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1 Department of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, NY, USA
2 Department of Pathology, College of Physicians and Surgeons of Columbia University, New York, NY, USA
* To whom correspondence should be addressed. E-mail: tl128{at}columbia.edu.
Local anesthetics are widely used during the perioperative period even in patients with pre-existing renal disease. However, local anesthestics have been shown to cause cell death in multiple cell lines including human kidney proximal tubule cells. We questioned whether local anesthetics potentiate renal dysfunction after ischemic-reperfusion (IR) injury in vivo. Rats were implanted with subcutaneous mini-osmotic pumps that continuously delivered lidocaine (2 mg/kg/hr), bupivacaine (0.4 mg/kg/hr), tetracaine (1 mg/kg/hr) or saline vehicle and six hours later the rats were subjected to 30 min. of renal ischemia or to sham operation. Renal function was assessed by measurement of plasma creatinine at 24 and 48 hrs after renal IR injury in the presence or absence of chronic infusions of local anesthetics and correlated to histological changes indicative of necrosis. The degree of renal apoptosis was assessed by three methods 1) DNA fragmentation detected by TUNEL staining, 2) DNA laddering detected following agarose gel electrophoresis and 3) morphologic identification of apoptotic tubules at the corticomedullary junction. We also measured the expression of the pro-inflammatory markers ICAM-1 and TNF
. Continuous local anesthetic infusion with renal IR injury resulted in an increased magnitude and duration of renal dysfunction compared to the saline infused IR group. Additionally, both apoptotic and necrotic renal cell death as well as inflammatory changes were significantly potentiated in local anesthetic treated rat kidneys. Local anesthetic infusion alone without IR injury had no effect on renal function. We conclude that local anesthetics potentiated renal injury after IR by increasing necrosis, apoptosis and inflammation.
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