Directly detected the pathophysiological basis of IAH-induced intestinal damage

In addition, bulkiness of fully structured WHy domain is more pronounced than that of intrinsically disordered hydrophilins. It was shown the larger the hydrodynamic radius of the dehydrins, the more effective their cryoprotant effect. LEAP class 2 and hydrophilins function as molecular shields, and their intrinsic disorder is required to be effective as cryoprotectant. LEAPs, hydrophilins and WHy domain protect membranes against dehydration, but their protective action differ. LEAPs intrinsic disorder may provide hydrophilic surfaces ordering water molecules around proteins that stabilize these proteins. Hydrophilins act as molecular shields via their intrinsic structural flexibility and prevent protein structure modification that is affected when water molecules are removed in the absence of a hydrophilin. It was also proposed that hydrophilins mediate interactions with their target proteins or stabilize active conformation of enzymes. Since recent studies provided no evidence for a membrane protective function of three LEAPs from class 8, it can be hypothesized that WHy domain protects against water deficit rather through stabilization of membrane-bound proteins. The assumption of Battaglia et al. was based on few LEAPs sequences. This works provide new insights in LEAPs family: hydrophilins are likely a subset of the LEAPs family and belong to LEAP class 2 also called dehydrins. Without timely and appropriate intervention, IAH may result in abdominal compartment syndrome, which is closely related to the pathophysiological changes caused by deteriorations in organ perfusion and microcirculation. Among the organ systems frequently affected by IAH, the intestine is the most susceptible. Ischemic injury and subsequent reperfusion-induced oxidative damage are involved in the development of IAH.Intestinal ischemia triggers the enhancement of intestinal permeability, bacterial translocation, and the subsequent systematic inflammatory response. These, in turn, cause capillary leakage that leads to bowel edema, thus further worsening the IAH and leading to a morbidity-ischemia cycle. They observed that rabbit intestinal microcirculatory blood flow was reduced by 40% after 2 h of 15-mmHg IAP. The blood flow was further reduced to 81% when the IAP was increased to 25 mmHg for 6 h. The IAH-induced endotoxemia, following increased permeability, may be correlated with tight junction damage. Although the adverse effects of IAH have received much attention, the effects of slightly elevated IAPs Perifosine Akt inhibitor remain unclear. Despite critically ill patients, the intraperitoneal pressures in adults are rarely more than 5–7 mmHg, which is within the acceptable normal range for such patients. In fact, based on the IAH diagnostic standards, 60% of adults in the intensive care unit have slightly elevated IAPs of 5–12 mmHg; the corresponding range for children is approximately 4–10 mmHg. This level of IAP is also considered to be dangerous. Sfez et al. and Baroncini et al. observed that mild elevations of IAP, induced by the carbon dioxide pneumoperitoneum that is commonly used during laparoscopic surgeries, influences the respiratory and cardiocirculatory parameters of children.

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