Introduction: Enoxaparin (Enox) is used in cardiovascular emergency and coronary angiography due to its effects on coagulation mechanisms. However, its effect on changing the structure of the exchange-inhibiting peptide present in the sodium-calcium exchanger, leading to the acceleration of its function and withdrawing calcium from the cell in overload situations could lead to a new therapeutic function, where the intracellular calcium overload would be deleterious, as in cardiac arrhythmias and myocardial infarction. Objective: To analyze the action of Enox on cardiac arrhythmias induced by ischemia and reperfusion (IR) in isolated rat hearts. Materials and method. Adult Wistar rats were sacrificed, hearts isolated and placed under perfusion in Langhendorf Model with Krebs solution (KS) and monitoring of the electrocardiogram. After 30 minutes in sinus rhythm, ischemia was performed with discontinuation of the KS for 5 min and then reconnected. They were divided into 2 groups: Control (n = 10), with IR without medication and Enox Group, with infusion of 2mg / kg, in the cannula that perfuses the heart, soon after initiation and support for 30 seconds of Ventricular Tachycardia (VT) or Torsade de Pointes (TP). In case of reversal of the arrhythmia, a new arrhythmia induction will be attempted with the same protocol. Monitoring is continued until asystole or completion scheduled for 60 minutes of experimentation. Results: The control group presented VT in 70% of hearts and total atrioventricular block (TAVB) in 30% of hearts, followed by asystole after 7 minutes in 100% of hearts, and no further attempt of ischemia was possible. In the Enox group, 60% of VT, 30% of TP and 10% of TAVB were observed. All arrhythmias were reversed between 10 and 15 seconds after infusion of Enox, with return and maintenance of sinus rhythm after medication. In this group, a new attempt was made to induce arrhythmia due to IR without success after 10 minutes of interruption of the arrhythmia by Enox and sinus rhythm was maintained until the interruption of the experimental protocol. Conclusion: Enoxaparin reverses arrhythmias triggered by IR, with its effect prolonging and protecting new events after infusion, as well as decreasing organ mortality in isolated hearts of rats.

Two similar proteolytic cascades lead to release of bradykinin and Lys‐bradykinin in tissues; these peptides act as autocoids, the first favouring blood clotting and endothelial protection, the second by initiating and maintaining tissue reactions to noxious stimuli. Kinin biological actions are mediated by two different receptor types, the constitutive B 2 which promotes initial reactions and the inducible B 1 which may later maintain mechanisms of defense and repair. Key Concepts Kinin–kallikrein system is a hormonal system that plays a major role in inflammation, blood pressure control, coagulation, pain and cellular proliferation. Kinin–kallikrein system involves coagulation factor XII (FXII), the complex of prekallikrein (PK) and high‐molecular‐weight kininogen (HK). Coagulation factor XII, also known as Hageman factor, is a plasma serine protease produced by hepatocytes. Factor XII activates factor XI and prekallikrein. Kallikreins (tissue and plasma kallikrein) are serine proteases that liberate kinins (bradykinin, BK and kallidin, KD) from the kininogens (HK and LK). High‐molecular‐weight kininogen and low‐molecular‐weight kininogen are precursors of the kinins, (HK) is precursor of BK and (LK) is precursor of KD. Bradykinin (BK) is a nonapeptide hormone with sequence Arg‐Pro‐Pro‐Gly‐Phe‐Ser‐Pro‐Phe‐Arg. BK is produced when kallikrein releases it from HK. Kallidin (KD) has the same amino acid sequence as Bradykinin with the addition of a Lysine at the N‐terminus, thus it is also called Lys‐BK. Kallidin is released from LK by tissue kallikrein. Kinins are potent hypotensive peptide hormones that are also involved in pain, neurotransmission, inflammation and cell proliferation processes. The various physiopathological actions of kinins are mediated by two receptor types, called B 1 R and B 2 R, which are G‐protein coupled receptors.

hospital stay had significantly lower enhancement in the late phase of preoperative MRI scan (290 vs. 365; p < 0.05). Conclusion: Preoperative MRI with liver specific contrast might be a helpful tool to identify patients endangered for postoperative death after extended liver resection.

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