Atenolol Attenuates Autonomic Dysfunction of Rat Jejunum Submitted to Cold Ischemic Preservation

In vitro studies have demonstrated that cold ischemic preservation (CIP) employed in small bowel transplantation produces loss of intestinal motility due to severe lesions of autonomic enteric nerves and that this autonomic dysfunction is attenuated by antioxidant agents. In this work, we investigated whether preservation with atenolol attenuated autonomic dysfunction of rat jejunum submitted to long-term CIP. Jejunal segments (2 cm) of Wistar rats (12 to 16 weeks old) were surgically isolated and preserved at 4°C in Ringer's lactate solution without (−) or with (+) 1 μmol/L atenolol (AT). After preservation for 12 hours, AT+ and AT− preparations were mounted in parallel in isolated organ baths containing 10 mL Tyrode's solution at 37°C for the study of neurogenic contractions evoked by electrical field stimulation (EFS; 10 to 30 Hz, 1-ms duration, 60 V) or by stimulation with nicotinic (nicotine, NIC) or muscarinic (carbachol, CCh) cholinoceptor agents as well as nicotine (hexamethonium, HEX) and muscarinic (atropine, ATR) antagonists. Contractions induced by EFS (30 Hz) were 46% higher in AT+ (0.38 ± 0.02 g) than AT− (0.26 ± 0.01 g), while contractions induced by NIC (1 mmol/L) were 84% higher in AT+ (0.46 ± 0.03 g) than in AT− (0.25 ± 0.02 g). In addition, contractions induced by CCh (1 mmol/L) were 34% higher in AT+ (0.87 ± 0.06 g) than in AT− (0.65 ± 0.08 g). EFS-, NIC-, and CCh-induced contractions were inhibited by pretreatment of jejunum with HEX or ATR (1 μmol/30 min), in AT+ and AT−. These results suggest that addition of atenolol in the preservation solution attenuated autonomic dysfunction of rat jejunum submitted to long-term CIP.