The effect of hemorrhagic shock on the reactivity of feline middle cerebral (MCA), mesenteric (MES), brachial (BRACH), renal (REN), and hepatic (HEP) arteries was studied in vitro. In sodium pentobarbital-treated cats, a steady level of hypotension (50 mm Hg) was reached by bleeding into a reservoir and maintained by further bleeding or autotransfusion during 2 h (shock). Rings of the arteries (from control animals and from animals after shock) were suspended for isometric tension recording in organ chambers. The experiments were performed in the presence of indomethacin and propranolol to inhibit cyclooxygenase and β-adrenoceptors, respectively. Contractions induced by norepinephrine were enhanced in REN, whereas serotonin-evoked contractions were facilitated in MCA and REN, and depressed in BRACH significantly. The responses to prostaglandin F(2α) remained unchanged in all vessels studied. Endothelium-dependent relaxations induced by acetylcholine were enhanced at lower (10-8 M) and inhibited at higher (10-6 M) concentrations in MCA and MES, and they were inhibited in REN, whereas the responses of BRACH and HEP were not affected significantly. Endothelium-dependent, ATP-induced dilations were inhibited in MCA, REN, and HEP and not affected in MES and BRACH. Adenosine-induced relaxations were inhibited only in MCA and MES. The present study suggests an impairment of the endothelial function in hemorrhagic shock, with marked regional heterogeneities. Possible mechanisms underlying the impairment of the endothelial function are discussed. The altered reactivity of the arteries might play a role in the development of various pathophysiological phenomena during hemorrhagic shock.
- Endothelium-dependent relaxation
- Endothelium-derived relaxing factor
- Hemorrhagic shock
- Isolated arteries
- Regional differences
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine