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At least 145 records · Page 8Linked to original sources
PubMed1996

[Ultrasound diagnosis, follow-up and therapy of cystic degeneration of the adventitia. 2 case reports and review of the literature].

Two Case Reports and Literature Review: Adventitial cystic disease of the popliteal artery is an unusual but important cause of intermittent claudication. Two cases of adventitial cystic disease were diagnosed by ultrasound investigation. The changing size of the cysts is correlated with the clinical symptoms of the patient. One patient was treated by resection with interposition of saphenous vein; the other by ultrasound guided needle aspiration of the fluid.

Arteritis↗
PubMed1997

The adventitia, endothelium and atherosclerosis.

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.

Animals↗
PubMed2002

[Cystic degeneration of the adventitia of the popliteal artery--case report].

Cystic adventitial disease (CAD) is a rare diagnosis with a higher number of the patients in recent years. The article gives a brief of the pathology and etiolopathogenesis of adventitial cystic disease and two case reports of the patients with CAD of the popliteal artery treated in our department between 1997 and 2001. Successful results are achieved only with surgical treatment.

Humans↗
PubMedDate not supplied

[A patient with cystic adventitia degeneration and entrapment syndrome of the popliteal artery].

Adventitial cystic disease and entrapment syndromes of the popliteal artery are rare causes of ischemia in the lower leg in younger patients without cardiovascular risk factors. The 38-year-old male patient described in this case report showed both types of these rare abnormalities in the same vessel, both usually requiring surgical revision even in causing only few symptoms.

Adult↗
PubMed1986

[Entrapment and cystic degeneration of the adventitia as a cause of occlusion of the popliteal artery].

The entrapment syndrome and the cystic adventitial degeneration of the popliteal artery are diseases affecting relative young patients. Four cases of entrapment and one case of cystic degeneration are demonstrated. In one patient also an entrapment of the popliteal vein is demonstrated. In all patients the outcome of vascular reconstruction was good. For the entrapment syndrome the posterior approach is prefered.

Adult↗
PubMed1985

Effect of prazosin on the efflux of 3H-norepinephrine and metabolites from the intima and adventitia of the rabbit ear artery.

The spontaneous and stimulation-induced (SI) effluxes of 3H-norepinephrine (3H-NE) and its metabolites from the intimal and adventitial surfaces of perfused segments of rabbit ear arteries were determined; vessels were previously incubated with 3H-NE (0.6 microM). The total SI adventitial efflux of 3H was approximately 10-fold greater than the intimal efflux, contained a higher percentage of unchanged 3H-NE (48 vs. 12%) and a lower percentage of O-methylated metabolites (17 vs. 55%); there was little difference between the percentages of deaminated catechols (35 vs. 31%). Prazosin, at a concentration (0.24 microM) which prevented the arteries constricting during stimulation, had little effect on the composition of the SI effluxes; however, it caused 2- to 3-fold increases in the effluxes of 3H-NE and its metabolites into the lumen during the period of stimulation. This effect is attributed to the failure of the vessel wall to thicken during stimulation, thus facilitating diffusion of 3H-NE and its intraneuronally formed metabolites across the media. Prazosin decreased the percentage of unchanged 3H-NE and increased that of the deaminated catechols in the spontaneous efflux; these effects are attributed to a direct effect of prazosin on the intra-neuronal metabolism of 3H-NE.

Animals↗