Anesth Prog. 1991;38:128–41.PubMed 11. Kahokehr A, Sammour T, Vather R, Taylor M, Stapelberg F, Hill AG. Systemic levels of local anaesthetic after intra-peritoneal application–a systematic review. Anaesth Intensive Care. 2010;38(4):623–38.PubMed 12. Benowitz NL, Meister W. Clinical Akt inhibitor pharmacokinetics of lignocaine. Clin Pharmacokinet. 1978;3:177–201. 13. Oral E, Olive DL, Arici A. The peritoneal environment in endometriosis. Hum Reprod Update. 1996;2(5):385–98.PubMedCrossRef 14. DiZerega GS, Rodgers KE. The peritoneum. New York: Springer; 1992. 15. Koninckx PR,

Kennedy SH, Barlow DH. Endometriotic disease: the role of peritoneal fluid. Hum Reprod Update. 1998;4(5):741–51.PubMedCrossRef 16. Narchi P, Benhamou D, Bouaziz H, Fernandez H, Mazoit JX. Serum concentrations of local anaesthetics following intraperitoneal ARN-509 price administration during laparoscopy. Eur J Clin Pharmacol. 1992;42:223–5.PubMedCrossRef 17. Wickström K, Bruse C, Sjösten A, Spira J, Edelstam G. Pertubation with lignocaine as a new treatment of dysmenorrhea due to endometriosis: a randomized controlled trial. Hum Reprod. 2012;27(3):695–701.PubMedCrossRef 18. Masse RI, Dunbar RW. Plasma lidocaine concentrations after caudal, lumbar, epidural, axillary block, and intravenous regional anesthesia. Anesthesiology. 1966;27(3):574–9.”
“1 Introduction

Acute myocardial infarction (AMI) CRT0066101 triggers an ischemic state in the myocardium, after which a process of remodeling is initiated by gradual myocardial ventricular dilation, hypertrophy, and distortion of left ventricular (LV) geometry [1]. The remodeling process, which can be categorized into the two phases of early (≤72 h) and late (>72 h) [2], is considered to be a determinant of mortality and morbidity in patients after AMI [3]. Several mechanisms contribute to the remodeling process, including myocardial cell death, fibrotic changes in cardiomyocytes following collagen synthesis, and inflammation due to increased

expression of pro-inflammatory cytokines [4–6]. Ischemia following AMI provoked an increase in the level of main pro-fibrotic cytokine, transforming growth factor (TGF)-β, which induces fibrotic depositions in the cardiomyocytes [7]. TGF-β plays a significant role in the pathogenesis of the remodeling process, as its inhibition in the proliferative Resveratrol phase of remodeling can prevent the LV from hypertrophy and decrease the extent of fibrosis in the non-infarcted segments of the myocardium and improve LV geometry [8, 9]. On the other hand, AMI is associated with acute up-regulation of pro-inflammatory cytokines, with tumor necrosis factor (TNF)-α being the most important [10]. TNF-α stimulated the remodeling process and provoked myocardial dysfunction after AMI [11–13]. Moreover, TNF-α can increase the expression of angiotensin receptor in the cardiac fibroblasts of animal models, which increased the activity of angiotensin and therefore induced fibrotic changes [14].