Electrophysiological alterations in diaphragm muscle caused by abdominal ischemia-reperfusion

Ischemia-reperfusion injury is the major complication of abdominal aortic surgery, and it mainly affects the lower extremities and remote organs. In the present study, the electrophysiological alterations in diaphragm that underlie the post-operative respiratory dysfunction were investigated. Wistar Albino rats were randomly divided into two groups: SHAM (only laparotomy was performed) and IR (abdominal aorta was clamped for 30min and reperfused for 2h). Following the operational period diaphragm muscles were isolated and electrophysiological experiments were carried out in-vitro. 3nM Ryanodine application, Na⁺ and K⁺ current blockage (0.3mM 4-Aminopyridine and 127mM N-methyl-d-glukamine) experiments were also conducted to further reveal any alterations. Twitch and tetanic force were decreased significantly. Action potential overshoot, amplitude and area were increased while diaphragm muscle cells were found to be hyperpolarized significantly. Mechanical alterations were shown to be caused by deterioration of Ca⁺⁺ homeostasis. At resting state, a decrease in persistent Na⁺ current was found. The reshaping of action potential, on the other hand, was shown to be due to altered kinetics of Na⁺ channels and delayed activation of voltage dependent K⁺ channels.