-43.

Exposure of vein grafts to arterial pressure increases the following nine mechanical factors: deformation in the circumferential, longitudinal, and radial directions; stresses in each of these three directions; pulsatile deformations and pulsatile stresses; and flow velocity. The experiments presented in this article demonstrate that intimal thickening is best correlated with low flow velocity, a correlate of low shear stress, whereas medial thickening is best correlated with deformation in the circumferential direction.

Posted June 2010