October 31, 2000CirculationOpen Access

Role of Monocyte Chemoattractant Protein-1 in Cardiovascular Remodeling Induced by Chronic Blockade of Nitric Oxide Synthesis

View Full Paper

Ask AI

Bookmark

Why the study?

Does a specific monoclonal anti-MCP-1 neutralizing antibody prevent cardiovascular remodeling in rats treated with L-NAME?

Population

Rats treated with N-nitro-L-arginine methyl ester to induce chronic blockade of nitric oxide synthesis

Comparison

Specific monoclonal anti-MCP-1 neutralizing… vs Control IgG

Design

Preclinical

Authors

MKMasamichi KoyanagiKyorin University Hospital KEKensuke EgashiraKyushu University SKShiro KitamotoNishikyushu University

Discussion

Member takes

Implication

MCP-1 inhibition selectively attenuates vascular changes in nitric oxide-deficient rats; leaves open broader remodeling mechanisms and clinical translation.

Structured PICO

Does a specific monoclonal anti-MCP-1 neutralizing antibody prevent cardiovascular remodeling in rats treated with L-NAME?

Population

Rats treated with N(omega)-nitro-L-arginine methyl ester (L-NAME) to induce chronic blockade of nitric oxide synthesis

Intervention

Specific monoclonal anti-MCP-1 neutralizing antibody

Comparator

Control IgG

Outcome

Cardiovascular remodeling (early inflammation, monocyte recruitment, coronary vascular medial thickening, and perivascular fibrosis)surrogate

In a rat model of chronic nitric oxide synthesis blockade, MCP-1 mediates early inflammation and coronary medial thickening, but not perivascular fibrosis or systolic pressure overload.

Cite This Study

Koyanagi et al. (2000) studied this question.

synapsesocial.com/papers/6a1a7acee916fa6dd3b8a444 https://doi.org/10.1161/01.cir.102.18.2243

Topics

Coronary artery disease

View Full Paper

Ask AI

Bookmark

Implication

MCP-1 inhibition selectively attenuates vascular changes in nitric oxide-deficient rats; leaves open broader remodeling mechanisms and clinical translation.