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Background and Objectives Interpleural anesthesia blocks pain perception from the thoracoabdominal wall without impairment of leg function. Bilateral interpleural anesthesia is not recommended because of possible bilateral impairment of respiratory function. Infiltration of the retromediastinum with local anesthetic might cause bilateral thoracoabdominal somatic block and block of sympathetic afferents from the abdominal cavity without impairing respiration. Method Distribution of stained fluid was studied after injection into the retromediastinum through a catheter placed about 10 cm cephalad to the diaphragm via the esophageal hiatus in three human cadavers of normal size and in six anesthetized pigs of 20-30 kg. In the pigs, serum levels of bupivacaine were measured after injection of 10 mL of 0.5% bupivacaine stained with 1 mL of methylene blue. Results The injected Dye stained intercostal nerves 6-11 in cadavers and 5-12 in pigs symmetrically on both sides, along with the adjacent parts of the sympathetic chain and both vagal nerves but not the phrenic nerves. During the sampling period of 50-60 minutes, bupivacaine serum concentrations rose slowly to a maximum of 4.2 μg/mL. Conclusions Block of pain perception from the abdominal wall and cavity is possible by injection of local anesthetic into the retromediastinum via a catheter introduced through the esophageal diaphragm hiatus. The block would not be expected to impair respiratory or leg function. Its efficacy and safety have yet to be established.

In present study, lipid peroxidation products (thiobarbituric acid reactive substances (TBARS) and diene conjugates (DC)) and markers of blood antioxidant status (serum antioxidative capacity (AOC) and red blood cells glutathione (RBC-GSH)) were measured to compare the extent of oxidative stress in 12 cardiac surgery and 10 septic general surgery patients. In heart surgery, arterial TBARS were significantly increased 15 min after the start and 15 min after cessation of cardiopulmonary bypass, while AOC at these times was decreased. Eighteen hours after surgery all parameters, except antioxidative capacity, had returned to preoperative levels. In septic patients, the preoperative level of lipid peroxidation was significantly higher and antioxidative capacity lower than in heart surgery patients. Surgery had no influence on oxidative stress markers in this group of patients. Increase in lipid peroxidation and reduction in blood antioxidant capacity, induced either by sepsis or cardiopulmonary bypass, were of comparable extent.

Oxidative stress and subsequent lipid peroxidation have been suggested as pathogenetically important for postischaemic reperfusion injury. We studied the time-course of oxidative stress in 14 adults undergoing cardiac surgery, evaluating serum levels of lipid peroxidation products--diene conjugates (DC) and basal and Fe-stimulated thiobarbituric acid reactive substances (TBARS, FeTEBARS)--as well as markers of blood antioxidant status--serum antioxidative capacity (AOC) and red blood cell glutathione (RBC-GSH) at 6 perioperative time-points. Arterial TBARS were significantly increased 15 minutes after start of cardiopulmonary bypass, 5 minutes after release of aortic cross-clamp and 15 minutes after cessation of bypass, compared with the preoperative levels (respective means 20.8, 38.5, 34.8 vs 7.5 nmol/g protein, p0.05). AOC had decreased at these times (means 21.3, 18.1, 23.2 vs 34.9%, p0.05). The TBARS changes correlated with AOC decrease (r = 0.30, p0.001). Changes in serum DC and RBC-GSH were not statistically significant. All lipid peroxidation parameters had returned to preoperative levels on the following morning, while antioxidative capacity remained suppressed (28.1%, p0.05). These data demonstrate a definite time-course of oxidative stress markers in arterial blood during open-heart surgery.