BackgroundIntra-abdominal hypertension and abdominal compartment syndrome contribute significantly to increased morbidity and mortality in critically ill patients. This study describes pathophysiologic effects of the acutely elevated intra-abdominal pressure on microvascular fluid exchange and microcirculation. The resulting changes could contribute to development of organ dysfunction or failure.Methods16 pigs were randomly allocated to a control-group (C-group) or an interventional group (P-group). After 60 min of stabilization, intra-abdominal pressure of the P-group animals was elevated to 15 mmHg by Helium insufflation and after 120 min to a level of 30 mmHg for two more hours. The C-group animals were observed without insufflation of gas. Laboratory and hemodynamic parameters, plasma volume, plasma colloid osmotic pressure, total tissue water content, tissue perfusion, markers of inflammation and cerebral energy metabolism were measured and net fluid balance and fluid extravasation rates calculated. Analysis of variance for repeated measurements with post-tests were used to evaluate the results with respect to differences within or between the groups.ResultsIn the C-group hematocrit, net fluid balance, plasma volume and the fluid extravasation rate remained essentially unchanged throughout the study as opposed to the increase in hematocrit (P < 0.001), fluid extravasation rate (P < 0.05) and decrease in plasma volume (P < 0.001) of the P-group. Hemodynamic parameters remained stable or were slightly elevated in the C-group while the P-group demonstrated an increase in femoral venous pressure (P < 0.001), right atrial pressure (P < 0.001), pulmonary capillary wedge pressure (P < 0.01) and mean pulmonary arterial pressure (P < 0.001). The protein mass decreased in both study groups but was significantly lower in the P-group as compared with the C-group, after 240 min of intervention. The increased intra-abdominal pressure was associated with elevated intracranial pressure and reduced tissue perfusion of the pancreas and the gastric- and intestinal mucosa.ConclusionElevation of intra-abdominal pressure has an immediate impact on microvascular fluid extravasation leading to plasma volume contraction, reduced cardiac output and deranged perfusion of abdominal organs.
No differences in fluid extravasation rates were observed between sevoflurane and isoflurane. The increased net fluid balance in the sevoflurane group during cardiopulmonary bypass was not associated with edema generation. Plasma volume was retained in the sevoflurane group, in contrast to the isoflurane group.
No differences in microvascular fluid exchange could be demonstrated as a direct effect of DHCA compared with DHLF. Thirty minutes of DHCA was associated with anaerobic cerebral metabolism and possible brain injury.
Background: The portal vein could play a major role in disseminating the local inflammation of acute bacterial peritonitis since it is responsible for the venous drainage of the gastrointestinal tract. We hypothesized that after peritoneal exposure to Escherichia coli, a gradient between the portal and systemic levels of cytokines would be expected. Methods: Acute peritonitis was induced by depositing 200 ml of broth with live E. coli in the peritoneal cavity of the animals in the B-group (n = 7). They were then observed for 4 h and compared with a control group (C-group, n = 7). Tumour necrosis factor alpha (TNF-α), interleukin (IL)-6, IL-10 and vascular endothelial growth factor were measured repeatedly in the portal vein and the femoral artery. Portal vein metabolic markers (microdialysis), haemodynamics, biochemistry, plasma volume (PV), fluid shifts and total tissue water content were recorded or calculated. Results: The intervention led to PV contraction, increased fluid extravasation, increased pulmonary vascular resistance and reduced urinary output in the B-group as compared with the C-group. The levels of glucose in the portal vein were reduced in both study groups with no between-group differences. The levels of TNF-α and IL-6 increased markedly in the portal vein as well as in the systemic circulation of the B-group, but no gradient was seen between them. The corresponding levels of TNF-α and IL-6 remained low and stable in the C-group. Conclusion: The portal vein appears to play a minor role in supplying TNF-α and IL-6 to the systemic circulation after peritoneal exposure to a substantial dose of E. coli.
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