Abstract

IntroductionIntra-abdominal hypertension (IAH) is known as a common, serious complication in critically ill patients. Bacterial translocation and permeability changes are considered the pathophysiological bases for IAH-induced enterogenic endotoxemia and subsequent multiorgan failure. Nevertheless, the effects of slightly elevated intra-abdominal pressures (IAPs) on the intestinal mucosa and the associated mechanisms remain unclear.MethodsTo investigate the acute effects of different nitrogen pneumoperitoneum grades on colonic mucosa, male Sprague-Dawley rats were assigned to six groups with different IAPs (0 [control], 4, 8, 12, 16, and 20 mmHg, n = 6/group). During 90 min of exposure, we dynamically monitored the heart rate and noninvasive hemodynamic parameters. After gradual decompression, arterial blood gas analyses were conducted. Thereafter, structural injuries to the colonic mucosa were identified using light microscopy. Colon permeability was determined using the expression of tight junction proteins, combined with fluorescein isothiocyanate dextran (FD-4) absorption. The pro-oxidant-antioxidant balance was determined based on the levels of malondialdehyde (MDA) and antioxidant enzymes.ResultsIAH significantly affected the histological scores of the colonic mucosa, tight junction protein expression, mucosal permeability, and pro-oxidant-antioxidant balance. Interestingly, elevations of IAP that were lower than the threshold for IAH also showed a similar, undesirable effect. In the 8 mmHg group, mild hyponatremia, hypocalcemia, and hypoxemia occurred, accompanied by reduced blood and abdominal perfusion pressures. Mild microscopic inflammatory infiltration and increased MDA levels were also detected. Moreover, an 8-mm Hg IAP markedly inhibited the expression of tight junction proteins, although no significant differences in FD-4 permeability were observed between the 0- and 8-mmHg groups.ConclusionsAcute exposure to slightly elevated IAP may result in adverse effects on intestinal permeability and the pro-oxidant-antioxidant balance. Therefore, in patients with critical illnesses, IAP should be dynamically monitored and corrected, as soon as possible, to prevent intestinal mucosal injury and subsequent gut-derived sepsis.

Highlights

  • Intra-abdominal hypertension (IAH) is known as a common, serious complication in critically ill patients

  • Without timely and appropriate intervention, IAH may result in abdominal compartment syndrome (ACS), which is closely related to the pathophysiological changes caused by deteriorations in organ perfusion and microcirculation [4]

  • The results indicated that intra-abdominal pressures (IAPs) equal to or higher than the threshold for IAH (12 mmHg in adults and 10 mmHg in children) significantly inhibited HR and blood pressure (BP)

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Summary

Introduction

Intra-abdominal hypertension (IAH) is known as a common, serious complication in critically ill patients. Bacterial translocation and permeability changes are considered the pathophysiological bases for IAH-induced enterogenic endotoxemia and subsequent multiorgan failure. Intra-abdominal hypertension (IAH, sustained elevation of intra-abdominal pressure above 12 mmHg in adults and above 10 mmHg in children)is currently known as a common, serious complication in critically ill patients [1]. Without timely and appropriate intervention, IAH may result in abdominal compartment syndrome (ACS), which is closely related to the pathophysiological changes caused by deteriorations in organ perfusion and microcirculation [4]. Cheng et al directly detected the pathophysiological basis of IAH-induced intestinal damage. They observed that rabbit intestinal microcirculatory blood flow was reduced by 40% after 2 h of 15-mmHg IAP. The IAH-induced endotoxemia, following increased permeability, may be correlated with tight junction (TJ) damage

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