Provider: - Institution: - Data provided by Europeana Collections- Cilj: Istražiti učinak akutnoga povećanja unosa soli na postokluzivni hiperemični protok krvi mikrocirkulacije kože, razjasniti ...ulogu ciklooksigenaza (COX 1, 2) i njihova vazokonstriktornog produkta tromboksana (TXA2) u regulaciji tkivnoga protoka krvi te odrediti učinak antagonizma receptora AT1 (losartanom) na krvni protok u mikrocirkulaciji i plazmatsku razinu TXA2. Metode: Ispitanice su (N=64) održavale dijetu s niskim udjelom soli (<40 mmol Na dnevno) tijekom sedam dana te su istovremeno podijeljene u skupinu na dijeti s visokim udjelom soli (HSD skupina; nadomjesna sol-200 mmol Na/dan) i skupinu na dijeti s niskim udjelom soli (LSD skupina; placebo-0 mmol Na/dan). Reaktivnost mikrocirkulacije mjerena je tehnikom laser Doppler (LDF). Jedna skupina primila je 100 mg indometacina 90 minuta, a druga skupina 200 mg celekoksiba 180 minuta prije ponovljenoga LDF mjerenja nakon HSD. Jedan dio ispitanica iz LSD skupine primala je 50 mg losartana dnevno tijekom sedam dana. Plazmatske koncentracije stabilnoga metabolita TXA2 (TXB2), staničnih adhezijskih molekula (ICAM-1, VCAM-1, E-selektin) i endokana izmjerene su prije i nakon HSD, a TXB2 i poslije LS+losartan protokola. Rezultati: Nije bilo razlike u krvnom tlaku i pulsu nakon HSD, dok se krvni tlak značajno smanjio nakon LSD protokola. LSD nije imao utjecaj, a HSD je izazvao značajno pogoršanje u reaktivnosti mikrocirkulacije. Koncentracija sCAMs nije se značajno mijenjala nakon oba protokola, dok je koncentracija endokana bila značajno smanjena nakon HSD protokola. Indometacin nakon HSD doveo je do oporavka vaskularne reaktivnosti, dok celekoksib nije potaknuo značajnije promjene postokluzivne hiperemije. Koncentracija TXB2 značajno je porasla nakon HSD. I celekoksib i indometacin značajno su smanjili koncentraciju TXB2. LSD+losartan protokol uzrokovao je porast TBX2, bez promjene u krvnome tlaku i/ili protoku mikrocirkulacije kože. Zaključak: Jedan tjedan HSD uzrokovao je pogoršanje vaskularne reaktivnost mikrocirkulacije, koja se oporavila nakon primjene indometacina, a nije bila promijenjena nakon primjene celekoksiba. Kako su se povišene vrijednosti TBX2 izazvane HSD protokolom snizile nakon primjene celekoksiba, čini se da neki drugi vazokonstriktorni metabolit podrijetlom od ciklooksigenaza ima značajnu ulogu u regulaciji protoka krvi u mikrocirkulaciji tijekom promjene količine soli u prehrani. Inhibicija receptora AT1 može voditi aktivaciji receptora AT2 i/ili interakciji s TXA2/prostanoid receptorom, koji održavaju hiperemiju, unatoč povišenoj razini vazokostriktora TXA2. - Objective: To investigate the effect of acute salt loading on skin microcirculatory hyperemic blood flow and in particular the role of cyclooxygenase (COX 1,2) and its derived vasoconstrictor thromboxane (TXA2) in tissue blood flow regulation. To determine the effect of AT1 receptor antagonism using losartan on microcirculatory blood flow and on plasma level of TXA2. Methods: All participants (N=64) maintained specific low salt diet (<40 mmol Na/day) through 7 days and simultaneously were divided in two groups: high salt diet (HSD) group (salt supplement-200 mmol Na/day) and low salt diet (LSD) group (placebo supplement-0 mmol Na/day). Microvascular reactivity was assessed by laser Doppler flowmetry (LDF). One group received 100 mg of indomethacin 90 minutes, and another group 200 mg of celecoxib 180 minutes before repeated LDF measurement after HSD. One group of participants on LSD was given 50 mg/per day of losartan (LSD+losartan group) for 7 days. Plasma concentration of stable TXA2 metabolite TXB2, cell adhesion molecules ICAM-1, VCAM-1 and E-selectin and endocan were measured before and after diet protocols. Results: No significant changes in BP and HR occures after HSD, while BP was significantly reduced after LSD. While LSD didn't has significant effect, HSD caused significant impairment in microvascular reactivity. sCAMs didn’t change after both HSD and LSD, while endocan concentration significantly decreased after HSD. Indomethacin administration after HSD restored microvascular reactivity to control values, while celecoxib administration didn't induce significant change in post occlusion blood flow. Plasma TXB2 was increased after HSD. Both celecoxib and indomethacin significantly decreased TXB2 levels after HSD. LSD+losartan significantly increased TXB2 plasma levels without causing changes in microvasular reactivity. Conclusion: These results have shown that one week of HSD impaired microvascular reactivity that was restored after indomethacin administration and wasn't changed after celecoxib administration. Increased levels of TXB2 after HSD were decreased after celecoxib administration what suggests that some other COX-1 derived vasoconstrictor metabolite may play more significant role in regulation of microvascular blood flow during sodium manipulation. Blockade of AT1 receptor could lead to activation of AT2 receptors and/or interaction with TXA2/prostanoid receptors, which maintain hyperemia, despite the increased level of TXA2.- All metadata published by Europeana are available free of restriction under the Creative Commons CC0 1.0 Universal Public Domain Dedication. 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