Acute systemic inflammation impairs endothelium-dependent dilatation in humans

Citation
Ad. Hingorani et al., Acute systemic inflammation impairs endothelium-dependent dilatation in humans, CIRCULATION, 102(9), 2000, pp. 994-999
Citations number
38
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CIRCULATION
ISSN journal
0009-7322 → ACNP
Volume
102
Issue
9
Year of publication
2000
Pages
994 - 999
Database
ISI
SICI code
0009-7322(20000829)102:9<994:ASIIED>2.0.ZU;2-U
Abstract
Background-We tested the hypothesis that endothelial dysfunction underlies the association between an acute inflammatory episode and the transiently i ncreased risk of a cardiovascular event by examining the effects of an expe rimental inflammatory stimulus on endothelium-dependent vasodilation. Methods and Results-Salmonella typhi vaccine was used to generate a systemi c inflammatory response in healthy volunteers. In 12 subjects, dilatation o f the brachial artery to flow and to sublingual nitroglycerin (NTG) was rec orded (conduit vessel response), and in 6 subjects, venous occlusion plethy smography was used to measure forearm blood flow during intrabrachial infus ion of the endothelium-dependent dilators acetylcholine (ACh) and bradykini n (BK) and the endothelium-independent dilators NTG and verapamil (resistan ce vessel response). Responses were assessed 16 hours before and 8 and 32 h ours after vaccination. Vaccination resulted in elevations in white cell co unt and serum levels of interleukin-6 and interleukin-1 receptor antagonist . Eight hours after vaccination, resistance vessel responses to BK (P=0.009 9) and ACh (P=0.0414) were markedly attenuated, and brachial artery flow-me diated dilatation was depressed. Resistance vessel responses to verapamil a nd NTG were unchanged, as was the conduit vessel response to NTG, Thirty-tw o hours after vaccination, resistance vessel responses to BK and ACh had re turned to normal. Conclusions-S typhi vaccine generates a mild inflammatory reaction associat ed with temporary but profound dysfunction of the arterial endothelium in b oth resistance and conduit vessels to both physical and pharmacological dil ator stimuli. This finding might explain the association between infection and inflammation and the enhanced risk of an acute cardiovascular event.