Objective. Our experiments were aimed at probing whether urocortin I postconditioning was beneficial for maintaining the mitochondrial respiratory function and inhibiting the surging of reactive oxygen species. In addition, our experiments also intended to reveal the relationships between urocortin I postconditioning and mitochondrial ATP-sensitive potassium channel. Methods. Langendorff and MPA perfusion systems were used to establish myocardial ischemia-reperfusion injury model and cardiomyocytes hypoxia-reoxygenation injury model in rats, respectively. Isolated hearts and cardiomyocytes were randomly divided into normal group, ischemia-reperfusion/hypoxia-reoxygenation group, urocortin I postconditioning group, and 5-hydroxysolanoic acid (5-HD)+urocortin I group. At the end of balance (T1) and reperfusion (T2), cardiac functions, mitochondrial state3 respiratory, respiratory control ratio, mitochondrial respiratory enzyme activity, and mitochondrial cardiolipin content were measured. Our experiments also observed the ultrastructure of myocardium. The changes of cardiomyocyte mitochondrial permeability transition pore, mitochondrial membrane potential, reactive oxygen species, expression of apoptosis protein, and cardiomyocytes activity were detected at the end of reoxygenation. Results. The cardiac functions, mitochondrial respiratory function, and enzyme activity of the normal group were better than other three groups at T2, and urocortin I postconditioning group was better than the IR group and 5-HD+urocortin I group. LVEDP, +dp/dtmax, mitochondrial respiratory function, and enzyme activity of IR group were worse than 5-HD+urocortin I group. Cardiolipin content of the normal group was higher than the other three groups at T2, urocortin I postconditioning group was higher than the IR group and 5-HD+urocortin I group, and 5-HD+urocortin I group was still higher than the IR group. The ultrastructure of the normal group maintained the most integrated than the other groups, IR group suffered the most serious damage, and ultrastructure of the urocortin I postconditioning group was better than the IR group and 5-HD+urocortin I group. At the end of reoxygenation, activity of mitochondrial permeability transition pore and generation of reactive oxygen species of normal group were lower than the other groups, HR group and 5-HD+urocortin I group were higher than the urocortin I postconditioning group, and 5-HD+urocortin I group was still higher than the urocortin I postconditioning group. Normal group had the highest level of mitochondrial membrane potential at the end of reoxygenation, and the urocortin I postconditioning group was higher than the HR group and 5-HD+urocortin I group. The normal group had the lowest expression level of Bax and the highest expression level of Bcl-2 at the end of reoxygenation. Urocortin I postconditioning group had lower Bax expression but higher Bcl-2 expression than the HR and 5-HD+urocortin I group. Accordingly, the normal group had the highest activity of cardiomyocytes, and the urocortin I postconditioning group was higher than the HR group and 5-HD+urocortin I group. Conclusions. Urocortin I postconditioning can protect the activity of cardiomyocytes after hypoxia-reoxygenation injury, improve the mitochondrial respiratory function, and enhance the contractility of isolated heart after myocardial ischemia-reperfusion injury. The alleviation of myocardial injury relates to the opening of mitochondrial ATP-sensitive potassium channel.

Hypertensive crisis and paroxysmal supraventricular tachycardia are serious adverse reactions that can lead to fatal consequences. We reported a 28-year-old woman who underwent emergency cesarean section of her first fetus due to pelvic outlet stenosis and had a hypertensive crisis, merging with paroxysmal supraventricular tachycardia after dezocine was administrated during the procedure. Her symptoms returned to normal after esmolol and urapidil were administrated. In order to rule out hypertension crisis caused by other diseases, the anesthesiologist immediately accessed the thyroid function, myocardial enzymes, catecholamines, and arterial blood gas analysis of the patient. No obvious abnormality was found in all the test results. We infer the conclusion that the symptoms of this patient during the operation were most likely related to dezocine administration. This case highlights the need to pay attention to possible malignant adverse reactions while using dezocine during cesarean section, and we recommend the immediate use of α-receptor blockers and/or β-receptor blockers in situations like to avoid serious complications caused by supraventricular tachycardia.

Background: Dezocine is a novel opioid receptor-antagonistic analgesic, which is widely used in clinic work. However, its usage in cesarean section is rare.Case presentation: A 28-year-old woman of 38 weeks' gestation (163cm, 79kg) underwent emergency cesarean section because of pelvic outlet stenosis in November 2021. There was no history of preeclampsia, anticoagulation, or hemorrhagic diathesis. The most recent electrocardiogram (ECG) during pregnancy was sinus tachycardia, and the heart rate (HR) was 108 beats/min. After the accomplishment of spinal anesthesia, the cesarean section started smoothly. After the fetus was delivered, the patient complained of pain when suturing the skin. The anesthesiologist gave her dezocine 5mg and the parturient presented with hypertensive crisis merging paroxysmal supraventricular tachycardia (PSVT). The fastest HR was 178 beats/min and the highest blood pressure (BP) was 190/128mmHg. After Esmolol 20mg and Urapidil 12.5mg were administrated, her HR and BP returned normal range 3min later. After observation, the patient returned to the ward one hour later and left hospital after 5 days. The patient denied the history of PSVT and hyperthyroidism.Conclusion: Nowadays，dizocine has been widely used in the area of postoperative analgesia. However, its usage is rare in obstetrics and gynecology. The malignant adverse reactions of dizocine needs to be highly vigilant.