Microcirculation dysfunction in endotoxic shock rabbits is associated with impaired S-nitrosohemoglobin-mediated nitric oxide release from red blood cells: a preliminary study.

ABSTRACT: BACKGROUND:Microcirculation dysfunction with blood flow heterogeneity is an important characteristic in sepsis shock. We hypothesized that impaired ability of red blood cells to release nitric oxide resulted in microcirculation dysfunction in sepsis shock. METHODS:4,4'-Diisothiocyanatostilbene-2,2'-disulfonic acid disodium salt hydrate (DIDS), an inhibitor of band3 protein, was used to inhibit S-nitrosohemoglobin-mediated nitric oxide release. Rabbits were randomly divided into four groups: control (n =?6), lipopolysaccharide (LPS) (n =?6), LPS + DIDS (n =?6), and control + DIDS group (n =?6). Macrocirculation (cardiac output and mean arterial pressure) and microcirculation (microvascular flow index and flow heterogeneity index) parameters were recorded. At 2-h time point, arterial and venous S-nitrosohemoglobin concentrations were measured. RESULTS:The arterial-venous difference for S-nitrosohemoglobin in the LPS group was lower than the control group (27.3?±?5.0 nmmol/L vs. 40.9?±?6.2 nmmol/L, P?

SUBMITTER: Yao B 

PROVIDER: S-EPMC6323059 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature