Studies of hemorrhagic and traumatic shock influence on liver oxygen tension: effects of a single large dose of dexamethasone.

Abstract

Liver surface oxygen tension in response to hemorrhagic shock (hs) and to combined hemorrhagic-traumatic shock (hts) as well as to hemorrhagic-traumatic shock with glucocorticoid application ( htsc ) has been studied using male rats (Wistar strain, 250-300 g b.w.). The animals were anaesthetized by i.p. injection of ketamine/xylazine. All animals were bled through a catheter inserted into the vena jugularis until a hypotension of 40 mm Hg mean arterial blood pressure (MAP) was attained. The hts rats were traumatized by fracturing the left tibia and crushing the adjacent muscle tissue with 45 N/2.25 cm2 for 5 minutes. The htsc animals were traumatized and treated with a single injection of a large pharmacological dose of dexamethasone (6-8 mg/kg b.w.). Initial surface Po2 of the liver was higher than published by others (29 +/- 7 mm Hg) probably due to the narcotic agents. Maximal blood withdrawal was 24.4 +/- 2.2 ml/kg b.w. for hs, 17.9 +/- 3.8 ml/kg b.w. for hts and 20.6 +/- 4.5 ml/kg b.w. for htsc rats. Liver surface Po2 decreased to zero mm Hg in response to hypovolemic hypotension in all rats. Retransfusion of the shed blood caused a MAP and surface Po2 increase to only about half of the initial levels in hts and htsc rats while in hs animals the initial values were approximated. The hts and htsc rats showed signs of progressive hypotension to about 45 mm Hg MAP within 90 minutes post retransfusion. Dexamethasone improved the arterial pH to 7.15 compared with 7.05 of the control. Pao2 was elevated to 60 mm Hg vs. 49 mm Hg of the control animals. The beneficial influence of glucocorticoids on liver surface Po2 has not been substantiated as would have been desirable for the patient. Nevertheless, from a physiological standpoint a positive trend in the liver O2 supply has been evaluated as a small right shift of the surface Po2 histogram as well as the blood gas and pH data.