Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In atherosclerotic rabbits (SCLER), decreases in vascular resistance in response to acetylcholine (ACH), an endothelium-dependent agent, are suppressed, whereas those to nitroprusside (NP), an endothelium-independent vasodilator, are preserved. To determine whether defective vasodilation in SCLER is related to altered reactivity of resistance vessels, we visualized arterioles of rabbit cremaster muscle by videomicroscopy. Arteriolar diameter was monitored during topical (superfusional) delivery of ACh and NO, interventions that did not affect systemic hemodynamics. Diameter changes in response to NP (0.01-100.0 microM) did not differ between SCLER and controls; maximal dilations amounted to 110 +/- 10% (mean +/- SE). In contrast, responses to ACH (0.001-100 microM) differed; maximal dilations averaged 54 +/- 4% in SCLER and 124 +/- 9% in controls (P less than 0.001). These differences persisted after blockade with phentolamine, propranolol, and indomethacin. Phenidone and hydroquinone blockers of endothelium-dependent vasodilation, inhibited arteriolar dilation to ACH without affecting that to NP. Microvascular responses to intra-arterial drug were similar to those elicited by topical drug. Thus, hypercholesterolemia and atherosclerosis in the rabbit appear to produce a microvascular defect characterized by an impaired endothelium-dependent dilation and a preserved endothelium-independent dilation. This defect could play a role in limiting vasodilator reserve in atherosclerosis.
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PMID:Videomicroscopic demonstration of defective cholinergic arteriolar vasodilation in atherosclerotic rabbit. 338 50

Our aim was to assess the potential role of lipoxygenase (LO) products in neointimal formation following vascular injury. We investigated the effect of LO pathway inhibition, by phenidone, on the concentration of 12- and 5-hydroxyeicosatetraenoic acid (12- and 5-HETE) in rat whole blood and in aortic tissue. We also examined the effect of phenidone on myoneointimal formation in balloon-injured rat carotid arteries. Phenidone significantly decreases the concentration of HETEs in aortic tissue, and decreases neointimal size even though there is no difference in the BrdU index. These data indicate that the LO product participates in developing neointima following balloon-induced vascular injury, and that the LO blocker phenidone decreases neointimal size possibly by suppressing migration of smooth muscle cells.
Atherosclerosis 1999 Nov 01
PMID:Lipoxygenase inhibition decreases neointimal formation following vascular injury. 1052 27