What question did this study set out to answer?

To evaluate the impact of short-term exposure to homocysteine on the contractile properties of rat aortic tissue using in vitro and in vivo models.

January 1, 2000Canadian Journal of Physiology and Pharmacology

Short-term exposure to homocysteine depresses rat aortic contractility by an endothelium-dependent mechanism

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Population

Rat aortic tissue (in vitro and in vivo models)

Comparison

Short-term exposure to homocysteine via culture… vs Saline, cysteine, or methionine injection…

Design

Preclinical

Follow-up

1 to 4 days

Authors

SWS. WangMarshall University GWGary L. WrightWestern Illinois University JHJean HarrahSan Francisco General Hospital

Discussion

Member takes

Implication

No clinical implications for hyperhomocysteinemia; leaves open endothelium-dependent mechanisms in vascular research.

Key Points

To evaluate the impact of short-term exposure to homocysteine on the contractile properties of rat aortic tissue using in vitro and in vivo models.
Assessed contractile responses in vitro using cultured rat aortic rings exposed to homocysteine for 1 or 4 days.
Evaluated in vivo effects using aortic rings harvested from rats injected with homocysteine, saline, cysteine, or methionine at 24 hours and 4 days.
Conducted mechanistic assays via endothelial denudation (intimal rubbing), pharmacological inhibition (L-NAME, indomethacin), and Western blot analysis of eNOS and iNOS expression.
In vitro culture with homocysteine for 1 to 4 days did not alter aortic ring contraction, whereas in vivo injection reduced K+-induced contraction within 24 hours and decreased responses to both K+ (-27%) and noradrenaline (-56%) at 4 days.
Endothelial removal via intimal rubbing completely reversed contractile attenuation to K+ and noradrenaline, while L-NAME provided partial recovery and indomethacin had no effect.
Homocysteine-injected rats demonstrated a 2-fold increase in endothelial nitric oxide synthase (eNOS) and a 3-fold increase in inducible nitric oxide synthase (iNOS) protein expression in aortic endothelial cells.

Structured PICO

Population

Rat aortic tissue (in vitro and in vivo models)

Intervention

Short-term exposure to homocysteine (Hcy) via culture or injection for 1 to 4 days

Comparator

Saline, cysteine, or methionine injection (in vivo); untreated controls (in vitro)

Outcome

Contractile response of aortic rings to K+ and noradrenalinesurrogate

Short-term in vivo exposure to homocysteine depresses vascular smooth muscle contractility via an endothelium-dependent mechanism likely involving increased nitric oxide production.

Cite This Study

Wang et al. (2000) studied this question.

synapsesocial.com/papers/6a91286fca59a4cbdea150f6 https://doi.org/10.1139/cjpp-78-6-500

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Short-term exposure to homocysteine depresses rat aortic contractility by an endothelium-dependent mechanism

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Short-term exposure to homocysteine depresses rat aortic contractility by an endothelium-dependent mechanism

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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