Abdominal organ perfusion and inflammation in experimental sepsis: a magnetic resonance imaging study.

Diffusion-weighted magnetic resonance imaging (DW-MRI) uses water as contrast and enables the study of perfusion in many organs simultaneously in situ. We used DW-MRI in a hypodynamic sepsis model, comparing abdominal organ perfusion with global hemodynamic measurements and inflammation. Sixteen anesthetized piglets were randomized into 3 groups: 2 intervention (sepsis) groups: HighMAP (mean arterial pressure, MAP > 65 mmHg) and LowMAP (MAP between 50 and 60 mmHg), and a Healthy Control group (HC). Sepsis was obtained with endotoxin and the desired MAP maintained with norepinephrine. After 6 h, DW-MRI was performed. Acute inflammation was assessed with IL-6 and TNFα in abdominal organs, ascites, and blood and by histology of intestine (duodenum). Perfusion of abdominal organs was reduced in the LowMAP group compared with the HighMAP group and HC. Liver perfusion was still reduced by 25% in the HighMAP group compared with HC. Intestinal perfusion did not differ significantly between the intervention groups. Cytokine concentrations were generally higher in the LowMAP group but did not correlate with global hemodynamics. However, cytokines correlated with regional perfusion and, for liver and intestine, also with intra-abdominal pressure. Histopathology of intestine worsened with decreasing perfusion. In conclusion, although a low MAP (≤60 mmHg) indicated impeded abdominal perfusion in experimental sepsis, it did not predict inflammation, nor did other global measures of circulation. Decreased abdominal perfusion partially predicted inflammation but intestine, occupying most of the abdomen, and liver were also affected by intra-abdominal pressure. NEW & NOTEWORTHY The study increases the knowledge of abdominal perfusion during sepsis. We used diffusion weighted imaging to assess perfusion simultaneously and noninvasively in different abdominal organs. The technique has not been used in a sepsis model before. Cytokine concentrations were measured in different abdominal organs and vascular beds and related to regional perfusion. Decreased abdominal perfusion, but not global measures of circulation, predicted inflammation. Intestine, occupying most of the abdomen, and liver were also affected by intra-abdominal pressure.

The Diaphragm Acts as a Brake during Expiration to Prevent Lung Collapse.

RATIONALE: The diaphragm is the major inspiratory muscle and is assumed to relax during expiration. However, electrical postinspiratory activity has been observed. Whether there is an expiratory diaphragmatic contraction that preserves lung patency has yet to be explored. OBJECTIVES: We hypothesized the occurrence of an expiratory diaphragmatic contraction directed at stabilizing peripheral airways and preventing or reducing cyclic expiratory lung collapse. METHODS: Mild acute respiratory distress syndrome was induced in 10 anesthetized, spontaneously breathing pigs. Lung volume was decreased by lowering end-expiratory airway pressure in a stepwise manner. We recorded the diaphragmatic electric activity during expiration, dynamic computed tomographic scans, and respiratory mechanics. In five pigs, the same protocol was repeated during mechanical ventilation after muscle paralysis. MEASUREMENTS AND MAIN RESULTS: Diaphragmatic electric activity during expiration increased by decreasing end-expiratory lung volume during spontaneous breathing. This enhanced the diaphragm muscle force, to a greater extent with lower lung volume, indicating a diaphragmatic electromechanical coupling during spontaneous expiration. In turn, the resulting diaphragmatic contraction delayed and reduced the expiratory collapse and increased lung aeration compared with mechanical ventilation with muscle paralysis and absence of diaphragmatic activity. CONCLUSIONS: The diaphragm is an important regulator of expiration. Its expiratory activity seems to preserve lung volume and to protect against lung collapse. The loss of diaphragmatic expiratory contraction during mechanical ventilation and muscle paralysis may be a contributing factor to unsuccessful respiratory support.