Dataset Information

Total sleep deprivation alters endothelial function in rats: a nonsympathetic mechanism.

ABSTRACT:

Study objectives

Sleep loss is suspected to induce endothelial dysfunction, a key factor in cardiovascular risk. We examined whether sympathetic activity is involved in the endothelial dysfunction caused by total sleep deprivation (TSD).

Design

TWO GROUPS: TSD (24-h wakefulness), using slowly rotating wheels, and wheel control (WC).

Participants

Seven-month-old male Wistar rats.

Interventions

Pharmacological sympathectomy (reserpine, 5 mg/kg, intraperitoneal), nitric oxide synthase (NOS) inhibition (N (G)-nitro-L-arginine, 20 mg/kg, intraperitoneally 30 min before experiment) and cyclooxygenase (COX) inhibition (indomethacin, 5 mg/kg, intraperitoneally 30 min before experiment).

Measurements and results

In protocol 1, changes in heart rate (HR) and blood pressure were continuously recorded in the sympathectomized and non-sympathectomized rats. Blood pressure and HR increased during TSD in non-sympathectomized rats. In protocol 2, changes in skin blood flow (vasodilation) were assessed in the sympathectomized and non-sympathectomized rats using laser-Doppler flowmetry coupled with iontophoretic delivery of acetylcholine (ACh), sodium nitroprusside (SNP), and anodal and cathodal currents. ACh- and cathodal current-induced vasodilations were significantly attenuated after TSD in non-sympathectomized and sympathectomized rats (51% and 60%, respectively). In protocol 3, ACh-induced vasodilation was attenuated after NOS and COX inhibition (66% and 49%, respectively). Cathodal current-induced vasodilation decreased by 40% after COX inhibition. In TSD compared to WC a decrease in ACh-induced vasodilation was still observed after COX inhibition. No changes in SNP- and anodal current-induced vasodilation were detected.

Conclusion

These results demonstrate that total sleep deprivation induces a reduction in endothelial-dependent vasodilation. This endothelial dysfunction is independent of blood pressure and sympathetic activity but associated with nitric oxide synthase and cyclooxygenase pathway alterations.

SUBMITTER: Sauvet F

PROVIDER: S-EPMC3920311 | biostudies-literature | 2014 Mar

REPOSITORIES: biostudies-literature

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Publications

Total sleep deprivation alters endothelial function in rats: a nonsympathetic mechanism.

Sauvet Fabien F Florence Geneviève G Van Beers Pascal P Drogou Catherine C Lagrume Christophe C Chaumes Cyrielle C Ciret Sylvain S Leftheriotis Georges G Chennaoui Mounir M

Sleep 20140301 3

<h4>Study objectives</h4>Sleep loss is suspected to induce endothelial dysfunction, a key factor in cardiovascular risk. We examined whether sympathetic activity is involved in the endothelial dysfunction caused by total sleep deprivation (TSD).<h4>Design</h4>TWO GROUPS: TSD (24-h wakefulness), using slowly rotating wheels, and wheel control (WC).<h4>Participants</h4>Seven-month-old male Wistar rats.<h4>Interventions</h4>Pharmacological sympathectomy (reserpine, 5 mg/kg, intraperitoneal), nitric ...[more]

PMID: 24587568

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Dataset Information

Total sleep deprivation alters endothelial function in rats: a nonsympathetic mechanism.

Study objectives

Design

Participants

Interventions

Measurements and results

Conclusion

Publications

Total sleep deprivation alters endothelial function in rats: a nonsympathetic mechanism.

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