2015年 · 第95卷第19期

Sudden out-of-hospital cardiac arrest (OHCA) is the main cause of death in developed countries, with an annual incidence rate of 36~128/100,000, and the incidence of sudden cardiac death in China is 41.8/100,000^[1,2,3]With the improvement of the pre-hospital "survival chain", the number of hospitalizations of resuscitation patients has gradually increased. Autopsy and emergency coronary angiography (CAG) studies have revealed that more than 70% of patients have obvious coronary lesions, and registered and observational studies have shown that emergency coronary diagnosis and treatment strategies [referring to CAG aimed at percutaneous coronary intervention (PCI)] significantly improve mortality and neurological recovery in patients with OHCA^[2]。 Although both European and American guidelines have made recommendations on coronary diagnosis and treatment strategies for surviving patients with OHCA, some key questions of clinical concern have not been answered^[2,4,5]。 It is necessary to explore some key issues when making clinical decisions about coronary diagnosis and treatment strategies in patients with OHCA.

Vitamin D is not only related to calcium and phosphorus metabolism, but also has the functions of immune regulation and inflammation control. Studies have shown that vitamin D deficiency in critically ill patients is closely related to poor prognosis, and vitamin D supplementation may benefit critically ill patients. Therefore, vitamin D may play a positive role in the treatment of critically ill patients, and may become a new target for the treatment of critically ill patients. Its application value and application prospect for the treatment of critically ill patients deserve our attention.

calpastatin (CAST) is an endogenous and specific inhibitor of calpain (CAPN). It can identify CAPN versus Ca^2＋Binding to the conformational changes caused by binding and specifically binding to it, plays a negative regulatory role. CAST is involved in the signal transduction process of numerous physiological and pathological changes, and is closely related to various diseases of the nervous system. In recent years, the role of CAST in neurological diseases has been widely paid attention to, and it is closely related to the pathogenesis of neurological diseases. The latest progress in this field is reviewed.

Sepsis and its caused septic shock are the most important causes of infection death worldwide, and the mortality rate of severe sepsis exceeds 20%^[1]。 Organ insufficiency caused by sepsis and its shock is the direct cause of threatening the life and quality of life of patients. Among them, the proportion of acute kidney injury (AKI) in patients with septic shock can be as high as 40% ~50%, the mortality of patients can be increased by 6~8 times, and the probability of renal fibrosis and progression to chronic kidney disease in patients is greatly increased^[2,3]。 The pathophysiological mechanisms of sepsis-associated AKI, or infectious acute kidney injury (SAKI), are not fully understood and may be responsible for its high morbidity and mortality. Renal hypoperfusion is one of the main causes of ischemic AKI. However, more and more animal and clinical evidence show that renal blood flow does not decrease or even increases when SAKI occurs^[4,5]。 Meanwhile, Murugan et al.^[6]In the study of nosocomial acquired pneumonia, it was found that in many patients with mild sepsis, although hemodynamics were not affected, SAKI could still occur. Therefore, the renal hypoperfusion of SAKI may be relative, and many previous studies have attempted to improve the prognosis of SAKI by moderately increasing the relative hypoperfusion. Unfortunately, it remains difficult to determine the degree of perfusion that can improve patient prognosis. Multiple large-scale RCT studies on fluid resuscitation in sepsis have shown that increased fluid infusion, increased red blood cell transfusion, more vasoactive drug use, or increased mean arterial pressure, although theoretically increased blood perfusion in the kidney, did not reduce the incidence and associated prognosis of AKI^[1,7,8]。 Obviously, in addition to hemodynamics, there are many factors involved in the pathophysiological process of SAKI. Probability of acute tubular necrosis (ATN) in renal epithelial cells in AKI<5%^[9,10]It can be seen that ATN is not the main pathological change of SAKI. After AKI, there were no obvious structural changes in renal tubular epithelial cells, but the pathological manifestations were heterogeneous changes in renal tubular epithelial cells, vacuolation in the brush margin of epithelial cells, less cell necrosis and apoptosis^[9,10,11]。

Acute respiratory distress syndrome (ARDS) is one of the leading causes of death in critically ill patients. Although the mortality rate of ARDS has decreased with the in-depth research and the continuous progress of clinical treatment measures, the research shows that the mortality rate of ARDS is still as high as 40%^[1]。 However, the clinical treatment of ARDS still stays at the level of supportive treatment such as mechanical ventilation and restricted fluid rehydration, and there is no effective drug treatment so far. Mesenchymal stem cells (MSC) have multidirectional differentiation potential. After migrating to the site of lung injury, they can differentiate into alveolar epithelial cells and pulmonary microvascular endothelial cells, thus repairing the damaged lung tissue structure and protecting lung function. In recent years, many studies have found that MSC can also paracrine a variety of protective factors^[2]Including growth factors, anti-apoptotic factors, anti-inflammatory and pro-inflammatory factors, chemokines, antimicrobial peptides, and the like^[3]They all play an active role in maintaining lung tissue structure and function^[4], is considered to be an extremely important mechanism for MSC to treat ARDS.