Key result
Brief intraarterial infusion of TNF-alpha significantly increased basal forearm vascular resistance from 30.5 to 39.9 units (p<0.01) in healthy volunteers.
Why the study?
Does intraarterial TNF-alpha infusion impair basal and stimulated endothelium-dependent vasomotion in healthy volunteers?
Does intraarterial TNF-alpha infusion impair basal and stimulated endothelium-dependent vasomotion in healthy volunteers?
Absolute Event Rate: 39.9% vs 30.5%
p-value: p=<0.01
Brief exposure to TNF-alpha increases basal forearm vascular resistance, likely by increasing vasoconstrictor prostaglandins and reducing NO bioavailability, though stimulated NO release can overwhelm this dysfunction in healthy humans.
TNF-alpha may impair basal resistance-vessel vasomotion in healthy volunteers; leaves open its role in clinical endothelial dysfunction.
The aim of this study was to determine whether tumor necrosis factor (TNF)-alpha would impair basal and stimulated endothelium-dependent vasomotion in human resistance vessel. Changes in baseline and acetylcholine (ACh)-induced forearm vascular resistance (FVR) were measured plethysmographically before and after a low-dose intraarterial forearm infusion of TNF-alpha according to the following three protocols in healthy volunteers. In the condition without pretreatment, basal FVR was significantly increased by TNF-alpha (from 30.5 +/- 4.8 to 39.9 +/- 5.9 units; p < 0.01), whereas ACh-induced minimal FVR did not differ between pre- and post-TNF-alpha states. In the condition after pretreatment with the cyclooxygenase inhibitor acetylsalicylic acid, although the vascular effects of TNF-alpha on basal FVR appeared to be blocked (37.1 +/- 5.3 vs. 37.6 +/- 5.2; NS), ACh-induced minimal FVR did not differ between pre- and post-TNF-alpha states. In the condition after pretreatment with the nitric oxide (NO) synthase inhibitor N(G)-monomethyl-L-arginine, the vascular effect of TNF-alpha on basal FVR was diminished, and the ACh-induced maximal dilatory response was significantly blunted after TNF-alpha compared with before TNF-alpha (minimal FVR: 30.4 +/- 12.0 vs. 12.3 +/- 4.2 units; p < 0.05). These findings suggest that brief exposure of the human forearm resistance artery to TNF-alpha may increase basal bioavailability of the vasoconstrictor prostaglandin and reduce basal bioavailability of NO. In the stimulated condition, TNF-alpha-induced vascular dysfunction may be overwhelmed by increased NO bioavailability in healthy humans.
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Nakamura et al. (2000) studied Healthy volunteers. Tumor necrosis factor (TNF)-alpha vs. Baseline (before TNF-alpha) was evaluated on Basal forearm vascular resistance (FVR) without pretreatment (p=<0.01). Brief intraarterial infusion of TNF-alpha significantly increased basal forearm vascular resistance from 30.5 to 39.9 units (p<0.01) in healthy volunteers.
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