Purpose: To study the effect of dexmedetomidine on myocardial ischemia-reperfusion injury (MI/RI)- induced imbalance on oxidant-prooxidant status and apoptotic changes in rats. Methods: Ninety (90) male Wistar rats were randomly divided into three groups – sham, model and post-treatment. In model rats, the anterior descending branch of the left coronary artery was ligated for 25 min, prior to their being subjected to reperfusion for 2 h. Rats in the post-treatment group were subjected to ligation at the anterior descending branch of the left coronary artery for 25 min, but they were intravenously injected with dexmedetomidine at a dose of 10 μg/kg prior to reperfusion. There was no ligation in the sham group. Malondialdehyde (MDA), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were assayed. Lactate dehydrogenase (LDH) and creatine kinase isoenzyme (CK-MB) levels were also evaluated. Apoptosis was measured with TdT-mediated dUTP nick end labeling (TUNEL) assay. Results: Compared with the sham group, MDA level in the model group was significantly rose, while SOD and GSH-Px activities were markedly decreased (p < 0.05). Moreover, there were higher LDH and CK-MB activities in model rats than in the sham rats, but they were significantly lower in the posttreatment group than in the model group (p < 0.05). Apoptosis was higher in model rats than in sham operation rats, but was markedly decreased in post-treatment rats than in model rats (p < 0.05). Conclusion: Post-treatment with dexmedetomidine exerts myocardial protective effect via significant reduction in oxidative stress-induced myocardial injury and apoptosis. Keywords: Dexmedetomidine, Myocardial ischemia-reperfusion injury, Antioxidant status, Programmed cell death

Purpose: To investigate the effect of morphine preconditioning on myocardial ischemia reperfusion injury in heart failure rats, and the  mechanism(s) of action involvedMethods: Seventy-two healthy male Sprague-Dawley rats were assigned to 4 groups: sham, model, morphine-preconditioning and SB203580 inhibitor groups, each with 18 rats. The expressions of P-p38, p-glycogen synthetase kinase-3, and p-gap junction protein 43 in rat myocardial cells were assayed by Western blotting. The mRNA expression levels of Bcl-2 and Bax, and Bcl-2/Bax were determined using real-time fluorescence quantitative PCR.Results: The expression levels of P-p38, p-glycogen synthetase kinase-3, p-gap junction protein 43, Bcl-2 mRNA and Bcl-2/Bax were significantly higher in the pretreatment group than in the model group, while Bax mRNA was significantly lower (p < 0.05). Moreover, the mRNA expression levels of P-p38, pglycogen synthetase kinase-3, p-gap junction protein, Bcl-2, and Bcl-2/Bax in inhibitor-treated rats decreased significantly, when compared to the values for pretreatment rats; furthermore, Bax mRNA was markedly upregulated (p < 0.05).Conclusion: Morphine preconditioning significantly inhibits the expressions of GSK-3β and Cx43 signaling proteins, as well as apoptosis-related gene, Bcl-2 and Bax. In addition, it inhibits the apoptosis of rat cardiomyocytes, and reduces myocardial injury, after ischemia reperfusion, via activation of the p38 MARK signaling pathway. This provides a new strategy for clinical reduction of myocardial injury after ischemia-reperfusion. Keywords: Morphine, Pretreatment, GSK-3β/Cx43 signaling protein, Bcl-2/Bax, Heart failure, Ischemiareperfusion injury

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This study was aimed at exploring the efficacy of morphine combined with mechanical ventilation in the treatment of heart failure with artificial intelligence algorithms. The cardiac magnetic resonance imaging (MRI) under the watershed segmentation algorithm was proposed, and the local grayscale clustering watershed (LGCW) model was designed in this study. A total of 136 patients with acute left heart failure were taken as the research objects and randomly divided into the control group (conventional treatment) and the experimental group (morphine combined with mechanical ventilation), with 68 cases in each group. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular ejection fraction (LVEF), N-terminal pro-brain natriuretic peptide (NT-proBNP), arterial partial pressure of oxygen (PaO2), and arterial partial pressure of carbon dioxide (PaCO2) were observed. The results showed that the mean absolute deviation (MAD) and maximum mean absolute deviation (max-MAD) of the LGCW model were lower than those of the fuzzy k-nearest neighbor (FKNN) algorithm and local gray-scale clustering model (LGSCm). The Dice metric was also significantly higher than that of other algorithms with statistically significant differences ( P < 0.05 ). After treatment, LVEDD, LVESD, and NT-proBNP of patients in the experimental group were significantly lower than those in the control group, and LVEF in the experimental group was higher than that in the control group ( P < 0.05 ). PaO2 of patients in the experimental group was also significantly higher than that in the control group ( P < 0.05 ). It suggested that the LGCW model had a better segmentation effect, and morphine combined with mechanical ventilation gave a better clinical efficacy in the treatment of acute left heart failure, improving the patients’ cardiac function and arterial blood gas effectively.