Background: Because hearts in acute myocardial infarction are often prone to ischemia-reperfusion damage during cardiac surgery, we investigated the influence of intracellular crystalloid cardioplegia solution (CCP) and extracellular blood cardioplegia solution (BCP) on cardiac function, metabolism, and infarct size in a rat heart model of myocardial infarction. Methods: Following euthanasia, the hearts of 50 rats were quickly excised, cannulated, and inserted into a blood-perfused isolated heart apparatus. A regional myocardial infarction was created in the infarction group (18 hearts) for 120 min; the control group (32 hearts) was not subjected to infarction. In each group, either Buckberg BCP or Bretschneider CCP was administered for an aortic clamping time of 90 min. Functional parameters were recorded during reperfusion: coronary blood flow, left ventricular developed pressure (LVDP) and contractility (dp/dt max). Infarct size was determined by planimetry. The results were compared between the groups using analysis of variance or parametric tests, as appropriate. Results: Cardiac function after acute myocardial infarction, 90 min of cardioplegic arrest, and 90 min of reperfusion was better preserved with Buckberg BCP than with Bretschneider CCP relative to baseline (BL) values (LVDP 54 ± 11% vs. 9 ± 2.9% [p = 0.0062]; dp/dt max. 73 ± 11% vs. 23 ± 2.7% [p = 0.0001]), whereas coronary flow was similarly impaired (BCP 55 ± 15%, CCP 63 ± 17% [p = 0.99]). The infarct in BCP-treated hearts was smaller (25% of myocardium) and limited to the area of coronary artery ligation, whereas in CCP hearts the infarct was larger (48% of myocardium; p = 0.029) and myocardial necrosis was distributed unevenly to the left ventricular wall. Conclusions: In a rat model of acute myocardial infarction followed by cardioplegic arrest, application of BCP leads to better myocardial recovery than CCP.

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Study Objectives: Recent studies have demonstrated that coagulopathy following snake envenomation is a venom-induced consumption coagulopathy (VICC), in which venom activates coagulation factors at specific points rather than an entire pathway. The objectives of this study were to determine what factors are consumed when severe coagulopathy after Korean viper (Gloydius species) bite develops and what factors should be used to monitor the venom activity.Methods: We retrospectively investigated the medical records of 244 patients who were admitted to our emergency department (ED) from 2011 to 2016 due to snake envenomation. There were 25 patients (10.2%) of severe coagulopathy defined as international normalized ratio (INR) > 3.0 with or without unmeasurable activated partial thromboplastin time (aPTT) and/or hypofibrinogenemia (< 100 mg/dl). Coagulation factor levels were checked at onset of severe coagulopathy. The onset time, treatment, and recovery time of severe coagulopathy were noted.Results: Most cases of severe coagulopathy (23/25, 88.0%) developed lately (> 12 hours after the bite). All patients (20/20) showed hypofibrinogenemia. Decreased levels of factors II, V, and VIII were observed in 2 (10.5%), 10 (52.6%), and 3 (15.8%) patients, respectively, of the total 19 patients. Among these, 2 patients showed severe coagulation factor deficiency (< 30%) rather than fibrinogen in factor V. Fibrin(ogen) degradation product (FDP) and d-dimer levels were increased in all patients who were tested. Only 2 patients (of 19) showed a mildly decreased anti-thrombin III level. Increase of fibrinogen levels was paralleled by decrease of FDP levels as treatment with antivenin and fibrinogenrich product were started.Conclusions: This study showed isolated hypofibrinogenemia and hyperfibrin(ogen)olysis are major hematologic findings of VICC following Korean viper bite. We suggest that the FDP level reflect the effect of venom and should be monitored during treatment for severe coagulopathy.