Szabó C, Faragó M, Horváth I, Lohinai Z, Kovách A G
Experimental Research Department, Semmelweis University Medical School, Budapest, Hungary.
Circ Shock. 1992 Mar;36(3):238-41.
The effect of hemorrhagic shock on the vasodilatory responses of the feline renal artery was studied in vitro. In sodium pentobarbital anaesthetized cats, a steady level of hypotension (50 mm Hg) was reached by bleeding into a reservoir and maintained at this level by further bleeding or autotransfusion for 2 hr (shock). One to 3 mm long rings of the arteries (from control and shocked animals) were suspended for isometric tension recording in organ chambers filled with modified Krebs-Henseleit solution, aerated with 95% O2-5% CO2 at 37 degrees C. The experiments were performed in the presence of indomethacin and propranolol to inhibit cyclooxygenase activity and beta-adrenoceptors, respectively. Endothelium-dependent relaxations induced by acetylcholine and ATP were significantly inhibited in the vessels after hemorrhagic shock. In contrast, endothelium-independent vasodilation induced by adenosine remained unchanged after this shock state. The present results suggest a marked and selective impairment of the endothelial function of the renal artery of hemorrhagic shock. This alteration of the renovascular reactivity might play an important role in the development of vasoconstriction in the renal vasculature during and after this hemorrhagic shock state.
