February 6, 2004Cardiovascular ResearchOpen Access

Swelling-activated chloride current is activated in guinea pig cardiomyocytes from endotoxic shock

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Population

Guinea pig model of endotoxic shock induced by intravenous lipopolysaccharides

Design

Preclinical

Follow-up

5 hours

Authors

CCC.‐H. ChiangTaipei Medical University Hospital

Discussion

Member takes

Implication

ICl,swell may mediate APD shortening in endotoxic shock; hypothesis-generating for chloride blockade in septic arrhythmias.

Structured PICO

Population

Guinea pig model of endotoxic shock induced by intravenous lipopolysaccharides (10 mg/kg) (papillary muscles and single ventricular myocytes)

Intervention

ICl,swell blockers (9-anthracene carboxylic acid [9-AC] and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid [DIDS]), iNOS inhibitors (L-NIL and 1400 W), PKC activators (PMA and PDD), and glibenclamide

Outcome

Action potential duration at 90% of repolarization (APD90) and membrane current activationsurrogate

Swelling-activated chloride current is activated in guinea pig hearts during endotoxic shock, which, along with ATP-sensitive K+ current activation, contributes to electrophysiological derangements.

Cite This Study

C.‐H. Chiang (2004) studied this question.

synapsesocial.com/papers/6a7caa21e6f41aaf0bcf82b3 https://doi.org/10.1016/j.cardiores.2004.01.007

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