Nitric Oxide: An Endogenous Inhibitor of Balloon Catheter-Induced Intimal Hyperplasia
Autor: | I-L. Chen, Dennis B. McNamara, Donald L. Akers, Thomas A. Osgood, Harmeet Aurora, Brenda Bedi, Philip J. Kadowitz, Raphael Santiago |
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Rok vydání: | 1995 |
Předmět: |
medicine.medical_specialty
Vascular smooth muscle Intimal hyperplasia Endothelium business.industry Balloon catheter Prostacyclin Vasodilation Balloon medicine.disease Nitric oxide chemistry.chemical_compound Endocrinology medicine.anatomical_structure chemistry Internal medicine cardiovascular system medicine business medicine.drug |
Zdroj: | Biochemical, Pharmacological, and Clinical Aspects of Nitric Oxide ISBN: 9781461357773 |
DOI: | 10.1007/978-1-4615-1903-4_21 |
Popis: | Regrowth of a neoendothelial vascular lining and intimal hyperplasia (IH) occur subsequent to balloon catheter injury to the vascular wall (Eldor et al., 1981; Barone et al., 1989; Weidinger et al., 1990; Saroyan et al., 1992). Prostacyclin (prostaglandin I2, PGI2) and nitric oxide (NO) are formed by the endothelium and have been reported to inhibit vascular smooth muscle proliferation (Garg and Hassid, 1989). However, the in vivo relationship between IH and PGI2 or endothelium-derived relaxing factor (EDRF) [which is thought to be NO] formation by the neoendothelium has yet to be firmly established. Earlier studies have demonstrated that balloon catheter-induced injury to the vascular wall is associated with a decrease (Eldor et al., 1981), an increase (Mehta et al., 1982), or no change in PGI2 formation (Hoover et al., 1989). Additionally, balloon catheter-induced injury has been reported to produce an initial decrease in EDRF generation with a return to control by 4 weeks, although the recovery of endothelium-dependent relaxation appears to depend on the severity of the initial injury (Weidinger et al., 1990). Others have shown a persistent defect in the response to various endothelium-dependent vasodilators (Shimokawa et al., 1987). Thus, although there is evidence that balloon injury and subsequent IH can alter both PGI2 and EDRF generation, there is little information on the effect of balloon catheter-induced vascular injury on the generation of PGI2 and EDRF in animals that received the same degree of injury. Therefore, the present study was undertaken to investigate the time course of recovery of vascular generation of PGI2 and EDRF following catheter-induced injury. We also tested the hypothesis that administration of LARG, the precursor of NO, inhibits balloon catheter-induced IH. |
Databáze: | OpenAIRE |
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