Attenuation of liver ischemia-reperfusion-induced atrial dysfunction by external pacing but not by isoproterenol

Abstract

Remote ischemia–reperfusion detrimentally affects myocardial function by initially interfering with the rate of contraction. We investigated the usefulness of isoproterenol versus external electrical pacing in attenuating secondary functional damage of isolated Wistar rat atria. Atrial strips (n = 10/group) were bathed within oxygenated Krebs–Henseleit solution that exited from isolated livers that had been either perfused normally (controls) or underwent no flow (ischemia) for 2 h. In addition to one noninterventional ischemia-exposed strip group, a second group was externally paced at a fixed rate (55 pulses·min–1, 6 V) and a third "ischemia" group was treated with isoproterenol (0.1 mM), both interventions commencing upon the strips' exposure to the hepatic effluents. Control strips displayed unaltered contraction rate and systolic-generated tension during the 2-h exposure. Nontreated strips exposed to ischemic reperfusate experienced bradycardia compared with baseline values (7 ± 2 vs. 50 ± 12 beats·min–1, p < 0.05), followed <1-min later by a fall in the generated tension (11 ± 4 vs. 20 ± 6 mmHg, p < 0.05). The paced-ischemic strips displayed unaltered rate and force of contraction, whereas the addition of isoproterenol did not prevent deterioration in the rate and force of contraction (8 ± 3 beats·min–1, 12 ± 4 mmHg, respectively; p < 0.05 vs. baseline control ischemia-paced strips). Thus, external electrical pacing prevented liver ischemia–reperfusion-induced atrial strips' bradycardia and loss of contractility, while isoproterenol did not.Key words: ischemia, reperfusion, liver, atrium, dysfunction, isoproterenol, pacing.