Arterial occlusion vasculature

The second model is usually known as the hydrone-phrotic rat kidney model, and was developed for in vivo visualization of the microcirculation [275] and involves 60 min renal artery occlusion combined with 3 weeks of ligation of the ureter. Atrophy of tubular structures leaves the cortical vasculature relatively intact and visualizable using planar microscopy in an illuminated observation chamber with nerve and blood supply left intact. Absolute and relative changes in lumen diameter of the major resistance vessels-inter-lobular arteries, afferent and efferent arterioles can be monitored in reponse to vasoactive stimuli. This model was adapted for in vitro perfusion by Loutzenhiser et al [276], removing systemic neurohumoral influences. 

Atherosclerosis (athero = fatty and sclerosis = scarring or hardening) of the coronary and peripheral vasculature is the leading cause of morbidity and mortality worldwide. Lesions (called plaque) are initiated by an injury to endothelium and thicken the intima of arteries, occlude the lumen, and compromise delivery of nutrients and oxygen to tissue (ischemia). Atherosclerotic lesions primarily occur in large and medium-sized elastic and muscular arteries and progress over decades of life. These lesions cause ischemia, which can result in infarction of the heart (myocardial infarction) or brain (stroke), as well as abnormalities of extremities. The proximate cause of occlusion in these pathological conditions is thrombus formation. 

Such a cerebral thrombosis is believed to occur as a result of atherosclerotic damage in the arterial wall. Narrowing of the arterial lumen slows the blood flow. The projection of rough-surfaced deposits into what is by then a trickle of blood may serve as a nucleus around which the thrombus will form, thereby completing the occlusion. A variation is the wandering of a blood clot, or embolus, through the vasculature until finally it becomes wedged in a cerebral artery. This is a cerebral embolism. 

In Apo E null mice increased Hey by a diet enriched with methionine but depleted in folate, Bg, and B12 increased atherosclerotic lesion area and complexity and enhanced expression of receptor for advanced glycation endproducts (AGE), VCAM-1, TF, and MMP-9 in the vasculature. These effects were suppressed in parallel with decreased plasma Hey levels upon dietary supplementation with folate, Bg, and B12 (7- 5). Also, methionine load increased vWF in patients with arterial or venous occlusive disease with or without hyperhomocysteinemia, suggesting endothelial dysfunction (146). 

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